Hospital Dermatology: Review of Research in 2023-2024

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Hospital Dermatology: Review of Research in 2023-2024

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13

In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

References
  1. Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
  2. Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
  3. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
  4. Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
  5. Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
  6. Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
  7. Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
  8. Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
  9. Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
  10. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
  11. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
  12. Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
  13. Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
  14. Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
  15. Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
  16. Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
  17. Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
  18. Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
  19. Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
  20. Chebani R, Lombart F, Chaby G, et al; French Study Group on ­Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
  21. Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
  22. Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
  23. Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
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Author and Disclosure Information

Dr. Wei is from the Department of Dermatology, University of Washington, Seattle. Dr. Micheletti is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Dr. Wei has no relevant financial disclosures to report. Dr. Micheletti is a consultant for Vertex and has received research grants from Amgen, Boehringer Ingelheim, Cabaletta Bio, and InflaRX.

Presented in part at the Society of Dermatology Hospitalists Annual Meeting; March 8, 2024; San Diego, California.

Correspondence: Robert G. Micheletti, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Blvd, PCAM 7 South, Room 724, Philadelphia, PA 19104 (robert.micheletti@pennmedicine.upenn.edu).

Cutis. 2024 November;114(5):156-158, 168. doi:10.12788/cutis.1126

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Author and Disclosure Information

Dr. Wei is from the Department of Dermatology, University of Washington, Seattle. Dr. Micheletti is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Dr. Wei has no relevant financial disclosures to report. Dr. Micheletti is a consultant for Vertex and has received research grants from Amgen, Boehringer Ingelheim, Cabaletta Bio, and InflaRX.

Presented in part at the Society of Dermatology Hospitalists Annual Meeting; March 8, 2024; San Diego, California.

Correspondence: Robert G. Micheletti, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Blvd, PCAM 7 South, Room 724, Philadelphia, PA 19104 (robert.micheletti@pennmedicine.upenn.edu).

Cutis. 2024 November;114(5):156-158, 168. doi:10.12788/cutis.1126

Author and Disclosure Information

Dr. Wei is from the Department of Dermatology, University of Washington, Seattle. Dr. Micheletti is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Dr. Wei has no relevant financial disclosures to report. Dr. Micheletti is a consultant for Vertex and has received research grants from Amgen, Boehringer Ingelheim, Cabaletta Bio, and InflaRX.

Presented in part at the Society of Dermatology Hospitalists Annual Meeting; March 8, 2024; San Diego, California.

Correspondence: Robert G. Micheletti, MD, Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Blvd, PCAM 7 South, Room 724, Philadelphia, PA 19104 (robert.micheletti@pennmedicine.upenn.edu).

Cutis. 2024 November;114(5):156-158, 168. doi:10.12788/cutis.1126

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Article PDF

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13

In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

Inpatient consultative dermatology has advanced as a subspecialty and increasingly gained recognition in recent years. Since its founding in 2009, the Society of Dermatology Hospitalists has fostered research and education in hospital dermatology. Last year, we reviewed the 2022-2023 literature with a focus on developments in severe cutaneous adverse reactions, supportive oncodermatology, cost of inpatient services, and teledermatology.1 In this review, we highlight 3 areas of interest from the 2023-2024 literature: severe cutaneous adverse drug reactions, skin and soft tissue infections, and autoimmune blistering diseases (AIBDs).

Severe Cutaneous Adverse Drug Reactions

Adverse drug reactions are among the most common diagnoses encountered by inpatient dermatology consultants.2,3 Severe cutaneous adverse drug reactions are associated with substantial morbidity and mortality. Efforts to characterize these conditions and standardize their diagnosis and management continue to be a major focus of ongoing research.

A single-center retrospective analysis of 102 cases of drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome evaluated differences in clinical manifestations depending on the culprit drug, offering insights into the heterogeneity of DRESS syndrome and the potential for diagnostic uncertainty.4 The shortest median latency was observed in a case caused by penicillin and cephalosporins (12 and 18 days, respectively), while DRESS syndrome secondary to allopurinol had the longest median latency (36 days). Nonsteroidal anti-inflammatory drug–induced DRESS syndrome was associated with the shortest hospital stay (6.5 days), while cephalosporin and vancomycin cases had the highest mortality rates.4

In the first international Delphi consensus study on the diagnostic workup, severity assessment, and management of DRESS syndrome, 54 dermatology and/or allergy experts reached consensus on 93 statements.5 Specific recommendations included basic evaluation with complete blood count with differential, kidney and liver function parameters, and electrocardiogram for all patients with suspected DRESS syndrome, with additional complementary workup considered in patients with evidence of specific organ damage and/or severe disease. In the proposed DRESS syndrome severity grading scheme, laboratory values that reached consensus for inclusion were hemoglobin, neutrophil, and platelet counts and creatinine, transaminases, and alkaline phosphatase levels. Although treatment of DRESS syndrome should be based on assessed disease severity, treatment with corticosteroids should be initiated in all patients with confirmed DRESS syndrome. Cyclosporine, antibodies interfering with the IL-5 axis, and intravenous immunoglobulins can be considered in patients with corticosteroid-refractory DRESS syndrome, and antiviral treatment can be considered in patients with a high serum cytomegalovirus viral load. Regularly following up with laboratory evaluation of involved organs; screening for autoantibodies, thyroid dysfunction, and steroid adverse effects; and offering of psychological support also were consensus recommendations.5

Identifying causative agents in drug hypersensitivity reactions remains challenging. A retrospective cohort study of 48 patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) highlighted the need for a systematic unbiased approach to identifying culprit drugs. Using the RegiSCAR database and algorithm for drug causality for epidermal necrolysis to analyze the cohort, more than half of causative agents were determined to be different from those initially identified by the treating physicians. Nine additional suspected culprit drugs were identified, while 43 drugs initially identified as allergens were exonerated.6

Etiology-associated definitions for blistering reactions in children have been proposed to replace the existing terms Stevens-Johnson syndrome, toxic epidermal necrolysis, and others.7 Investigators in a recent study reclassified cases of SJS and TEN as reactive infectious mucocutaneous eruption (RIME) or drug-induced epidermal necrolysis (DEN), respectively. In RIME cases, Mycoplasma pneumoniae was the most commonly identified trigger, and in DEN cases, anticonvulsants were the most common class of culprit medications. Cases of RIME were less severe and were most often treated with antibiotics, whereas patients with DEN were more likely to receive supportive care, corticosteroids, intravenous immunoglobulins, and other immunosuppressive therapies.7

In addition to causing acute devastating mucocutaneous complications, SJS and TEN have long-lasting effects that require ongoing care. In a cohort of 6552 incident SJS/TEN cases over an 11-year period, survivors of SJS/TEN endured a mean loss of 9.4 years in life expectancy and excess health care expenditures of $3752 per year compared with age- and sex-matched controls. Patients with more severe disease, comorbid malignancy, diabetes, end-stage renal disease, or SJS/TEN sequelae experienced greater loss in life expectancy and lifetime health care expenditures.8 Separately, a qualitative study investigating the psychological impact of SJS/TEN in pediatric patients described sequelae including night terrors, posttraumatic stress disorder, depression, and anxiety for many years after the acute phase. Many patients reported a desire for increased support for their physical and emotional needs following hospital discharge.9

Skin and Soft Tissue Infections: Diagnosis, Management, and Prevention

Dermatology consultation has been shown to be a cost-effective intervention to improve outcomes in hospitalized patients with skin and soft tissue infections.10,11 In particular, cellulitis frequently is misdiagnosed, leading to unnecessary antibiotic use, hospitalizations, and major health care expenditures.12 Recognizing this challenge, researchers have worked to develop objective tools to improve diagnostic accuracy. In a large prospective prognostic validation study, Pulia et al13 found that thermal imaging alone or in combination with the ALT-70 prediction model (asymmetry, leukocytosis, tachycardia, and age ≥70 years) could be used successfully to reduce overdiagnosis of cellulitis. Both thermal imaging and the ALT-70 prediction model demonstrated robust sensitivity (93.5% and 98.8%, respectively) but low specificity (38.4% and 22.0%, respectively, and 53.9% when combined).13

In a systematic review, Kovacs et al14 analyzed case reports of pseudocellulitis caused by chemotherapeutic medications. Of the 81 cases selected, 58 (71.6%) were associated with gemcitabine, with the remaining 23 (28.4%) attributed to pemetrexed. Within this group, two-thirds of the patients received antibiotic treatment prior to receiving the correct diagnosis, and 36% experienced interruptions to their oncologic therapies. In contrast to infectious cellulitis, which tends to be unilateral and associated with elevated erythrocyte sedimentation rate or C-reactive protein, most chemotherapy-induced pseudocellulitis cases occurred bilaterally on the lower extremities, while erythrocyte sedimentation rate and C-reactive protein seldom were elevated.14

Necrotizing soft tissue infections (NSTIs) are severe life-threatening conditions characterized by widespread tissue destruction, signs of systemic toxicity, hemodynamic collapse, organ failure, and high mortality. Surgical inspection along with intraoperative tissue culture is the gold standard for diagnosis. Early detection, prompt surgical intervention, and appropriate antibiotic treatment are essential to reduce mortality and improve outcomes.15 A retrospective study of patients with surgically confirmed NSTIs assessed the incidence and risk factors for recurrence within 1 year following an initial NSTI of the lower extremity. Among 93 included patients, 32 (34.4%) had recurrence within 1 year, and more than half of recurrences occurred in the first 3 months (median, 66 days). The comparison of patients with and without recurrence showed similar proportions of antibiotic prophylaxis use after the first NSTI. There was significantly less compression therapy use (33.3% vs 62.3%; P=.13) and more negative pressure wound therapy use (83.3% vs 63.3%; P=.03) in the recurrence group, though the authors acknowledged that factors such as severity of pain and size of soft tissue defect may have affected the decisions for compression and negative pressure wound therapy.16

Residents of nursing homes are a particularly vulnerable population at high risk for health care–associated infections due to older age and a higher likelihood of having wounds, indwelling medical devices, and/or coexisting conditions.17 One cluster-randomized trial compared universal decolonization with routine-care bathing practices in nursing homes (N=28,956 residents). Decolonization entailed the use of chlorhexidine for all routine bathing and showering and administration of nasal povidone-iodine twice daily for the first 5 days after admission and then twice daily for 5 days every other week. Transfer to a hospital due to infection decreased from 62.9% to 52.2% with decolonization, for a difference in risk ratio of 16.6% (P<.001) compared with routine care. Additionally, the difference in risk ratio of the secondary end point (transfer to a hospital for any reason) was 14.6%. The number needed to treat was 9.7 to prevent 1 infection-related hospitalization and 8.9 to prevent 1 hospitalization for any reason.17

Autoimmune Blistering Diseases

Although rare, AIBDs are potentially life-threatening cutaneous diseases that often require inpatient management. While corticosteroids remain the mainstay of initial AIBD management, rituximab is now well recognized as the steroid-sparing treatment of choice for patients with moderate to severe pemphigus. In a long-term follow-up study of Ritux 318—the trial that led to the US Food and Drug Administration approval of rituximab in the treatment of moderate to severe pemphigus vulgaris—researchers assessed the long-term efficacy and safety of rituximab as a first-line treatment in patients with pemphigus.19 The 5- and 7-year disease-free survival rates without corticosteroid therapy for patients treated with rituximab were 76.7% and 72.1%, respectively, compared with 35.3% and 35.3% in those treated with prednisone alone (P<.001). Fewer serious adverse events were reported in those treated with rituximab plus prednisone compared with those treated with prednisone alone. None of the patients who maintained complete remission off corticosteroid therapy received any additional maintenance infusions of rituximab after the end of the Ritux 3 regimen (1 g of rituximab at day 0 and day 14, then 500 mg at months 12 and 18).19

By contrast, treatment of severe bullous pemphigoid (BP) often is less clear-cut, as no single therapeutic option has been shown to be superior to other immunomodulatory and immunosuppressive regimens, and the medical comorbidities of elderly patients with BP can be limiting. Fortunately, newer therapies with favorable safety profiles have emerged in recent years. In a multicenter retrospective study, 100 patients with BP received omalizumab after previously failing to respond to at least one alternative therapy. Disease control was obtained after a median of 10 days, and complete remission was achieved in 77% of patients in a median time of 3 months.20 In a multicenter retrospective cohort study of 146 patients with BP treated with dupilumab following the atopic dermatitis dosing schedule (one 600-mg dose followed by 300 mg every 2 weeks), disease control was achieved in a median of 14 days, while complete remission was achieved in 35.6% of patients, with 8.9% relapsing during the observation period.21 A retrospective case series of 30 patients with BP treated with dupilumab with maintenance dosing frequency tailored to individual patient response showed complete remission or marked response in 76.7% (23/30) of patients.22 A phase 2/3 randomized controlled trial of dupilumab in BP is currently ongoing (ClinicalTrials.gov identifier NCT04206553).

Pemphigoid gestationis is a rare autoimmune subepidermal bullous dermatosis of pregnancy that may be difficult to distinguish clinically from polymorphic eruption of pregnancy but confers notably different maternal and fetal risks. Researchers developed and validated a scoring system using clinical factors—history of pemphigoid gestationis, primigravidae, timing of rash onset, and specific clinical examination findings—that was able to differentiate between the 2 diseases with 79% sensitivity, 95% specificity, and an area under the curve of 0.93 without the need for advanced immunologic testing.23

Final Thoughts

Highlights of the literature from 2023-2024 demonstrate advancements in hospital-based dermatology as well as ongoing challenges. This year’s review emphasizes key developments in severe cutaneous adverse drug reactions, skin and soft tissue infections, and AIBDs. Continued expansion of knowledge in these areas and others informs patient care and demonstrates the value of dermatologic expertise in the inpatient setting.

References
  1. Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
  2. Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
  3. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
  4. Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
  5. Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
  6. Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
  7. Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
  8. Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
  9. Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
  10. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
  11. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
  12. Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
  13. Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
  14. Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
  15. Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
  16. Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
  17. Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
  18. Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
  19. Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
  20. Chebani R, Lombart F, Chaby G, et al; French Study Group on ­Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
  21. Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
  22. Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
  23. Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
References
  1. Berk-Krauss J, Micheletti RG. Hospital dermatology: review of research in 2022-2023. Cutis. 2023;112:236-239.
  2. Falanga V, Schachner LA, Rae V, et al. Dermatologic consultations in the hospital setting. Arch Dermatol. 1994;130:1022-1025.
  3. Kroshinsky D, Cotliar J, Hughey LC, et al. Association of dermatology consultation with accuracy of cutaneous disorder diagnoses in hospitalized patients: a multicenter analysis. JAMA Dermatol. 2016;152:477-480.
  4. Blumenthal KG, Alvarez-Arango S, Kroshinsky D, et al. Drug reaction eosinophilia and systemic symptoms: clinical phenotypic patterns according to causative drug. J Am Acad Dermatol. 2024;90:1240-1242.
  5. Brüggen MC, Walsh S, Ameri MM, et al. Management of adult patients with drug reaction with eosinophilia and systemic symptoms: a Delphi-based international consensus. JAMA Dermatol. 2024;160:37-44.
  6. Li DJ, Velasquez GA, Romar GA, et al. Assessment of need for improved identification of a culprit drug in Stevens-Johnson syndrome/toxic epidermal necrolysis. JAMA Dermatol. 2023;159:830-836.
  7. Martinez-Cabriales S, Coulombe J, Aaron M, et al. Preliminary summary and reclassification of cases from the Pediatric Research of Management in Stevens-Johnson syndrome and Epidermonecrolysis (PROMISE) study: a North American, multisite retrospective cohort. J Am Acad Dermatol. 2024;90:635-637.
  8. Chiu YM, Chiu HY. Lifetime risk, life expectancy, loss-of-life expectancy and lifetime healthcare expenditure for Stevens-Johnson syndrome/toxic epidermal necrolysis in Taiwan: follow-up of a nationwide cohort from 2008 to 2019. Br J Dermatol. 2023;189:553-560.
  9. Phillips C, Russell E, McNiven A, et al. A qualitative study of psychological morbidity in paediatric survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis. Br J Dermatol. 2024;191:293-295.
  10. Li DG, Xia FD, Khosravi H, et al. Outcomes of early dermatology consultation for inpatients diagnosed with cellulitis. JAMA Dermatol. 2018;154:537-543.
  11. Milani-Nejad N, Zhang M, Kaffenberger BH. Association of dermatology consultations with patient care outcomes in hospitalized patients with inflammatory skin diseases. JAMA Dermatol. 2017;153:523-528.
  12. Weng QY, Raff AB, Cohen JM, et al. Costs and consequences associated with misdiagnosed lower extremity cellulitis. JAMA Dermatol. 2017;153:141-146.
  13. Pulia MS, Schwei RJ, Alexandridis R, et al. Validation of thermal imaging and the ALT-70 prediction model to differentiate cellulitis from pseudocellulitis. JAMA Dermatol. 2024;160:511-517.
  14. Kovacs LD, O’Donoghue M, Cogen AL. Chemotherapy-induced pseudocellulitis without prior radiation exposure: a systematic review. JAMA Dermatol. 2023;159:870-874.
  15. Yildiz H, Yombi JC. Necrotizing soft-tissue infections. comment. N Engl J Med. 2018;378:970.
  16. Traineau H, Charpentier C, Lepeule R, et al. First-year recurrence rate of skin and soft tissue infections following an initial necrotizing soft tissue infection of the lower extremities: a retrospective cohort study of 93 patients. J Am Acad Dermatol. 2023;88:1360-1363.
  17. Miller LG, McKinnell JA, Singh RD, et al. Decolonization in nursing homes to prevent infection and hospitalization. N Engl J Med. 2023;389:1766-1777.
  18. Joly P, Maho-Vaillant M, Prost-Squarcioni C, et al; French Study Group on Autoimmune Bullous Skin Diseases. First-line rituximab combined with short-term prednisone versus prednisone alone for the treatment of pemphigus (Ritux 3): a prospective, multicentre, parallel-group, open-label randomised trial. Lancet. 2017;389:2031-2040.
  19. Tedbirt B, Maho-Vaillant M, Houivet E, et al; French Reference Center for Autoimmune Blistering Diseases MALIBUL. Sustained remission without corticosteroids among patients with pemphigus who had rituximab as first-line therapy: follow-up of the Ritux 3 Trial. JAMA Dermatol. 2024;160:290-296.
  20. Chebani R, Lombart F, Chaby G, et al; French Study Group on ­Autoimmune Bullous Diseases. Omalizumab in the treatment of bullous pemphigoid resistant to first-line therapy: a French national multicentre retrospective study of 100 patients. Br J Dermatol. 2024;190:258-265.
  21. Zhao L, Wang Q, Liang G, et al. Evaluation of dupilumab in patients with bullous pemphigoid. JAMA Dermatol. 2023;159:953-960.
  22. Miller AC, Temiz LA, Adjei S, et al. Treatment of bullous pemphigoid with dupilumab: a case series of 30 patients. J Drugs Dermatol. 2024;23:E144-E148.
  23. Xie F, Davis DMR, Baban F, et al. Development and multicenter international validation of a diagnostic tool to differentiate between pemphigoid gestationis and polymorphic eruption of pregnancy. J Am Acad Dermatol. 2023;89:106-113.
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  • An international Delphi study reached consensus on 93 statements regarding workup, severity assessment, and management of DRESS syndrome.
  • In nursing homes, universal decolonization with chlorhexidine and nasal iodophor greatly reduced the risk for hospital transfers due to infection compared to routine care.
  • Rituximab as the first-line therapy for pemphigus vulgaris is associated with long-term sustained complete remission without corticosteroid therapy.
  • Dupilumab and omalizumab are emerging safe and effective treatment options for bullous pemphigoid.
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Emerging Insights in Keloid Pathogenesis and Therapeutics

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Emerging Insights in Keloid Pathogenesis and Therapeutics

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.1 While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.2 Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.3 There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,4 there is a considerable lack of focus on this population in the literature.5 Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.8

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.5 One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%9; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.8

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.18

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO2, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.19

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.20 To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices21; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO2 laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.22 Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.23 This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.23 This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.30 Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).31 These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.32

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.33 Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.34 Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

References
  1. Téot L, Mustoe TA, Middelkoop E, eds. Textbook on Scar Management: State of the Art Management and Emerging Technologies. Springer; 2020.
  2. Davis SA, Feldman SR, McMichael AJ. Management of keloids in the United States, 1990-2009: an analysis of the National Ambulatory Medical Care Survey. Dermatol Surg. 2013;39:988-994. doi:10.1111/dsu.12182
  3. Kassi K, Kouame K, Kouassi A, et al. Quality of life in black African patients with keloid scars. Dermatol Reports. 2020;12:8312. doi:10.4081/dr.2020.8312
  4. Delaleu J, Charvet E, Petit A. Keloid disease: review with clinical atlas. part I: definitions, history, epidemiology, clinics and diagnosis. Ann Dermatol Venereol. 2023;150:3-15. doi:10.1016/j.annder.2022.08.010
  5. Bronte J, Zhou C, Vempati A, et al. A comprehensive review of non-surgical treatments for hypertrophic and keloid scars in skin of color. Clin Cosmet Investig Dermatol. 2024;17:1459-1469. doi:10.2147/CCID.S470997
  6. Davison SP, Dayan JH, Clemens MW, et al. Efficacy of intralesional 5-fluorouracil and triamcinolone in the treatment of keloids. Aesthet Surg J. 2009;29:40-46. doi:10.1016/j.asj.2008.11.006
  7. Azzam OA, Bassiouny DA, El-Hawary MS, et al. Treatment of hypertrophic scars and keloids by fractional carbon dioxide laser: a clinical, histological, and immunohistochemical study. Lasers Med Sci. 2016;31:9-18. doi:10.1007/s10103-015-1824-4
  8. Ekstein SF, Wyles SP, Moran SL, et al. Keloids: a review of therapeutic management. Int J Dermatol. 2021;60:661-671. doi:10.1111/ijd.15159
  9. Morelli Coppola M, Salzillo R, Segreto F, et al. Triamcinolone acetonide intralesional injection for the treatment of keloid scars: patient selection and perspectives. Clin Cosmet Investig Dermatol. 2018;11:387-396. doi:10.2147/CCID.S133672
  10. Kant SB, van den Kerckhove E, Colla C, et al. A new treatment of hypertrophic and keloid scars with combined triamcinolone and verapamil: a retrospective study. Eur J Plast Surg. 2018;41:69-80. doi:10.1007/s00238-017-1322-y
  11. Cohen AJ, Talasila S, Lazarevic B, et al. Combination cryotherapy and intralesional corticosteroid versus steroid monotherapy in the treatment of keloids. J Cosmet Dermatol. 2023;22:932-936. doi:10.1111/jocd.15520
  12. Tawaranurak N, Pliensiri P, Tawaranurak K. Combination of fractional carbon dioxide laser and topical triamcinolone vs intralesional triamcinolone for keloid treatment: a randomised clinical trial. Int Wound J. 2022;19:1729-1735. doi:10.1111/iwj.13775
  13. Belie O, Ugburo AO, Mofikoya BO, et al. A comparison of intralesional verapamil and triamcinolone monotherapy in the treatment of keloids in an African population. Niger J Clin Pract. 2021;24:986-992. doi:10.4103/njcp.njcp_474_20
  14. Khalid FA, Mehrose MY, Saleem M, et al. Comparison of efficacy and safety of intralesional triamcinolone and combination of triamcinolone with 5-fluorouracil in the treatment of keloids and hypertrophic scars: randomised control trial. Burns. 2019;45:69-75. doi:10.1016/j.burns.2018.08.011
  15. Asilian A, Darougheh A, Shariati F. New combination of triamcinolone, 5-Fluorouracil, and pulsed-dye laser for treatment of keloid and hypertrophic scars. Dermatol Surg. 2006;32:907-915. doi:10.1111/j.1524-4725.2006.32195.x
  16. Kim WI, Kim S, Cho SW, et al. The efficacy of bleomycin for treating keloid and hypertrophic scar: a systematic review and meta-analysis. J Cosmet Dermatol. 2020;19:3357-3366. doi:10.1111/jocd.13390
  17. Kabel A, Sabry H, Sorour N, et al. Comparative study between intralesional injection of bleomycin and 5-fluorouracil in the treatment of keloids and hypertrophic scars. J Dermatol Dermatol Surg. 2016;20:32-38.
  18. Yang HA, Jheng WL, Yu J, et al. Comparative efficacy of drug interventions for keloids: a network meta-analysis. Ann Plast Surg. 2024;92(1S suppl 1):S52-S59. doi:10.1097/SAP.0000000000003759
  19. Preissig J, Hamilton K, Markus R. Current laser resurfacing technologies: a review that delves beneath the surface. Semin Plast Surg. 2012;26:109-116. doi:10.1055/s-0032-1329413
  20. Bin Dakhil A, Shadid A, Altalhab S. Post-inflammatory hyperpigmentation after carbon dioxide laser: review of prevention and risk factors. Dermatol Reports. 2023;15:9703. doi:10.4081/dr.2023.9703
  21. Kaushik SB, Alexis AF. Nonablative fractional laser resurfacing in skin of color: evidence-based review. J Clin Aesthet Dermatol. 2017;10:51-67.
  22. Foppiani JA, Khaity A, Al-Dardery NM, et al. Laser therapy in hypertrophic and keloid scars: a systematic review and network meta-analysis. Aesthetic Plast Surg. Published May 17, 2024. doi:10.1007/s00266-024-04027-9
  23. Diaz A, Tan K, He H, et al. Keloid lesions show increased IL-4/IL-13 signaling and respond to Th2-targeting dupilumab therapy. J Eur Acad Dermatol Venereol. 2020;34:E161-E164. doi:10.1111/jdv.16097
  24. Min MS, Mazori DR, Lee MS, et al. Successful treatment of keloids and hypertrophic scars with systemic and intralesional dupilumab. J Drugs Dermatol. 2023;22:1220-1222. doi:10.36849/JDD.6385
  25. Wittmer A, Finklea L, Joseph J. Effects of dupilumab on keloid stabilization and prevention. JAAD Case Rep. 2023;37:103-105. doi:10.1016/j.jdcr.2023.05.001
  26. Luk K, Fakhoury J, Ozog D. Nonresponse and progression of diffuse keloids to dupilumab therapy. J Drugs Dermatol. 2022;21:197-199. doi:10.36849/jdd.6252
  27. Tirgan MH, Uitto J. Lack of efficacy of dupilumab in the treatment of keloid disorder. J Eur Acad Dermatol Venereol. 2022;36:E120-E122. doi:10.1111/jdv.17669
  28. Berman B, Duncan MR. Pentoxifylline inhibits the proliferation of human fibroblasts derived from keloid, scleroderma and morphoea skin and their production of collagen, glycosaminoglycans and fibronectin. Br J Dermatol. 1990;123:339-346. doi:10.1111/j.1365-2133.1990.tb06294.x
  29. Berman B, Duncan MR. Pentoxifylline inhibits normal human dermal fibroblast in vitro proliferation, collagen, glycosaminoglycan, and fibronectin production, and increases collagenase activity. J Invest Dermatol. 1989;92:605-610.
  30. Tan A, Martinez Luna O, Glass DA 2nd. Pentoxifylline for the prevention of postsurgical keloid recurrence. Dermatol Surg. 2020;46:1353-1356. doi:10.1097/DSS.0000000000002090
  31. Serag-Eldin YMA, Mahmoud WH, Gamea MM, et al. Intralesional pentoxifylline, triamcinolone acetonide, and their combination for treatment of keloid scars. J Cosmet Dermatol. 2021;20:3330-3340. doi:10.1111/jocd.14305
  32. Zhou T, Chen Y, Wang C, et al. SIRT6 inhibits the proliferation and collagen synthesis of keloid fibroblasts through MAPK/ERK pathway. Discov Med. 2024;36:1430-1440. doi:10.24976/Discov.Med.202436186.133
  33. Zhang J, Zhang X, Guo X, et al. Remdesivir alleviates skin fibrosis by suppressing TGF-β1 signaling pathway. PLoS One. 2024;19:E0305927. doi:10.1371/journal.pone.0305927
  34. Zhao J, Zhai X, Xu Z, et al. Novel needle-type electrocoagulation and combination pharmacotherapy: basic and clinical studies on efficacy and safety in treating keloids. J Cosmet Dermatol. doi:10.1111/jocd.16453
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Noelle Desir is from Weill Cornell Medical College, New York, New York. Iain Noel Encarnacion is from Eastern Virginia Medical School, Norfolk. Dr. Taylor is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Noelle Desir and Iain Noel Encarnacion have no relevant financial disclosures to report. Dr. Taylor has served as a consultant, advisory board member, investigator, and/or speaker for AbbVie, Allergan Aesthetics, Arcutis, Armis Biopharma, Avita Medical, Beiersdorf, Biorez, Bristol-Myers Squibb, Cara Therapeutics, Catalyst Medical Education, Concert Pharmaceuticals, Croma-Pharma GmbH, Dermsquared, Dior, Eli Lilly and Company, EPI Health, Estée Lauder, Evolus, Galderma, GloGetter, Hugel America, Incyte, Johnson & Johnson Innovate Medicine, LearnSkin, L’Oreal USA, Medscape, MJH Life Sciences, Pfizer, Piction Health, Sanofi, Scientis US, UCB, and Vichy Laboratories. She also serves on the board of directors for Mercer Strategies; has received stock options for Armis Biopharma, GloGetter, and Piction Health; and has received royalties from McGraw-Hill.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA 19104 (susan.taylor@pennmedicine.upenn.edu).

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Noelle Desir is from Weill Cornell Medical College, New York, New York. Iain Noel Encarnacion is from Eastern Virginia Medical School, Norfolk. Dr. Taylor is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Noelle Desir and Iain Noel Encarnacion have no relevant financial disclosures to report. Dr. Taylor has served as a consultant, advisory board member, investigator, and/or speaker for AbbVie, Allergan Aesthetics, Arcutis, Armis Biopharma, Avita Medical, Beiersdorf, Biorez, Bristol-Myers Squibb, Cara Therapeutics, Catalyst Medical Education, Concert Pharmaceuticals, Croma-Pharma GmbH, Dermsquared, Dior, Eli Lilly and Company, EPI Health, Estée Lauder, Evolus, Galderma, GloGetter, Hugel America, Incyte, Johnson & Johnson Innovate Medicine, LearnSkin, L’Oreal USA, Medscape, MJH Life Sciences, Pfizer, Piction Health, Sanofi, Scientis US, UCB, and Vichy Laboratories. She also serves on the board of directors for Mercer Strategies; has received stock options for Armis Biopharma, GloGetter, and Piction Health; and has received royalties from McGraw-Hill.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA 19104 (susan.taylor@pennmedicine.upenn.edu).

Cutis. 2024 November;114(5):137-139. doi:10.12788/cutis.1122

Author and Disclosure Information

Noelle Desir is from Weill Cornell Medical College, New York, New York. Iain Noel Encarnacion is from Eastern Virginia Medical School, Norfolk. Dr. Taylor is from the Department of Dermatology, Perelman School of Medicine, University of Pennsylvania, Philadelphia.

Noelle Desir and Iain Noel Encarnacion have no relevant financial disclosures to report. Dr. Taylor has served as a consultant, advisory board member, investigator, and/or speaker for AbbVie, Allergan Aesthetics, Arcutis, Armis Biopharma, Avita Medical, Beiersdorf, Biorez, Bristol-Myers Squibb, Cara Therapeutics, Catalyst Medical Education, Concert Pharmaceuticals, Croma-Pharma GmbH, Dermsquared, Dior, Eli Lilly and Company, EPI Health, Estée Lauder, Evolus, Galderma, GloGetter, Hugel America, Incyte, Johnson & Johnson Innovate Medicine, LearnSkin, L’Oreal USA, Medscape, MJH Life Sciences, Pfizer, Piction Health, Sanofi, Scientis US, UCB, and Vichy Laboratories. She also serves on the board of directors for Mercer Strategies; has received stock options for Armis Biopharma, GloGetter, and Piction Health; and has received royalties from McGraw-Hill.

Correspondence: Susan C. Taylor, MD, Department of Dermatology, Perelman School of Medicine at the University of Pennsylvania, 3400 Civic Center Blvd, Philadelphia, PA 19104 (susan.taylor@pennmedicine.upenn.edu).

Cutis. 2024 November;114(5):137-139. doi:10.12788/cutis.1122

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Article PDF

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.1 While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.2 Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.3 There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,4 there is a considerable lack of focus on this population in the literature.5 Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.8

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.5 One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%9; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.8

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.18

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO2, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.19

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.20 To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices21; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO2 laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.22 Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.23 This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.23 This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.30 Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).31 These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.32

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.33 Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.34 Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

Keloids are fibroproliferative lesions caused by aberrant wound healing in predisposed individuals.1 While keloids have been reported in patients of all races and ethnicities, they most commonly develop in individuals of African or Asian descent.2 Often associated with symptoms such as pain and itching, keloids can be disfiguring and result in poorer quality of life.3 There is a paucity of research on keloid pathogenesis and efficacious therapeutics, particularly in patients with skin of color (SOC). Herein, we outline the current research on keloid treatment and highlight promising new therapies ranging from innovative intralesional techniques to advanced laser-based and biologic therapies.

Deficiencies in Skin of Color Research

Although keloids are 17 times more prevalent in patients with SOC,4 there is a considerable lack of focus on this population in the literature.5 Studies on keloids that include individuals with SOC often group patients of all skin types together, and subgroup analyses are not always performed.6,7 As a result, dermatologists may face considerable challenges in providing effective treatments for keloids in patients with SOC. With few evidence-based options available, patients with SOC who have keloids continue to experience impairments in quality of life.

Common Keloid Therapies

There currently is no gold-standard treatment for keloids. Common therapeutic modalities include intralesional corticosteroids (ILCs), antineoplastic agents and neuromodulators, laser-based devices, and surgical therapies (eg, excision), as well as combined medical and surgical techniques.8

Intralesional Corticosteroids—Minimally invasive ILCs are the first-line treatment in all patients with keloids, regardless of skin phototype. Because keloid formation results from trauma to the skin, ILCs often are recommended to minimize further skin damage.5 One meta-analysis found that ILCs have demonstrated success rates of 50% to 100%9; however, these studies frequently combine ILCs with other treatment modalities, and few studies have focused on the efficacy of ILC monotherapy in patients with SOC.6,10-13

Antineoplastic Agents and Neuromodulators—Certain antineoplastic agents (eg, 5-fluorouracil [5-FU] and bleomycin) and neuromodulators (eg, botulinum toxin A [BTA]) also have been studied in keloid management.8

5-Fluorouracil frequently is combined with ILCs such as triamcinolone (TAC). Combined therapy is more effective than TAC monotherapy in scar height reduction.14,15 Rates of adverse events such as dyspigmentation, atrophy, and telangiectasias also were lower in patients who received combined therapy.14,15 A systematic review found that intralesional bleomycin may be more effective than TAC alone, 5-FU alone, TAC combined with 5-FU, and TAC combined with cryotherapy; however, hyperpigmentation was a common adverse event, occurring in roughly 70% (42/60) of patients.16,17 Additionally, a 2024 meta-analysis evaluated 20 randomized controlled trials comprising 1114 patients treated with intralesional TAC, 5-FU, BTA, verapamil, and/or bleomycin. Botulinum toxin A and TAC plus 5-FU were found to have outstanding therapeutic efficacy for keloids, and rates of adverse events were similar among users of TAC, 5-FU, BTA, and TAC plus 5-FU.18

While antineoplastic agents and BTA may be promising keloid therapies, further studies demonstrating their efficacy and safety profiles are necessary, particularly regarding dyspigmentation as a potential adverse event, as this may be of concern in patients with darker phototypes.

Laser Therapies—Of all treatment modalities, laser-based keloid therapies have been the most robustly studied in SOC. The 2 main types are ablative (eg, CO2, Er:YAG) and nonablative (eg, pulsed dye, Nd:YAG) lasers. Ablative lasers rapidly heat water molecules within the skin, thereby vaporizing the skin cells in a controlled precise process that reduces scar tissue by removing layers of skin. Nonablative lasers target hemoglobin in blood vessels, reducing oxygen supply and inducing collagen remodeling without damaging the epidermis.19

For patients with SOC, lasers carry a risk for postinflammatory hyperpigmentation.20 To address this risk, recent advancements in laser technology and procedural protocols have aimed to minimize the number of passes and utilize cooling devices21; however, many of these recommendations are based on retrospective reviews and small case series. A 2024 meta-analysis comprising 550 patients found that the combination of fractional CO2 laser therapy and 5-FU was the most effective intervention, markedly reducing Vancouver Scar Scale and pliability scores as well as keloid thickness.22 Conversely, pulsed dye lasers were the least effective in terms of improving scar thickness, pigmentation, and pliability when compared to other treatments.

Randomized controlled trials of laser-based therapies in patients with SOC are lacking in the literature. Future studies should focus on calibrating laser-based therapies for those with darker skin tones and examine the efficacy and adverse effects of ablative and nonablative lasers in patients with SOC.

Promising New Keloid Therapies

Keloid disease pathogenesis is incompletely understood, but several new therapeutic targets have been highlighted in the literature, including dupilumab, pentoxifylline, sirtuin 6 (SIRT6) modulators, remdesivir, and needle-assisted electrocoagulation plus pharmacotherapy.

Dupilumab—An anti–IL-4 and IL-13 monoclonal antibody, dupilumab was first approved for the treatment of severe atopic dermatitis. Its use has broadened since its approval, and keloids have been identified as a potential therapeutic target. A 2019 case study described a 53-year-old Black man with severe atopic dermatitis and chronic keloids that regressed with systemic dupilumab therapy.23 This prompted a follow-up case-control study using real-time polymerase chain reaction testing to evaluate Th2 gene expression (IL-4R, IL-13, and CCL18) of lesional and nonlesional tissue in 3 Black patients with chronic keloids and no concurrent atopic dermatitis vs 5 healthy Black controls.Despite the limited sample size, a significant increase in IL-13 and the Th2 chemokine CCL18 was found in patients with keloids compared to controls (P<.05), suggesting that the entire integument of patients with severe keloids is abnormal.23 This finding supports the use of systemic treatments for chronic and multifocal keloid disease. Several subsequent case reports have corroborated the efficacy of systemic and/or intralesional dupilumab.24,25 However, some studies have reported contradictory findings, suggesting the need for high-quality clinical trials.26,27

Pentoxifylline—Pentoxifylline is a methylated xanthine derivative and a nonspecific phosphodiesterase ­inhibitor used to treat claudication from peripheral artery disease. It also inhibits the proliferation and rate of collagen synthesis of fibroblasts from keloids in vitro.28,29 A 2019 retrospective, open-label pilot study analyzed postsurgical keloid recurrence in 45 patients with 67 unique keloids that were stratified into low- and high-risk groups based on clinical factors including multiple symptomatic keloids, history of recurrence, and family history.30 Both the low- and the high-risk groups were treated with 40 mg/mL intralesional triamcinolone acetonide monthly for 6 months; however, some of the high-risk keloids also received pentoxifylline 300 mg 3 times daily for 6 months. There was a statistically significant decrease in keloid recurrence rate between the high-risk group treated with pentoxifylline and the low-risk group for whom pentoxifylline was not prescribed (P=.015).

Similarly, a randomized clinical trial comparing the efficacy of combination intralesional pentoxifylline and intralesional triamcinolone vs monotherapy with pentoxifylline or triamcinolone found the most significant improvement in the combination cohort with reduction in keloid height (P=.04), pliability (P=.003), and vascularity (P=.05).31 These findings highlight the need for supplementary studies on the use of pentoxifylline for keloid therapy.

SIRT6 Modulators—SIRT6 modulators are an exciting future therapeutic target. In a recent case-control study evaluating the histologic milieu of keloid tissue vs normal skin specimens, the researchers found that selective overexpression of SIRT6 via the use of a recombinant adenovirus in keloid fibroblasts attenuated proliferation, invasion, and collagen synthesis while fostering apoptosis, likely through the suppression of MAPK/ERK pathway activity.32

Remdesivir—The antiviral drug remdesivir has been reported to have pharmacologic activities in a wide range of fibrotic diseases, including keloids. A 2024 study explored the potential effect and mechanisms of remdesivir on skin fibrosis both in vitro and in rodents.33 Remdesivir was found to decrease skin fibrosis and attenuate the gross weight of keloid tissues in vivo, suppress fibroblast activation and autophagy both in vivo and in vitro, dampen fibroblast activation by the TGF-β1/Smad signaling pathway, and inhibit fibroblasts autophagy by the PI3K/Akt/mTOR signaling pathway. These results demonstrate the therapeutic potential of remdesivir for keloid management.

Needle-Assisted Electrocoagulation Plus Pharmacotherapy—A novel needle-assisted electrocoagulation technique combined with pharmacotherapy (corticosteroid and 5-FU injections) was effective in a Chinese clinical trial involving 6 patients with keloids.34 Investigators used Vancouver Scar Scale and both Patient and Observer Scar Assessment Scale scores to grade patients’ scars before treatment and 1 month after the first treatment cycle. They found that ablation combined with pharmacotherapy significantly reduced all 3 scores without any obvious adverse events (P=.004, P=.006, and P=.017, respectively). This novel combination treatment may serve as a safe and effective therapeutic approach for keloid removal.

Final Thoughts

Emerging treatments offer promising new horizons in keloid management; however, the lack of robust, high-quality clinical trials, especially those focusing on SOC, underscores a pressing need for comprehensive and inclusive studies. There is much work to be done to close the existing knowledge gap, and future studies must be more intentional with recruitment, assuring that the patients who are disproportionately affected by these lesions are represented in study populations.

References
  1. Téot L, Mustoe TA, Middelkoop E, eds. Textbook on Scar Management: State of the Art Management and Emerging Technologies. Springer; 2020.
  2. Davis SA, Feldman SR, McMichael AJ. Management of keloids in the United States, 1990-2009: an analysis of the National Ambulatory Medical Care Survey. Dermatol Surg. 2013;39:988-994. doi:10.1111/dsu.12182
  3. Kassi K, Kouame K, Kouassi A, et al. Quality of life in black African patients with keloid scars. Dermatol Reports. 2020;12:8312. doi:10.4081/dr.2020.8312
  4. Delaleu J, Charvet E, Petit A. Keloid disease: review with clinical atlas. part I: definitions, history, epidemiology, clinics and diagnosis. Ann Dermatol Venereol. 2023;150:3-15. doi:10.1016/j.annder.2022.08.010
  5. Bronte J, Zhou C, Vempati A, et al. A comprehensive review of non-surgical treatments for hypertrophic and keloid scars in skin of color. Clin Cosmet Investig Dermatol. 2024;17:1459-1469. doi:10.2147/CCID.S470997
  6. Davison SP, Dayan JH, Clemens MW, et al. Efficacy of intralesional 5-fluorouracil and triamcinolone in the treatment of keloids. Aesthet Surg J. 2009;29:40-46. doi:10.1016/j.asj.2008.11.006
  7. Azzam OA, Bassiouny DA, El-Hawary MS, et al. Treatment of hypertrophic scars and keloids by fractional carbon dioxide laser: a clinical, histological, and immunohistochemical study. Lasers Med Sci. 2016;31:9-18. doi:10.1007/s10103-015-1824-4
  8. Ekstein SF, Wyles SP, Moran SL, et al. Keloids: a review of therapeutic management. Int J Dermatol. 2021;60:661-671. doi:10.1111/ijd.15159
  9. Morelli Coppola M, Salzillo R, Segreto F, et al. Triamcinolone acetonide intralesional injection for the treatment of keloid scars: patient selection and perspectives. Clin Cosmet Investig Dermatol. 2018;11:387-396. doi:10.2147/CCID.S133672
  10. Kant SB, van den Kerckhove E, Colla C, et al. A new treatment of hypertrophic and keloid scars with combined triamcinolone and verapamil: a retrospective study. Eur J Plast Surg. 2018;41:69-80. doi:10.1007/s00238-017-1322-y
  11. Cohen AJ, Talasila S, Lazarevic B, et al. Combination cryotherapy and intralesional corticosteroid versus steroid monotherapy in the treatment of keloids. J Cosmet Dermatol. 2023;22:932-936. doi:10.1111/jocd.15520
  12. Tawaranurak N, Pliensiri P, Tawaranurak K. Combination of fractional carbon dioxide laser and topical triamcinolone vs intralesional triamcinolone for keloid treatment: a randomised clinical trial. Int Wound J. 2022;19:1729-1735. doi:10.1111/iwj.13775
  13. Belie O, Ugburo AO, Mofikoya BO, et al. A comparison of intralesional verapamil and triamcinolone monotherapy in the treatment of keloids in an African population. Niger J Clin Pract. 2021;24:986-992. doi:10.4103/njcp.njcp_474_20
  14. Khalid FA, Mehrose MY, Saleem M, et al. Comparison of efficacy and safety of intralesional triamcinolone and combination of triamcinolone with 5-fluorouracil in the treatment of keloids and hypertrophic scars: randomised control trial. Burns. 2019;45:69-75. doi:10.1016/j.burns.2018.08.011
  15. Asilian A, Darougheh A, Shariati F. New combination of triamcinolone, 5-Fluorouracil, and pulsed-dye laser for treatment of keloid and hypertrophic scars. Dermatol Surg. 2006;32:907-915. doi:10.1111/j.1524-4725.2006.32195.x
  16. Kim WI, Kim S, Cho SW, et al. The efficacy of bleomycin for treating keloid and hypertrophic scar: a systematic review and meta-analysis. J Cosmet Dermatol. 2020;19:3357-3366. doi:10.1111/jocd.13390
  17. Kabel A, Sabry H, Sorour N, et al. Comparative study between intralesional injection of bleomycin and 5-fluorouracil in the treatment of keloids and hypertrophic scars. J Dermatol Dermatol Surg. 2016;20:32-38.
  18. Yang HA, Jheng WL, Yu J, et al. Comparative efficacy of drug interventions for keloids: a network meta-analysis. Ann Plast Surg. 2024;92(1S suppl 1):S52-S59. doi:10.1097/SAP.0000000000003759
  19. Preissig J, Hamilton K, Markus R. Current laser resurfacing technologies: a review that delves beneath the surface. Semin Plast Surg. 2012;26:109-116. doi:10.1055/s-0032-1329413
  20. Bin Dakhil A, Shadid A, Altalhab S. Post-inflammatory hyperpigmentation after carbon dioxide laser: review of prevention and risk factors. Dermatol Reports. 2023;15:9703. doi:10.4081/dr.2023.9703
  21. Kaushik SB, Alexis AF. Nonablative fractional laser resurfacing in skin of color: evidence-based review. J Clin Aesthet Dermatol. 2017;10:51-67.
  22. Foppiani JA, Khaity A, Al-Dardery NM, et al. Laser therapy in hypertrophic and keloid scars: a systematic review and network meta-analysis. Aesthetic Plast Surg. Published May 17, 2024. doi:10.1007/s00266-024-04027-9
  23. Diaz A, Tan K, He H, et al. Keloid lesions show increased IL-4/IL-13 signaling and respond to Th2-targeting dupilumab therapy. J Eur Acad Dermatol Venereol. 2020;34:E161-E164. doi:10.1111/jdv.16097
  24. Min MS, Mazori DR, Lee MS, et al. Successful treatment of keloids and hypertrophic scars with systemic and intralesional dupilumab. J Drugs Dermatol. 2023;22:1220-1222. doi:10.36849/JDD.6385
  25. Wittmer A, Finklea L, Joseph J. Effects of dupilumab on keloid stabilization and prevention. JAAD Case Rep. 2023;37:103-105. doi:10.1016/j.jdcr.2023.05.001
  26. Luk K, Fakhoury J, Ozog D. Nonresponse and progression of diffuse keloids to dupilumab therapy. J Drugs Dermatol. 2022;21:197-199. doi:10.36849/jdd.6252
  27. Tirgan MH, Uitto J. Lack of efficacy of dupilumab in the treatment of keloid disorder. J Eur Acad Dermatol Venereol. 2022;36:E120-E122. doi:10.1111/jdv.17669
  28. Berman B, Duncan MR. Pentoxifylline inhibits the proliferation of human fibroblasts derived from keloid, scleroderma and morphoea skin and their production of collagen, glycosaminoglycans and fibronectin. Br J Dermatol. 1990;123:339-346. doi:10.1111/j.1365-2133.1990.tb06294.x
  29. Berman B, Duncan MR. Pentoxifylline inhibits normal human dermal fibroblast in vitro proliferation, collagen, glycosaminoglycan, and fibronectin production, and increases collagenase activity. J Invest Dermatol. 1989;92:605-610.
  30. Tan A, Martinez Luna O, Glass DA 2nd. Pentoxifylline for the prevention of postsurgical keloid recurrence. Dermatol Surg. 2020;46:1353-1356. doi:10.1097/DSS.0000000000002090
  31. Serag-Eldin YMA, Mahmoud WH, Gamea MM, et al. Intralesional pentoxifylline, triamcinolone acetonide, and their combination for treatment of keloid scars. J Cosmet Dermatol. 2021;20:3330-3340. doi:10.1111/jocd.14305
  32. Zhou T, Chen Y, Wang C, et al. SIRT6 inhibits the proliferation and collagen synthesis of keloid fibroblasts through MAPK/ERK pathway. Discov Med. 2024;36:1430-1440. doi:10.24976/Discov.Med.202436186.133
  33. Zhang J, Zhang X, Guo X, et al. Remdesivir alleviates skin fibrosis by suppressing TGF-β1 signaling pathway. PLoS One. 2024;19:E0305927. doi:10.1371/journal.pone.0305927
  34. Zhao J, Zhai X, Xu Z, et al. Novel needle-type electrocoagulation and combination pharmacotherapy: basic and clinical studies on efficacy and safety in treating keloids. J Cosmet Dermatol. doi:10.1111/jocd.16453
References
  1. Téot L, Mustoe TA, Middelkoop E, eds. Textbook on Scar Management: State of the Art Management and Emerging Technologies. Springer; 2020.
  2. Davis SA, Feldman SR, McMichael AJ. Management of keloids in the United States, 1990-2009: an analysis of the National Ambulatory Medical Care Survey. Dermatol Surg. 2013;39:988-994. doi:10.1111/dsu.12182
  3. Kassi K, Kouame K, Kouassi A, et al. Quality of life in black African patients with keloid scars. Dermatol Reports. 2020;12:8312. doi:10.4081/dr.2020.8312
  4. Delaleu J, Charvet E, Petit A. Keloid disease: review with clinical atlas. part I: definitions, history, epidemiology, clinics and diagnosis. Ann Dermatol Venereol. 2023;150:3-15. doi:10.1016/j.annder.2022.08.010
  5. Bronte J, Zhou C, Vempati A, et al. A comprehensive review of non-surgical treatments for hypertrophic and keloid scars in skin of color. Clin Cosmet Investig Dermatol. 2024;17:1459-1469. doi:10.2147/CCID.S470997
  6. Davison SP, Dayan JH, Clemens MW, et al. Efficacy of intralesional 5-fluorouracil and triamcinolone in the treatment of keloids. Aesthet Surg J. 2009;29:40-46. doi:10.1016/j.asj.2008.11.006
  7. Azzam OA, Bassiouny DA, El-Hawary MS, et al. Treatment of hypertrophic scars and keloids by fractional carbon dioxide laser: a clinical, histological, and immunohistochemical study. Lasers Med Sci. 2016;31:9-18. doi:10.1007/s10103-015-1824-4
  8. Ekstein SF, Wyles SP, Moran SL, et al. Keloids: a review of therapeutic management. Int J Dermatol. 2021;60:661-671. doi:10.1111/ijd.15159
  9. Morelli Coppola M, Salzillo R, Segreto F, et al. Triamcinolone acetonide intralesional injection for the treatment of keloid scars: patient selection and perspectives. Clin Cosmet Investig Dermatol. 2018;11:387-396. doi:10.2147/CCID.S133672
  10. Kant SB, van den Kerckhove E, Colla C, et al. A new treatment of hypertrophic and keloid scars with combined triamcinolone and verapamil: a retrospective study. Eur J Plast Surg. 2018;41:69-80. doi:10.1007/s00238-017-1322-y
  11. Cohen AJ, Talasila S, Lazarevic B, et al. Combination cryotherapy and intralesional corticosteroid versus steroid monotherapy in the treatment of keloids. J Cosmet Dermatol. 2023;22:932-936. doi:10.1111/jocd.15520
  12. Tawaranurak N, Pliensiri P, Tawaranurak K. Combination of fractional carbon dioxide laser and topical triamcinolone vs intralesional triamcinolone for keloid treatment: a randomised clinical trial. Int Wound J. 2022;19:1729-1735. doi:10.1111/iwj.13775
  13. Belie O, Ugburo AO, Mofikoya BO, et al. A comparison of intralesional verapamil and triamcinolone monotherapy in the treatment of keloids in an African population. Niger J Clin Pract. 2021;24:986-992. doi:10.4103/njcp.njcp_474_20
  14. Khalid FA, Mehrose MY, Saleem M, et al. Comparison of efficacy and safety of intralesional triamcinolone and combination of triamcinolone with 5-fluorouracil in the treatment of keloids and hypertrophic scars: randomised control trial. Burns. 2019;45:69-75. doi:10.1016/j.burns.2018.08.011
  15. Asilian A, Darougheh A, Shariati F. New combination of triamcinolone, 5-Fluorouracil, and pulsed-dye laser for treatment of keloid and hypertrophic scars. Dermatol Surg. 2006;32:907-915. doi:10.1111/j.1524-4725.2006.32195.x
  16. Kim WI, Kim S, Cho SW, et al. The efficacy of bleomycin for treating keloid and hypertrophic scar: a systematic review and meta-analysis. J Cosmet Dermatol. 2020;19:3357-3366. doi:10.1111/jocd.13390
  17. Kabel A, Sabry H, Sorour N, et al. Comparative study between intralesional injection of bleomycin and 5-fluorouracil in the treatment of keloids and hypertrophic scars. J Dermatol Dermatol Surg. 2016;20:32-38.
  18. Yang HA, Jheng WL, Yu J, et al. Comparative efficacy of drug interventions for keloids: a network meta-analysis. Ann Plast Surg. 2024;92(1S suppl 1):S52-S59. doi:10.1097/SAP.0000000000003759
  19. Preissig J, Hamilton K, Markus R. Current laser resurfacing technologies: a review that delves beneath the surface. Semin Plast Surg. 2012;26:109-116. doi:10.1055/s-0032-1329413
  20. Bin Dakhil A, Shadid A, Altalhab S. Post-inflammatory hyperpigmentation after carbon dioxide laser: review of prevention and risk factors. Dermatol Reports. 2023;15:9703. doi:10.4081/dr.2023.9703
  21. Kaushik SB, Alexis AF. Nonablative fractional laser resurfacing in skin of color: evidence-based review. J Clin Aesthet Dermatol. 2017;10:51-67.
  22. Foppiani JA, Khaity A, Al-Dardery NM, et al. Laser therapy in hypertrophic and keloid scars: a systematic review and network meta-analysis. Aesthetic Plast Surg. Published May 17, 2024. doi:10.1007/s00266-024-04027-9
  23. Diaz A, Tan K, He H, et al. Keloid lesions show increased IL-4/IL-13 signaling and respond to Th2-targeting dupilumab therapy. J Eur Acad Dermatol Venereol. 2020;34:E161-E164. doi:10.1111/jdv.16097
  24. Min MS, Mazori DR, Lee MS, et al. Successful treatment of keloids and hypertrophic scars with systemic and intralesional dupilumab. J Drugs Dermatol. 2023;22:1220-1222. doi:10.36849/JDD.6385
  25. Wittmer A, Finklea L, Joseph J. Effects of dupilumab on keloid stabilization and prevention. JAAD Case Rep. 2023;37:103-105. doi:10.1016/j.jdcr.2023.05.001
  26. Luk K, Fakhoury J, Ozog D. Nonresponse and progression of diffuse keloids to dupilumab therapy. J Drugs Dermatol. 2022;21:197-199. doi:10.36849/jdd.6252
  27. Tirgan MH, Uitto J. Lack of efficacy of dupilumab in the treatment of keloid disorder. J Eur Acad Dermatol Venereol. 2022;36:E120-E122. doi:10.1111/jdv.17669
  28. Berman B, Duncan MR. Pentoxifylline inhibits the proliferation of human fibroblasts derived from keloid, scleroderma and morphoea skin and their production of collagen, glycosaminoglycans and fibronectin. Br J Dermatol. 1990;123:339-346. doi:10.1111/j.1365-2133.1990.tb06294.x
  29. Berman B, Duncan MR. Pentoxifylline inhibits normal human dermal fibroblast in vitro proliferation, collagen, glycosaminoglycan, and fibronectin production, and increases collagenase activity. J Invest Dermatol. 1989;92:605-610.
  30. Tan A, Martinez Luna O, Glass DA 2nd. Pentoxifylline for the prevention of postsurgical keloid recurrence. Dermatol Surg. 2020;46:1353-1356. doi:10.1097/DSS.0000000000002090
  31. Serag-Eldin YMA, Mahmoud WH, Gamea MM, et al. Intralesional pentoxifylline, triamcinolone acetonide, and their combination for treatment of keloid scars. J Cosmet Dermatol. 2021;20:3330-3340. doi:10.1111/jocd.14305
  32. Zhou T, Chen Y, Wang C, et al. SIRT6 inhibits the proliferation and collagen synthesis of keloid fibroblasts through MAPK/ERK pathway. Discov Med. 2024;36:1430-1440. doi:10.24976/Discov.Med.202436186.133
  33. Zhang J, Zhang X, Guo X, et al. Remdesivir alleviates skin fibrosis by suppressing TGF-β1 signaling pathway. PLoS One. 2024;19:E0305927. doi:10.1371/journal.pone.0305927
  34. Zhao J, Zhai X, Xu Z, et al. Novel needle-type electrocoagulation and combination pharmacotherapy: basic and clinical studies on efficacy and safety in treating keloids. J Cosmet Dermatol. doi:10.1111/jocd.16453
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When Your Malpractice Insurer Investigates You: What to Know

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Thu, 11/07/2024 - 15:31

When psychiatrist Paul Sartain, MD (not his real name), received a letter from his state’s medical board, he was concerned. A patient’s family complained that he made sexual advances to a young woman he treated for psychotic depression.

“There was absolutely no evidence, and the claims were vague,” he said. “I think the family was angry at me and with the system — the woman had not gotten better.” Sartain reviewed his medical records and then called his malpractice insurer.

The insurer asked about his involvement with the patient’s case, if there was anything credible to the patient’s complaint, and if he had thorough documentation. Then, the carrier offered Sartain his choice of several attorneys who could represent him. The medical board ultimately closed the case with no findings against him, and the patient’s family never sued him.

While Sartain said he trusted his carrier-provided attorney, he would have considered hiring his own attorney as well if a criminal issue was also alleged.

“If I’m wrongly accused, I’m defended (by the carrier). If I had stolen money or had a sexual relationship with the patient, then you’re acting outside the bounds of what is protected (by the carrier),” he said.
 

How Medical Board and Malpractice Insurer Investigations Differ

Medical board complaints differ from malpractice claims, in which patients seek damages. The investigation process also varies.

When a patient reports a doctor to a state medical board, they may also sue the doctor for monetary damages in civil court. The medical board responds to patient complaints made directly to them, but it also may also initiate its own investigations. Those can be prompted by a malpractice claim resolution, with a court verdict against the doctor, or a settlement recorded in the National Practitioner Data Bank.

Malpractice insurers may offer limited legal representation for medical board investigations, requiring the doctor to report the medical board issue to them before the doctor takes any action. Often, they will cover up to $50,000 in defense costs but not cover any subsequent medical board fines or required classes or medical board fees.

When a doctor contacts the carrier about a medical board investigation, the carrier may ask for the medical board document and the medical records, said Alex Keoskey, a partner in Frier Levitt’s life sciences group.

The carrier may want to ask about the patient, staff members involved, the doctor’s background, if there have been previous medical board investigations or lawsuits against this doctor, and the doctor’s opinion of the allegations. The doctor should be transparent with the carrier, Keoskey said.

Some carriers conduct more in-depth investigations, examining record-keeping, prescription practices, patient consent processes, and continuing medical education status. That’s because the medical board may inquire about these as well should its own investigation expand.

Not all carriers explore cases like these, even if reimbursing for defense costs, said Karen Frisella, director of professional liability claims at BETA Healthcare Group in California. In her experience, a licensing investigation usually follows a claim resolution that was already worked up by the carrier. If a complaint was made directly to the licensing board without an accompanying liability claim, the carrier’s ability to initiate an investigation on the incident depends on the policy terms or coverage available.

“Typically, a professional liability policy requires that the insured report a claim to trigger coverage. The carrier can’t unilaterally decide to open a claim,” she said. A licensing board investigation is not a claim by definition and therefore does not provide a mechanism for the carrier to open a liability claim file, she added.

If the medical board ultimately restricts the doctor’s license or puts the doctor on probation, that becomes public, and the underwriting department may then look into it.

Malpractice insurers routinely monitor licensing board discipline notices. A reprimand or restrictions on a doctor’s license could trigger a review of the physician’s future insurability and lead to higher premiums or even nonrenewal, Frisella said.

If a carrier investigates a reported claim and determines there are issues with the care rendered, whether there is an accompanying medical board action, that also can affect underwriting decisions, Frisella said.
 

 

 

Who Is Your Attorney Really Working for?

The doctor should understand whose interests the attorney represents. In a medical board claim, the attorney — even if defense is paid by the carrier — represents the doctor.

Frisella said her organization provides pass-through coverage, meaning it reimburses the doctor for medical board defense costs. “Because the carrier isn’t directing the medical board defense, it is not generally privy to the work product.”

If a patient files a malpractice claim, however, the attorney ultimately represents the insurance company.

“The panel counsel who works for the insurer does not work for the doctor, and that’s always important to remember,” Keoskey said. While the attorney will do their best to aggressively defend the doctor, “he’s going to protect the insurer’s interest before the doctor’s.”

Physicians who find any conflict of interest with their insurer should seek counsel.

Such conflicts could include:

  • Disagreements over the case’s ultimate worth. For example, a physician might want a case to settle for less than their carrier is willing to pay.
  • The legal judgment may exceed the carrier’s policy limits, or there are punitive damages or allegations of criminal acts that the insurer does not cover.

In these cases, the insurance company should recommend the doctor get personal counsel. They will send a reservation of rights letter saying they will defend the doctor for now, but if the facts show the doctor committed some type of misconduct, they may decline coverage, said Keoskey. Some states, including California, require that the carrier pay for this independent counsel.

Unless there is a conflict of interest, though, having a personal attorney just makes the situation more complicated, said Frisella.

A version of this article first appeared on Medscape.com.

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When psychiatrist Paul Sartain, MD (not his real name), received a letter from his state’s medical board, he was concerned. A patient’s family complained that he made sexual advances to a young woman he treated for psychotic depression.

“There was absolutely no evidence, and the claims were vague,” he said. “I think the family was angry at me and with the system — the woman had not gotten better.” Sartain reviewed his medical records and then called his malpractice insurer.

The insurer asked about his involvement with the patient’s case, if there was anything credible to the patient’s complaint, and if he had thorough documentation. Then, the carrier offered Sartain his choice of several attorneys who could represent him. The medical board ultimately closed the case with no findings against him, and the patient’s family never sued him.

While Sartain said he trusted his carrier-provided attorney, he would have considered hiring his own attorney as well if a criminal issue was also alleged.

“If I’m wrongly accused, I’m defended (by the carrier). If I had stolen money or had a sexual relationship with the patient, then you’re acting outside the bounds of what is protected (by the carrier),” he said.
 

How Medical Board and Malpractice Insurer Investigations Differ

Medical board complaints differ from malpractice claims, in which patients seek damages. The investigation process also varies.

When a patient reports a doctor to a state medical board, they may also sue the doctor for monetary damages in civil court. The medical board responds to patient complaints made directly to them, but it also may also initiate its own investigations. Those can be prompted by a malpractice claim resolution, with a court verdict against the doctor, or a settlement recorded in the National Practitioner Data Bank.

Malpractice insurers may offer limited legal representation for medical board investigations, requiring the doctor to report the medical board issue to them before the doctor takes any action. Often, they will cover up to $50,000 in defense costs but not cover any subsequent medical board fines or required classes or medical board fees.

When a doctor contacts the carrier about a medical board investigation, the carrier may ask for the medical board document and the medical records, said Alex Keoskey, a partner in Frier Levitt’s life sciences group.

The carrier may want to ask about the patient, staff members involved, the doctor’s background, if there have been previous medical board investigations or lawsuits against this doctor, and the doctor’s opinion of the allegations. The doctor should be transparent with the carrier, Keoskey said.

Some carriers conduct more in-depth investigations, examining record-keeping, prescription practices, patient consent processes, and continuing medical education status. That’s because the medical board may inquire about these as well should its own investigation expand.

Not all carriers explore cases like these, even if reimbursing for defense costs, said Karen Frisella, director of professional liability claims at BETA Healthcare Group in California. In her experience, a licensing investigation usually follows a claim resolution that was already worked up by the carrier. If a complaint was made directly to the licensing board without an accompanying liability claim, the carrier’s ability to initiate an investigation on the incident depends on the policy terms or coverage available.

“Typically, a professional liability policy requires that the insured report a claim to trigger coverage. The carrier can’t unilaterally decide to open a claim,” she said. A licensing board investigation is not a claim by definition and therefore does not provide a mechanism for the carrier to open a liability claim file, she added.

If the medical board ultimately restricts the doctor’s license or puts the doctor on probation, that becomes public, and the underwriting department may then look into it.

Malpractice insurers routinely monitor licensing board discipline notices. A reprimand or restrictions on a doctor’s license could trigger a review of the physician’s future insurability and lead to higher premiums or even nonrenewal, Frisella said.

If a carrier investigates a reported claim and determines there are issues with the care rendered, whether there is an accompanying medical board action, that also can affect underwriting decisions, Frisella said.
 

 

 

Who Is Your Attorney Really Working for?

The doctor should understand whose interests the attorney represents. In a medical board claim, the attorney — even if defense is paid by the carrier — represents the doctor.

Frisella said her organization provides pass-through coverage, meaning it reimburses the doctor for medical board defense costs. “Because the carrier isn’t directing the medical board defense, it is not generally privy to the work product.”

If a patient files a malpractice claim, however, the attorney ultimately represents the insurance company.

“The panel counsel who works for the insurer does not work for the doctor, and that’s always important to remember,” Keoskey said. While the attorney will do their best to aggressively defend the doctor, “he’s going to protect the insurer’s interest before the doctor’s.”

Physicians who find any conflict of interest with their insurer should seek counsel.

Such conflicts could include:

  • Disagreements over the case’s ultimate worth. For example, a physician might want a case to settle for less than their carrier is willing to pay.
  • The legal judgment may exceed the carrier’s policy limits, or there are punitive damages or allegations of criminal acts that the insurer does not cover.

In these cases, the insurance company should recommend the doctor get personal counsel. They will send a reservation of rights letter saying they will defend the doctor for now, but if the facts show the doctor committed some type of misconduct, they may decline coverage, said Keoskey. Some states, including California, require that the carrier pay for this independent counsel.

Unless there is a conflict of interest, though, having a personal attorney just makes the situation more complicated, said Frisella.

A version of this article first appeared on Medscape.com.

When psychiatrist Paul Sartain, MD (not his real name), received a letter from his state’s medical board, he was concerned. A patient’s family complained that he made sexual advances to a young woman he treated for psychotic depression.

“There was absolutely no evidence, and the claims were vague,” he said. “I think the family was angry at me and with the system — the woman had not gotten better.” Sartain reviewed his medical records and then called his malpractice insurer.

The insurer asked about his involvement with the patient’s case, if there was anything credible to the patient’s complaint, and if he had thorough documentation. Then, the carrier offered Sartain his choice of several attorneys who could represent him. The medical board ultimately closed the case with no findings against him, and the patient’s family never sued him.

While Sartain said he trusted his carrier-provided attorney, he would have considered hiring his own attorney as well if a criminal issue was also alleged.

“If I’m wrongly accused, I’m defended (by the carrier). If I had stolen money or had a sexual relationship with the patient, then you’re acting outside the bounds of what is protected (by the carrier),” he said.
 

How Medical Board and Malpractice Insurer Investigations Differ

Medical board complaints differ from malpractice claims, in which patients seek damages. The investigation process also varies.

When a patient reports a doctor to a state medical board, they may also sue the doctor for monetary damages in civil court. The medical board responds to patient complaints made directly to them, but it also may also initiate its own investigations. Those can be prompted by a malpractice claim resolution, with a court verdict against the doctor, or a settlement recorded in the National Practitioner Data Bank.

Malpractice insurers may offer limited legal representation for medical board investigations, requiring the doctor to report the medical board issue to them before the doctor takes any action. Often, they will cover up to $50,000 in defense costs but not cover any subsequent medical board fines or required classes or medical board fees.

When a doctor contacts the carrier about a medical board investigation, the carrier may ask for the medical board document and the medical records, said Alex Keoskey, a partner in Frier Levitt’s life sciences group.

The carrier may want to ask about the patient, staff members involved, the doctor’s background, if there have been previous medical board investigations or lawsuits against this doctor, and the doctor’s opinion of the allegations. The doctor should be transparent with the carrier, Keoskey said.

Some carriers conduct more in-depth investigations, examining record-keeping, prescription practices, patient consent processes, and continuing medical education status. That’s because the medical board may inquire about these as well should its own investigation expand.

Not all carriers explore cases like these, even if reimbursing for defense costs, said Karen Frisella, director of professional liability claims at BETA Healthcare Group in California. In her experience, a licensing investigation usually follows a claim resolution that was already worked up by the carrier. If a complaint was made directly to the licensing board without an accompanying liability claim, the carrier’s ability to initiate an investigation on the incident depends on the policy terms or coverage available.

“Typically, a professional liability policy requires that the insured report a claim to trigger coverage. The carrier can’t unilaterally decide to open a claim,” she said. A licensing board investigation is not a claim by definition and therefore does not provide a mechanism for the carrier to open a liability claim file, she added.

If the medical board ultimately restricts the doctor’s license or puts the doctor on probation, that becomes public, and the underwriting department may then look into it.

Malpractice insurers routinely monitor licensing board discipline notices. A reprimand or restrictions on a doctor’s license could trigger a review of the physician’s future insurability and lead to higher premiums or even nonrenewal, Frisella said.

If a carrier investigates a reported claim and determines there are issues with the care rendered, whether there is an accompanying medical board action, that also can affect underwriting decisions, Frisella said.
 

 

 

Who Is Your Attorney Really Working for?

The doctor should understand whose interests the attorney represents. In a medical board claim, the attorney — even if defense is paid by the carrier — represents the doctor.

Frisella said her organization provides pass-through coverage, meaning it reimburses the doctor for medical board defense costs. “Because the carrier isn’t directing the medical board defense, it is not generally privy to the work product.”

If a patient files a malpractice claim, however, the attorney ultimately represents the insurance company.

“The panel counsel who works for the insurer does not work for the doctor, and that’s always important to remember,” Keoskey said. While the attorney will do their best to aggressively defend the doctor, “he’s going to protect the insurer’s interest before the doctor’s.”

Physicians who find any conflict of interest with their insurer should seek counsel.

Such conflicts could include:

  • Disagreements over the case’s ultimate worth. For example, a physician might want a case to settle for less than their carrier is willing to pay.
  • The legal judgment may exceed the carrier’s policy limits, or there are punitive damages or allegations of criminal acts that the insurer does not cover.

In these cases, the insurance company should recommend the doctor get personal counsel. They will send a reservation of rights letter saying they will defend the doctor for now, but if the facts show the doctor committed some type of misconduct, they may decline coverage, said Keoskey. Some states, including California, require that the carrier pay for this independent counsel.

Unless there is a conflict of interest, though, having a personal attorney just makes the situation more complicated, said Frisella.

A version of this article first appeared on Medscape.com.

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The Rise of Sham Peer Reviews

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While a medical peer review occurs once a patient, fellow doctor, or staff member reports that a physician failed to treat a patient up to standards or acted improperly, a “sham peer review” is undertaken for ulterior motives.

Sham peer reviews can be used to attack a doctor for unrelated professional, personal, or nonmedical reasons; intimidate, silence, or target a physician; or to carry out a personal vendetta. They’re typically undertaken due to professional competition or institutional politics rather than to promote quality care or uphold professional standards.

Physicians should be concerned. In a soon-to-be-published Medscape report on peer reviews, 56% of US physicians surveyed expressed higher levels of concern that a peer review could be misused to punish a physician for reasons unrelated to the matter being reviewed.

This is a troublesome issue, and many doctors may not be aware of it or how often it occurs.

“The biggest misconception about sham peer reviews is a denial of how pervasive they are,” said Andy Schlafly, general counsel for the Association of American Physicians and Surgeons (AAPS), which offers a free legal consultation service for physicians facing a sham peer review. “Many hospital administrations are as dangerous to good physicians as street gangs can be in a crime-ridden neighborhood.”

“Physicians should become aware of whether sham peer reviews are prevalent at their hospital and, if so, those physicians should look to practice somewhere else,” Schlafly said in an interview.

Unfortunately, there are limited data on how often this happens. When it does, it can be a career killer, said Lawrence Huntoon, MD, PhD, who has run the AAPS sham peer review hotline for over 20 years.

The physicians at the most risk for a sham peer review tend to be those who work for large hospital systems — as this is one way for hospitals to get rid of the doctors they don’t want to retain on staff, Huntoon said.

“Hospitals want a model whereby every physician on the medical staff is an employee,” Huntoon added. “This gives them complete power and control over these physicians, including the way they practice and how many patients they see per day, which, for some, is 20-50 a day to generate sufficient revenue.”

Complaints are generally filed via incident reporting software.

“The complaint could be that the physician is ‘disruptive,’ which can include facial expression, tone of voice, and body language — for example, ‘I found his facial expression demeaning’ or ‘I found her tone condescending’ — and this can be used to prosecute a doctor,” Huntoon said.

After the complaint is filed, the leaders of a hospital’s peer review committee meet to discuss the incident, followed by a panel of fellow physicians convened to review the matter. Once the date for a meeting is set, the accused doctor is allowed to testify, offer evidence, and have attorney representation.

The entire experience can take a physician by surprise.

“A sham peer review is difficult to prepare for because no physician thinks this is going to happen to them,” said Laurie L. York, a medical law attorney in Austin, Texas.

York added that there may also be a misperception of what is actually happening.

“When a physician becomes aware of an investigation, it initially may look like a regular peer review, and the physician may feel there has been a ‘misunderstanding’ that they can make right by explaining things,” York said. “The window of opportunity to shut down a sham peer review happens quickly. That’s why the physician needs the help of an experienced attorney as early in the process as possible.”
 

 

 

If You’re a Victim of a Sham Peer Review

Be vigilant. The most important thing you should think about when it comes to sham peer reviews is that this can, indeed, happen to you, Huntoon said. “I’ve written articles to help educate physicians about the tactics that are used,” he said. “You need to be educated and read medical staff bylaws to know your rights before something bad happens.”

Stay in your job. No matter what, if you’re under review, do not resign your position, no matter how difficult this may be. “A resignation during a sham peer review triggers an adverse report to the National Practitioner Data Bank [NPDB],” Schlafly said. The NPDB is a flagging system created by Congress to improve healthcare quality and reduce healthcare fraud and abuse. “A resignation also waives the physician’s right to contest the unfair review. In addition, leverage to negotiate a favorable settlement is lost if the physician simply resigns.”

Get a lawyer on board early. This is the only way to protect your rights. “Don’t wait a year to get an attorney involved,” Huntoon said. But this also can’t be any lawyer. It’s critical to find someone who specializes in sham peer reviews, so be sure to ask about their experience in handling peer review matters in hospitals and how knowledgeable they are about databank reporting requirements. “Sometimes, doctors will hire a malpractice attorney with no knowledge of what happens with sham peer reviews, and they may give bad advice,” he said. “Others may hire an employment attorney and that attorney will be up on employment law but has no experience with peer review matters in hospitals.”

Given the seriousness of a sham peer review, following these guidelines can help.

Contact the AAPA right away. There are things that can be done early on like getting a withdrawal of the request for corrective action as well as obtaining a preliminary injunction. Preparing for the fallout that may occur can be just as challenging.

“After this situation, the doctor is damaged goods,” Huntoon said. “What hospital will want to hire damaged goods to be part of their medical staff? Finding employment is going to be challenging and opening your own practice may also be difficult because the insurers have access to data bank reports.”

Ultimately, the best advice Huntoon can offer is to do your best to stay one step ahead of any work issues that could even lead to a sham peer review.

“Try and shield yourself from a sham peer review and be prepared should it happen,” he said. “I’ve seen careers end in the blink of an eye — wrongfully.”

A version of this article first appeared on Medscape.com.

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While a medical peer review occurs once a patient, fellow doctor, or staff member reports that a physician failed to treat a patient up to standards or acted improperly, a “sham peer review” is undertaken for ulterior motives.

Sham peer reviews can be used to attack a doctor for unrelated professional, personal, or nonmedical reasons; intimidate, silence, or target a physician; or to carry out a personal vendetta. They’re typically undertaken due to professional competition or institutional politics rather than to promote quality care or uphold professional standards.

Physicians should be concerned. In a soon-to-be-published Medscape report on peer reviews, 56% of US physicians surveyed expressed higher levels of concern that a peer review could be misused to punish a physician for reasons unrelated to the matter being reviewed.

This is a troublesome issue, and many doctors may not be aware of it or how often it occurs.

“The biggest misconception about sham peer reviews is a denial of how pervasive they are,” said Andy Schlafly, general counsel for the Association of American Physicians and Surgeons (AAPS), which offers a free legal consultation service for physicians facing a sham peer review. “Many hospital administrations are as dangerous to good physicians as street gangs can be in a crime-ridden neighborhood.”

“Physicians should become aware of whether sham peer reviews are prevalent at their hospital and, if so, those physicians should look to practice somewhere else,” Schlafly said in an interview.

Unfortunately, there are limited data on how often this happens. When it does, it can be a career killer, said Lawrence Huntoon, MD, PhD, who has run the AAPS sham peer review hotline for over 20 years.

The physicians at the most risk for a sham peer review tend to be those who work for large hospital systems — as this is one way for hospitals to get rid of the doctors they don’t want to retain on staff, Huntoon said.

“Hospitals want a model whereby every physician on the medical staff is an employee,” Huntoon added. “This gives them complete power and control over these physicians, including the way they practice and how many patients they see per day, which, for some, is 20-50 a day to generate sufficient revenue.”

Complaints are generally filed via incident reporting software.

“The complaint could be that the physician is ‘disruptive,’ which can include facial expression, tone of voice, and body language — for example, ‘I found his facial expression demeaning’ or ‘I found her tone condescending’ — and this can be used to prosecute a doctor,” Huntoon said.

After the complaint is filed, the leaders of a hospital’s peer review committee meet to discuss the incident, followed by a panel of fellow physicians convened to review the matter. Once the date for a meeting is set, the accused doctor is allowed to testify, offer evidence, and have attorney representation.

The entire experience can take a physician by surprise.

“A sham peer review is difficult to prepare for because no physician thinks this is going to happen to them,” said Laurie L. York, a medical law attorney in Austin, Texas.

York added that there may also be a misperception of what is actually happening.

“When a physician becomes aware of an investigation, it initially may look like a regular peer review, and the physician may feel there has been a ‘misunderstanding’ that they can make right by explaining things,” York said. “The window of opportunity to shut down a sham peer review happens quickly. That’s why the physician needs the help of an experienced attorney as early in the process as possible.”
 

 

 

If You’re a Victim of a Sham Peer Review

Be vigilant. The most important thing you should think about when it comes to sham peer reviews is that this can, indeed, happen to you, Huntoon said. “I’ve written articles to help educate physicians about the tactics that are used,” he said. “You need to be educated and read medical staff bylaws to know your rights before something bad happens.”

Stay in your job. No matter what, if you’re under review, do not resign your position, no matter how difficult this may be. “A resignation during a sham peer review triggers an adverse report to the National Practitioner Data Bank [NPDB],” Schlafly said. The NPDB is a flagging system created by Congress to improve healthcare quality and reduce healthcare fraud and abuse. “A resignation also waives the physician’s right to contest the unfair review. In addition, leverage to negotiate a favorable settlement is lost if the physician simply resigns.”

Get a lawyer on board early. This is the only way to protect your rights. “Don’t wait a year to get an attorney involved,” Huntoon said. But this also can’t be any lawyer. It’s critical to find someone who specializes in sham peer reviews, so be sure to ask about their experience in handling peer review matters in hospitals and how knowledgeable they are about databank reporting requirements. “Sometimes, doctors will hire a malpractice attorney with no knowledge of what happens with sham peer reviews, and they may give bad advice,” he said. “Others may hire an employment attorney and that attorney will be up on employment law but has no experience with peer review matters in hospitals.”

Given the seriousness of a sham peer review, following these guidelines can help.

Contact the AAPA right away. There are things that can be done early on like getting a withdrawal of the request for corrective action as well as obtaining a preliminary injunction. Preparing for the fallout that may occur can be just as challenging.

“After this situation, the doctor is damaged goods,” Huntoon said. “What hospital will want to hire damaged goods to be part of their medical staff? Finding employment is going to be challenging and opening your own practice may also be difficult because the insurers have access to data bank reports.”

Ultimately, the best advice Huntoon can offer is to do your best to stay one step ahead of any work issues that could even lead to a sham peer review.

“Try and shield yourself from a sham peer review and be prepared should it happen,” he said. “I’ve seen careers end in the blink of an eye — wrongfully.”

A version of this article first appeared on Medscape.com.

While a medical peer review occurs once a patient, fellow doctor, or staff member reports that a physician failed to treat a patient up to standards or acted improperly, a “sham peer review” is undertaken for ulterior motives.

Sham peer reviews can be used to attack a doctor for unrelated professional, personal, or nonmedical reasons; intimidate, silence, or target a physician; or to carry out a personal vendetta. They’re typically undertaken due to professional competition or institutional politics rather than to promote quality care or uphold professional standards.

Physicians should be concerned. In a soon-to-be-published Medscape report on peer reviews, 56% of US physicians surveyed expressed higher levels of concern that a peer review could be misused to punish a physician for reasons unrelated to the matter being reviewed.

This is a troublesome issue, and many doctors may not be aware of it or how often it occurs.

“The biggest misconception about sham peer reviews is a denial of how pervasive they are,” said Andy Schlafly, general counsel for the Association of American Physicians and Surgeons (AAPS), which offers a free legal consultation service for physicians facing a sham peer review. “Many hospital administrations are as dangerous to good physicians as street gangs can be in a crime-ridden neighborhood.”

“Physicians should become aware of whether sham peer reviews are prevalent at their hospital and, if so, those physicians should look to practice somewhere else,” Schlafly said in an interview.

Unfortunately, there are limited data on how often this happens. When it does, it can be a career killer, said Lawrence Huntoon, MD, PhD, who has run the AAPS sham peer review hotline for over 20 years.

The physicians at the most risk for a sham peer review tend to be those who work for large hospital systems — as this is one way for hospitals to get rid of the doctors they don’t want to retain on staff, Huntoon said.

“Hospitals want a model whereby every physician on the medical staff is an employee,” Huntoon added. “This gives them complete power and control over these physicians, including the way they practice and how many patients they see per day, which, for some, is 20-50 a day to generate sufficient revenue.”

Complaints are generally filed via incident reporting software.

“The complaint could be that the physician is ‘disruptive,’ which can include facial expression, tone of voice, and body language — for example, ‘I found his facial expression demeaning’ or ‘I found her tone condescending’ — and this can be used to prosecute a doctor,” Huntoon said.

After the complaint is filed, the leaders of a hospital’s peer review committee meet to discuss the incident, followed by a panel of fellow physicians convened to review the matter. Once the date for a meeting is set, the accused doctor is allowed to testify, offer evidence, and have attorney representation.

The entire experience can take a physician by surprise.

“A sham peer review is difficult to prepare for because no physician thinks this is going to happen to them,” said Laurie L. York, a medical law attorney in Austin, Texas.

York added that there may also be a misperception of what is actually happening.

“When a physician becomes aware of an investigation, it initially may look like a regular peer review, and the physician may feel there has been a ‘misunderstanding’ that they can make right by explaining things,” York said. “The window of opportunity to shut down a sham peer review happens quickly. That’s why the physician needs the help of an experienced attorney as early in the process as possible.”
 

 

 

If You’re a Victim of a Sham Peer Review

Be vigilant. The most important thing you should think about when it comes to sham peer reviews is that this can, indeed, happen to you, Huntoon said. “I’ve written articles to help educate physicians about the tactics that are used,” he said. “You need to be educated and read medical staff bylaws to know your rights before something bad happens.”

Stay in your job. No matter what, if you’re under review, do not resign your position, no matter how difficult this may be. “A resignation during a sham peer review triggers an adverse report to the National Practitioner Data Bank [NPDB],” Schlafly said. The NPDB is a flagging system created by Congress to improve healthcare quality and reduce healthcare fraud and abuse. “A resignation also waives the physician’s right to contest the unfair review. In addition, leverage to negotiate a favorable settlement is lost if the physician simply resigns.”

Get a lawyer on board early. This is the only way to protect your rights. “Don’t wait a year to get an attorney involved,” Huntoon said. But this also can’t be any lawyer. It’s critical to find someone who specializes in sham peer reviews, so be sure to ask about their experience in handling peer review matters in hospitals and how knowledgeable they are about databank reporting requirements. “Sometimes, doctors will hire a malpractice attorney with no knowledge of what happens with sham peer reviews, and they may give bad advice,” he said. “Others may hire an employment attorney and that attorney will be up on employment law but has no experience with peer review matters in hospitals.”

Given the seriousness of a sham peer review, following these guidelines can help.

Contact the AAPA right away. There are things that can be done early on like getting a withdrawal of the request for corrective action as well as obtaining a preliminary injunction. Preparing for the fallout that may occur can be just as challenging.

“After this situation, the doctor is damaged goods,” Huntoon said. “What hospital will want to hire damaged goods to be part of their medical staff? Finding employment is going to be challenging and opening your own practice may also be difficult because the insurers have access to data bank reports.”

Ultimately, the best advice Huntoon can offer is to do your best to stay one step ahead of any work issues that could even lead to a sham peer review.

“Try and shield yourself from a sham peer review and be prepared should it happen,” he said. “I’ve seen careers end in the blink of an eye — wrongfully.”

A version of this article first appeared on Medscape.com.

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Sulfites: The 2024 American Contact Dermatitis Society Allergen of the Year

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Sulfites: The 2024 American Contact Dermatitis Society Allergen of the Year

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.1 Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO32-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.2 Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.3 It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.1

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,7 antibiotics,8 antifungals,9 hemorrhoidal preparations,10 local anesthetics,11 and urinary catheterization gel,12 highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.13 Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,7 which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.1

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.1

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.4 This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.14 While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.15 There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.16

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).17 A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).18 However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.1

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.1

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.4 Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,20 the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.21 However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.17

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.22

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 201817 to 3.3% (N=4115) in 2019 and 202023 among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.17 However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.5 Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

References
  1. Ekstein SF, Warshaw EM. Sulfites: allergen of the year 2024. Dermatitis. 2024;35:6-12. doi:10.1089/derm.2023.0154
  2. Gunnison AF, Jacobsen DW. Sulfite hypersensitivity. a critical review. CRC Crit Rev Toxicol. 1987;17:185-214. doi:10.3109/10408448709071208
  3. Clough SR. Sodium sulfite. In: Wexler P, ed. Encyclopedia of Toxicology. 3rd ed. Academic Press; 2014: 341-343.
  4. Vally H, Misso NL, Madan V. Clinical effects of sulphite additives. Clin Exp Allergy. 2009;39:1643-1651. doi:10.1111/j.1365-2222.2009.03362.x
  5. Ralph N, Verma S, Merry S, et al. What is the relevance of contact allergy to sodium metabisulfite and which concentration of the allergen should we use? Dermatitis. 2015;26:162-165. doi:10.1097/der.0000000000000120
  6. Madan V, Walker SL, Beck MH. Sodium metabisulfite allergy is common but is it relevant? Contact Dermatitis. 2007;57:173-176. doi:10.1111/j.1600-0536.2007.01188.x
  7. García-Gavín J, Parente J, Goossens A. Allergic contact dermatitis caused by sodium metabisulfite: a challenging allergen. a case series and literature review. Contact Dermatitis. 2012;67:260-269. doi:10.1111/j.1600-0536.2012.02135.x
  8. Milpied B, van Wassenhove L, Larousse C, et al. Contact dermatitis from rifamycin. Contact Dermatitis. 1986;14:252-253. doi:10.1111/j.1600-0536.1986.tb01240.x
  9. Lodi A, Chiarelli G, Mancini LL, et al. Contact allergy to sodium sulfite contained in an antifungal preparation. Contact Dermatitis. 1993;29:97. doi:10.1111/j.1600-0536.1993.tb03493.x
  10. Sánchez-Pérez J, Abajo P, Córdoba S, et al. Allergic contact dermatitis from sodium metabisulfite in an antihemorrhoidal cream. Contact Dermatitis. 2000;42:176-177.
  11. Boyd AH, Warshaw EM. Sulfites: no longer a zebra? Dermatitis. 2017;28:364-366. doi:10.1097/der.0000000000000312
  12. Grosch E, Mahler V. Allergic contact dermatitis caused by a catheter system containing sodium metabisulfite. Contact Dermatitis. 2017;76:186-187. doi:10.1111/cod.12675
  13. Shaver RL, Warshaw EM. Contact allergens in prescription topical ophthalmic medications. Dermatitis. 2022;33:135-143. doi:10.1097/der.0000000000000751
  14. Dendooven E, Darrigade AS, Foubert K, et al. The presence of sulfites in ‘natural rubber latex’ and ‘synthetic’ rubber gloves: an experimental pilot study. Br J Dermatol. 2020;182:1054-1055. doi:10.1111/bjd.18608
  15. Nater JP. Allergic contact dermatitis caused by potassium metabisulfite. Dermatologica. 1968;136:477-478. doi:10.1159/000254143
  16. Borges AS, Valejo Coelho MM, Fernandes C, et al. Systemic allergic dermatitis caused by sodium metabisulfite in rectal enemas. Contact Dermatitis. 2018;78:429-430. doi:10.1111/cod.12971
  17. Warshaw EM, Buonomo M, DeKoven JG, et al. Patch testing with sodium disulfite: North American Contact Dermatitis Group experience, 2017 to 2018. Contact Dermatitis. 2021;85:285-296. doi:10.1111/cod.13860
  18. Häberle M, Geier J, Mahler V. Contact allergy to sulfites: clinical and occupational relevance—new data from the German ­Contact ­Dermatitis Research Group and the Information Network of ­Departments of ­Dermatology (IVDK). J Dtsch Dermatol Ges. 2016;14:938-941. doi:10.1111/ddg.13009
  19. Tan MG, Li HO, Pratt MD. Systemic allergic dermatitis to sodium metabisulfite in local anesthetic solution. Contact Dermatitis. 2022;86:120-121. doi:10.1111/cod.13978
  20. D’Amore T, Di Taranto A, Berardi G, et al. Sulfites in meat: occurrence, activity, toxicity, regulation, and detection. a comprehensive review. Compr Rev Food Sci Food Saf. 2020;19:2701-2720. doi:10.1111/1541-4337.12607
  21. Grotheer P, Marshall M, Simonne A. Sulfites: separating fact from fiction. May 11, 2022. UF IFAS Extension. University of Florida. Accessed October 4, 2024. https://edis.ifas.ufl.edu/publication/FY731
  22. Silva M, Gama J, Pinto N, et al. Sulfite concentration and the occurrence of headache in young adults: a prospective study. Eur J Clin Nutr. 2019;73:1316-1322. doi:10.1038/s41430-019-0420-2
  23. DeKoven JG, Warshaw EM, Reeder MJ, et al. North American Contact Dermatitis Group patch test results: 2019-2020. Dermatitis. 2023;34:90-104. doi:10.1089/derm.2022.29017.jdk
  24. T.R.U.E. Test. Thin-layer rapid use epicutaneous patch test. SmartPractice Dermatology Allergy. Accessed October 4, 2024. https://www.smartpractice.com/shop/category?id=581719&m=SPA
  25. Schalock PC, Dunnick CA, Nedorost, et al; American Contact Dermatitis Society Core Allergen Series Committee. American ­Contact Dermatitis Society Core Allergen Series: 2020 update. Dermatitis. 2020;31:279-282.
  26. Kaaman AC, Boman A, Wrangsjö K, et al. Contact allergy to sodium metabisulfite: an occupational problem. Contact Dermatitis. 2010;63:110-112. doi:10.1111/j.1600-0536.2010.01756.x
  27. Vena GA, Foti C, Angelini G. Sulfite contact allergy. Contact Dermatitis. 1994;31:172-175. doi:10.1111/j.1600-0536.1994.tb01959.x
Article PDF
Author and Disclosure Information

Solbie Choi is from the Albert Einstein College of Medicine, Bronx, New York. Sarak K. Zemlok is from the University of Connecticut School of Medicine, Farmington. Dr. Yu is from the Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston. Dr. Adler is from the Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles.

Solbie Choi has no relevant financial disclosures to report. Sarah K. Zemlok receives royalties from Kadmon Pharmaceuticals and Sanofi. Dr. Yu has served as a consultant, advisory board member, and/or investigator for and/or has received income or honoraria from AbbVie, Arcutis Biotherapeutics, Astria Therapeutics, Dermatology Foundation, Dermavant Sciences Ltd, Dynamed, Eli Lilly and Company, Incyte, iRhythm, LEO Pharma, National Eczema Association, O’Glacée, Pediatric Dermatology Research Alliance, Pfizer, Sanofi, SmartPractice, Sol-Gel Technologies, and UptoDate, Inc. He also is the Director and President-Elect of the American Contact Dermatitis Society. Dr. Adler has received research grants from AbbVie and Dermavant Sciences Ltd and serves as chair of the Contact Allergen Management Program Council for the American Contact Dermatitis Society.

The views expressed in this article are those of the authors and do not represent the opinions of the American Contact Dermatitis Society.

Correspondence: Brandon L. Adler, MD, 1441 Eastlake Ave, Ezralow Tower, Ste 5301, Los Angeles, CA 90033 (Brandon.Adler@med.usc.edu).

Cutis. 2024 November;114(5):141-143. doi:10.12788/cutis.1124

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Author and Disclosure Information

Solbie Choi is from the Albert Einstein College of Medicine, Bronx, New York. Sarak K. Zemlok is from the University of Connecticut School of Medicine, Farmington. Dr. Yu is from the Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston. Dr. Adler is from the Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles.

Solbie Choi has no relevant financial disclosures to report. Sarah K. Zemlok receives royalties from Kadmon Pharmaceuticals and Sanofi. Dr. Yu has served as a consultant, advisory board member, and/or investigator for and/or has received income or honoraria from AbbVie, Arcutis Biotherapeutics, Astria Therapeutics, Dermatology Foundation, Dermavant Sciences Ltd, Dynamed, Eli Lilly and Company, Incyte, iRhythm, LEO Pharma, National Eczema Association, O’Glacée, Pediatric Dermatology Research Alliance, Pfizer, Sanofi, SmartPractice, Sol-Gel Technologies, and UptoDate, Inc. He also is the Director and President-Elect of the American Contact Dermatitis Society. Dr. Adler has received research grants from AbbVie and Dermavant Sciences Ltd and serves as chair of the Contact Allergen Management Program Council for the American Contact Dermatitis Society.

The views expressed in this article are those of the authors and do not represent the opinions of the American Contact Dermatitis Society.

Correspondence: Brandon L. Adler, MD, 1441 Eastlake Ave, Ezralow Tower, Ste 5301, Los Angeles, CA 90033 (Brandon.Adler@med.usc.edu).

Cutis. 2024 November;114(5):141-143. doi:10.12788/cutis.1124

Author and Disclosure Information

Solbie Choi is from the Albert Einstein College of Medicine, Bronx, New York. Sarak K. Zemlok is from the University of Connecticut School of Medicine, Farmington. Dr. Yu is from the Department of Dermatology, Massachusetts General Hospital, Harvard Medical School, Boston. Dr. Adler is from the Department of Dermatology, Keck School of Medicine, University of Southern California, Los Angeles.

Solbie Choi has no relevant financial disclosures to report. Sarah K. Zemlok receives royalties from Kadmon Pharmaceuticals and Sanofi. Dr. Yu has served as a consultant, advisory board member, and/or investigator for and/or has received income or honoraria from AbbVie, Arcutis Biotherapeutics, Astria Therapeutics, Dermatology Foundation, Dermavant Sciences Ltd, Dynamed, Eli Lilly and Company, Incyte, iRhythm, LEO Pharma, National Eczema Association, O’Glacée, Pediatric Dermatology Research Alliance, Pfizer, Sanofi, SmartPractice, Sol-Gel Technologies, and UptoDate, Inc. He also is the Director and President-Elect of the American Contact Dermatitis Society. Dr. Adler has received research grants from AbbVie and Dermavant Sciences Ltd and serves as chair of the Contact Allergen Management Program Council for the American Contact Dermatitis Society.

The views expressed in this article are those of the authors and do not represent the opinions of the American Contact Dermatitis Society.

Correspondence: Brandon L. Adler, MD, 1441 Eastlake Ave, Ezralow Tower, Ste 5301, Los Angeles, CA 90033 (Brandon.Adler@med.usc.edu).

Cutis. 2024 November;114(5):141-143. doi:10.12788/cutis.1124

Article PDF
Article PDF

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.1 Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO32-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.2 Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.3 It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.1

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,7 antibiotics,8 antifungals,9 hemorrhoidal preparations,10 local anesthetics,11 and urinary catheterization gel,12 highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.13 Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,7 which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.1

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.1

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.4 This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.14 While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.15 There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.16

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).17 A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).18 However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.1

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.1

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.4 Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,20 the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.21 However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.17

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.22

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 201817 to 3.3% (N=4115) in 2019 and 202023 among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.17 However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.5 Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

The American Contact Dermatitis Society (ACDS) selected sulfites as the 2024 Allergen of the Year.1 Due to their preservative and antioxidant properties, sulfites are prevalent in a variety of foods, beverages, medications, and personal care products; however, sulfites also have been implicated as a potential contact allergen. In this article, we review common sources of sulfite exposure, clinical manifestations of allergic contact dermatitis (ACD) to sulfites, and patch testing considerations for this emerging allergen.

What Are Sulfites?

Sulfiting agents are compounds that contain the sulfite ion SO32-, including sulfur dioxide, sodium disulfite (sodium metabisulfite), and potassium metabisulfite.2 Sulfites occur naturally in the environment and commonly are used as preservatives, antibrowning agents, and antioxidants in various foods, beverages, medications, cosmetics, and skin care products. As antibrowning agents and antioxidants, sulfites help maintain the natural appearance of foods and other products and prevent premature spoiling by inactivating oxidative enzymes.3 It should be noted that sulfites and sulfates are distinct and unrelated compounds that do not cross-react.1

Common Sources of Sulfite Exposure

From a morning glass of juice to an evening shower, in the pharmacy and at the hair salon, sulfite exposure is ubiquitous in most daily routines. Sulfites are present in many foods and beverages, either as a byproduct of natural fermentation or as an additive to prevent spoiling and color change. The Table provides examples of foods with high sulfite content.1,4-6 In particular, dried fruit, bottled lemon juice, wine, grape juice, sauerkraut juice, and pickled onions have high sulfite content.

Topical medications and personal care products represent other potential sources of sulfite exposure. A number of reports have shown that sulfites may be included in topical steroids,7 antibiotics,8 antifungals,9 hemorrhoidal preparations,10 local anesthetics,11 and urinary catheterization gel,12 highlighting their many potential applications. In addition, a comprehensive ingredient analysis of 264 ophthalmic medications found that 3.8% of the products contained sodium disulfite.13 Sulfites may be found in personal care products, including facial and hand cleansers, shampoos, moisturizers, and toothpastes. Hair dyes also commonly contain sulfites,7 which are listed in as many as 90% of hair dye kits in the ACDS Contact Allergen Management Program database.1

Occupational exposures also are widespread, as sulfites are extensively utilized across diverse industries such as pharmaceuticals, health care, leather manufacturing, mineral extraction, food preparation, chemical manufacturing, textiles, alcohol brewing, and wine production.1

Sulfites also are used in the rubber industry—­particularly in gloves—due to their anticoagulant and preservative properties.4 This is relevant to health care providers, who may use dozens of disposable gloves in a single day. In an experimental pilot study, ­researchers detected sulfites in 83% (5/6) of natural rubber latex gloves, 96% (23/24) of synthetic (nitrile) gloves, and 0% (0/5) of polyvinyl chloride gloves.14 While this study was limited to a small sample size, it demonstrates the common use of sulfites in certain rubber gloves and encourages future studies to determine whether there is a quantitative threshold to elicit allergic reactions.

Sulfite Allergy

In 1968, an early case report of ACD to sulfites was published involving a pharmaceutical worker who developed hand eczema after working at a factory for 3 months and had a positive patch test to potassium metabisulfite.15 There have been other cases published in the literature since then, including localized ACD as well as less common cases of systemic contact dermatitis following oral, injectable, and rectal sulfite exposures.16

The North American Contact Dermatitis Group found that, among 132 (2.7%) of 4885 patients with positive patch tests to sodium disulfite from 2017 to 2018, the most commonly involved body sites were the face (28.8%) and hands (20.5%) followed by a scattered/generalized distribution (13.6%). Involvement of the face and hands may correlate with the most frequent sources of exposure that were identified, including personal care products (particularly hair dyes)(18.9%), medications (9.1%), and foods (7.6%).17 A multicenter analysis of patch test results from Germany, Austria, and Switzerland from 1999 to 2013 showed that 357 (2.9%) of 12,156 patients had positive reactions to sodium disulfite, with the most commonly identified exposure sources being topical pharmaceutical agents (59.3%); cosmetics, creams, and sunscreens (13.6%); and systemic drugs (6.8%).18 However, it is not always possible to determine the clinical relevance of a positive patch test to sulfites.1

Other than the face and hands, there have been other unexpected anatomic locations for sulfite ACD (eg, the lower back), and systemic contact dermatitis has manifested with widespread rashes due to oral, rectal, and parenteral exposure.4,16,19 There is no definitive link between sulfite contact allergy and patient sex, but there seems to be a higher prevalence in patients older than 40 years, perhaps related to overall lifetime exposure.1

Immediate hypersensitivity reactions to sulfites also have been reported, including urticaria, angioedema, and anaphylaxis.4 Due to multiple cases of severe dermatologic and respiratory reactions to food products containing sulfites,20 the US Food and Drug Administration prohibited their use in fresh fruit and vegetables as antibrowning agents in 1986 and required labels on packaged foods that contained sulfites at more than 10 parts per million.21 However, food and drinks produced in restaurants, bakeries, and cafes as well as those that are distributed directly to consumers from the preparation site are exempt from these rules.17

In addition, consuming high amounts of dietary sulfites has been linked to headaches through unclear (ie, not necessarily allergic) mechanisms.4,22 One study found that wine with a higher sulfite concentration was associated with increased risk for headaches in participants who had a history of headaches related to wine consumption.22

Patch Testing to Sulfites

The North American Contact Dermatitis Group has tested sodium disulfite since 2017 and found an increased frequency of positive patch tests from 2.7% (N=4885) in 2017 and 201817 to 3.3% (N=4115) in 2019 and 202023 among patients referred for testing. Similarly, patch testing to sodium disulfite in nearly 40,000 patients in 9 European countries showed a pooled prevalence of reactions of 3.1%.17 However, this contact allergy may go unrecognized, as sulfites are not included in common patch test series, including the thin-layer rapid use epicutaneous test and the ACDS Core Allergen Series.24,25 The relatively high patch test positivity to sulfites along with the prevalence of daily exposures supports the addition of sulfites to more patch test screening series.

The recommended patch test concentration for sodium disulfite is 1% in petrolatum.5 Testing in aqueous solutions is not recommended because they can cause sulfites to break down, potentially producing false-positive or irritant patch test reactions.7,26,27

Recommendations for Patients With Sulfite Allergies

Individuals with contact allergies to sulfites should be counseled on exposure sources and should be given resources providing a list of safe products, such as the ACDS Contact Allergen Management Program (https://www.acdscamp.org/login) or SkinSAFE ­(https://www.skinsafeproducts.com/). Prescribers should be cognizant of sulfites that are present in prescription medications. Just because a patient has a positive patch test to sulfites does not automatically imply that they will need to modify their diet to avoid sulfite-containing foods; in the absence of cheilitis or a distribution suggestive of systemic contact dermatitis (eg, vesicular hand/foot dermatitis, intertriginous eruptions), this step may be unnecessary. On the other hand, individuals who have experienced immediate hypersensitivity reactions to sulfites should avoid sulfite-containing foods and carry an epinephrine autoinjector.

Final Interpretation

Sulfites are ubiquitous compounds found in various foods, beverages, medications, and personal care products in addition to a range of occupational exposures. The face and hands are the most common sites of sulfite ACD. Despite patch test positivity in as many as 3% of tested patients,17,23 sulfite allergy may be missed due to lack of routine testing on standard screening series.

References
  1. Ekstein SF, Warshaw EM. Sulfites: allergen of the year 2024. Dermatitis. 2024;35:6-12. doi:10.1089/derm.2023.0154
  2. Gunnison AF, Jacobsen DW. Sulfite hypersensitivity. a critical review. CRC Crit Rev Toxicol. 1987;17:185-214. doi:10.3109/10408448709071208
  3. Clough SR. Sodium sulfite. In: Wexler P, ed. Encyclopedia of Toxicology. 3rd ed. Academic Press; 2014: 341-343.
  4. Vally H, Misso NL, Madan V. Clinical effects of sulphite additives. Clin Exp Allergy. 2009;39:1643-1651. doi:10.1111/j.1365-2222.2009.03362.x
  5. Ralph N, Verma S, Merry S, et al. What is the relevance of contact allergy to sodium metabisulfite and which concentration of the allergen should we use? Dermatitis. 2015;26:162-165. doi:10.1097/der.0000000000000120
  6. Madan V, Walker SL, Beck MH. Sodium metabisulfite allergy is common but is it relevant? Contact Dermatitis. 2007;57:173-176. doi:10.1111/j.1600-0536.2007.01188.x
  7. García-Gavín J, Parente J, Goossens A. Allergic contact dermatitis caused by sodium metabisulfite: a challenging allergen. a case series and literature review. Contact Dermatitis. 2012;67:260-269. doi:10.1111/j.1600-0536.2012.02135.x
  8. Milpied B, van Wassenhove L, Larousse C, et al. Contact dermatitis from rifamycin. Contact Dermatitis. 1986;14:252-253. doi:10.1111/j.1600-0536.1986.tb01240.x
  9. Lodi A, Chiarelli G, Mancini LL, et al. Contact allergy to sodium sulfite contained in an antifungal preparation. Contact Dermatitis. 1993;29:97. doi:10.1111/j.1600-0536.1993.tb03493.x
  10. Sánchez-Pérez J, Abajo P, Córdoba S, et al. Allergic contact dermatitis from sodium metabisulfite in an antihemorrhoidal cream. Contact Dermatitis. 2000;42:176-177.
  11. Boyd AH, Warshaw EM. Sulfites: no longer a zebra? Dermatitis. 2017;28:364-366. doi:10.1097/der.0000000000000312
  12. Grosch E, Mahler V. Allergic contact dermatitis caused by a catheter system containing sodium metabisulfite. Contact Dermatitis. 2017;76:186-187. doi:10.1111/cod.12675
  13. Shaver RL, Warshaw EM. Contact allergens in prescription topical ophthalmic medications. Dermatitis. 2022;33:135-143. doi:10.1097/der.0000000000000751
  14. Dendooven E, Darrigade AS, Foubert K, et al. The presence of sulfites in ‘natural rubber latex’ and ‘synthetic’ rubber gloves: an experimental pilot study. Br J Dermatol. 2020;182:1054-1055. doi:10.1111/bjd.18608
  15. Nater JP. Allergic contact dermatitis caused by potassium metabisulfite. Dermatologica. 1968;136:477-478. doi:10.1159/000254143
  16. Borges AS, Valejo Coelho MM, Fernandes C, et al. Systemic allergic dermatitis caused by sodium metabisulfite in rectal enemas. Contact Dermatitis. 2018;78:429-430. doi:10.1111/cod.12971
  17. Warshaw EM, Buonomo M, DeKoven JG, et al. Patch testing with sodium disulfite: North American Contact Dermatitis Group experience, 2017 to 2018. Contact Dermatitis. 2021;85:285-296. doi:10.1111/cod.13860
  18. Häberle M, Geier J, Mahler V. Contact allergy to sulfites: clinical and occupational relevance—new data from the German ­Contact ­Dermatitis Research Group and the Information Network of ­Departments of ­Dermatology (IVDK). J Dtsch Dermatol Ges. 2016;14:938-941. doi:10.1111/ddg.13009
  19. Tan MG, Li HO, Pratt MD. Systemic allergic dermatitis to sodium metabisulfite in local anesthetic solution. Contact Dermatitis. 2022;86:120-121. doi:10.1111/cod.13978
  20. D’Amore T, Di Taranto A, Berardi G, et al. Sulfites in meat: occurrence, activity, toxicity, regulation, and detection. a comprehensive review. Compr Rev Food Sci Food Saf. 2020;19:2701-2720. doi:10.1111/1541-4337.12607
  21. Grotheer P, Marshall M, Simonne A. Sulfites: separating fact from fiction. May 11, 2022. UF IFAS Extension. University of Florida. Accessed October 4, 2024. https://edis.ifas.ufl.edu/publication/FY731
  22. Silva M, Gama J, Pinto N, et al. Sulfite concentration and the occurrence of headache in young adults: a prospective study. Eur J Clin Nutr. 2019;73:1316-1322. doi:10.1038/s41430-019-0420-2
  23. DeKoven JG, Warshaw EM, Reeder MJ, et al. North American Contact Dermatitis Group patch test results: 2019-2020. Dermatitis. 2023;34:90-104. doi:10.1089/derm.2022.29017.jdk
  24. T.R.U.E. Test. Thin-layer rapid use epicutaneous patch test. SmartPractice Dermatology Allergy. Accessed October 4, 2024. https://www.smartpractice.com/shop/category?id=581719&m=SPA
  25. Schalock PC, Dunnick CA, Nedorost, et al; American Contact Dermatitis Society Core Allergen Series Committee. American ­Contact Dermatitis Society Core Allergen Series: 2020 update. Dermatitis. 2020;31:279-282.
  26. Kaaman AC, Boman A, Wrangsjö K, et al. Contact allergy to sodium metabisulfite: an occupational problem. Contact Dermatitis. 2010;63:110-112. doi:10.1111/j.1600-0536.2010.01756.x
  27. Vena GA, Foti C, Angelini G. Sulfite contact allergy. Contact Dermatitis. 1994;31:172-175. doi:10.1111/j.1600-0536.1994.tb01959.x
References
  1. Ekstein SF, Warshaw EM. Sulfites: allergen of the year 2024. Dermatitis. 2024;35:6-12. doi:10.1089/derm.2023.0154
  2. Gunnison AF, Jacobsen DW. Sulfite hypersensitivity. a critical review. CRC Crit Rev Toxicol. 1987;17:185-214. doi:10.3109/10408448709071208
  3. Clough SR. Sodium sulfite. In: Wexler P, ed. Encyclopedia of Toxicology. 3rd ed. Academic Press; 2014: 341-343.
  4. Vally H, Misso NL, Madan V. Clinical effects of sulphite additives. Clin Exp Allergy. 2009;39:1643-1651. doi:10.1111/j.1365-2222.2009.03362.x
  5. Ralph N, Verma S, Merry S, et al. What is the relevance of contact allergy to sodium metabisulfite and which concentration of the allergen should we use? Dermatitis. 2015;26:162-165. doi:10.1097/der.0000000000000120
  6. Madan V, Walker SL, Beck MH. Sodium metabisulfite allergy is common but is it relevant? Contact Dermatitis. 2007;57:173-176. doi:10.1111/j.1600-0536.2007.01188.x
  7. García-Gavín J, Parente J, Goossens A. Allergic contact dermatitis caused by sodium metabisulfite: a challenging allergen. a case series and literature review. Contact Dermatitis. 2012;67:260-269. doi:10.1111/j.1600-0536.2012.02135.x
  8. Milpied B, van Wassenhove L, Larousse C, et al. Contact dermatitis from rifamycin. Contact Dermatitis. 1986;14:252-253. doi:10.1111/j.1600-0536.1986.tb01240.x
  9. Lodi A, Chiarelli G, Mancini LL, et al. Contact allergy to sodium sulfite contained in an antifungal preparation. Contact Dermatitis. 1993;29:97. doi:10.1111/j.1600-0536.1993.tb03493.x
  10. Sánchez-Pérez J, Abajo P, Córdoba S, et al. Allergic contact dermatitis from sodium metabisulfite in an antihemorrhoidal cream. Contact Dermatitis. 2000;42:176-177.
  11. Boyd AH, Warshaw EM. Sulfites: no longer a zebra? Dermatitis. 2017;28:364-366. doi:10.1097/der.0000000000000312
  12. Grosch E, Mahler V. Allergic contact dermatitis caused by a catheter system containing sodium metabisulfite. Contact Dermatitis. 2017;76:186-187. doi:10.1111/cod.12675
  13. Shaver RL, Warshaw EM. Contact allergens in prescription topical ophthalmic medications. Dermatitis. 2022;33:135-143. doi:10.1097/der.0000000000000751
  14. Dendooven E, Darrigade AS, Foubert K, et al. The presence of sulfites in ‘natural rubber latex’ and ‘synthetic’ rubber gloves: an experimental pilot study. Br J Dermatol. 2020;182:1054-1055. doi:10.1111/bjd.18608
  15. Nater JP. Allergic contact dermatitis caused by potassium metabisulfite. Dermatologica. 1968;136:477-478. doi:10.1159/000254143
  16. Borges AS, Valejo Coelho MM, Fernandes C, et al. Systemic allergic dermatitis caused by sodium metabisulfite in rectal enemas. Contact Dermatitis. 2018;78:429-430. doi:10.1111/cod.12971
  17. Warshaw EM, Buonomo M, DeKoven JG, et al. Patch testing with sodium disulfite: North American Contact Dermatitis Group experience, 2017 to 2018. Contact Dermatitis. 2021;85:285-296. doi:10.1111/cod.13860
  18. Häberle M, Geier J, Mahler V. Contact allergy to sulfites: clinical and occupational relevance—new data from the German ­Contact ­Dermatitis Research Group and the Information Network of ­Departments of ­Dermatology (IVDK). J Dtsch Dermatol Ges. 2016;14:938-941. doi:10.1111/ddg.13009
  19. Tan MG, Li HO, Pratt MD. Systemic allergic dermatitis to sodium metabisulfite in local anesthetic solution. Contact Dermatitis. 2022;86:120-121. doi:10.1111/cod.13978
  20. D’Amore T, Di Taranto A, Berardi G, et al. Sulfites in meat: occurrence, activity, toxicity, regulation, and detection. a comprehensive review. Compr Rev Food Sci Food Saf. 2020;19:2701-2720. doi:10.1111/1541-4337.12607
  21. Grotheer P, Marshall M, Simonne A. Sulfites: separating fact from fiction. May 11, 2022. UF IFAS Extension. University of Florida. Accessed October 4, 2024. https://edis.ifas.ufl.edu/publication/FY731
  22. Silva M, Gama J, Pinto N, et al. Sulfite concentration and the occurrence of headache in young adults: a prospective study. Eur J Clin Nutr. 2019;73:1316-1322. doi:10.1038/s41430-019-0420-2
  23. DeKoven JG, Warshaw EM, Reeder MJ, et al. North American Contact Dermatitis Group patch test results: 2019-2020. Dermatitis. 2023;34:90-104. doi:10.1089/derm.2022.29017.jdk
  24. T.R.U.E. Test. Thin-layer rapid use epicutaneous patch test. SmartPractice Dermatology Allergy. Accessed October 4, 2024. https://www.smartpractice.com/shop/category?id=581719&m=SPA
  25. Schalock PC, Dunnick CA, Nedorost, et al; American Contact Dermatitis Society Core Allergen Series Committee. American ­Contact Dermatitis Society Core Allergen Series: 2020 update. Dermatitis. 2020;31:279-282.
  26. Kaaman AC, Boman A, Wrangsjö K, et al. Contact allergy to sodium metabisulfite: an occupational problem. Contact Dermatitis. 2010;63:110-112. doi:10.1111/j.1600-0536.2010.01756.x
  27. Vena GA, Foti C, Angelini G. Sulfite contact allergy. Contact Dermatitis. 1994;31:172-175. doi:10.1111/j.1600-0536.1994.tb01959.x
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Practice Points

  • Sulfites are ubiquitous compounds that serve as preservatives and antioxidants in various foods, beverages, medications, and personal care products.
  • Allergic contact dermatitis to sulfites most commonly affects the face and hands.
  • Because sulfites are not included in most patch test screening series, contact allergy to sulfites may be missed unless expanded testing is performed.
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At Last, a Nasal Epinephrine Spray

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This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

  • It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
  • It’s easier to carry than many larger devices (though not the AUVI-Q).
  • It cannot be injected incorrectly. 
  • Expiration is 8 months longer than the EAI.
  • There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

 

 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

A version of this article first appeared on Medscape.com.

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This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

  • It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
  • It’s easier to carry than many larger devices (though not the AUVI-Q).
  • It cannot be injected incorrectly. 
  • Expiration is 8 months longer than the EAI.
  • There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

 

 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

A version of this article first appeared on Medscape.com.

This summer, the US Food and Drug Administration (FDA) fast-tracked approval of the first-in-its-class nasal epinephrine (neffy). It’s a very welcome addition to our anaphylaxis treatment armamentarium. As the FDA announcement notes, patients with anaphylaxis at times “delay or avoid” anaphylaxis “treatment due to fear of injections.” Neffy was approved on the basis of pharmacokinetic studies. In healthy volunteers, neffy achieved similar serum epinephrine levels, rises in blood pressure, and pulse compared with IM epinephrine. 

The Need for Neffy

It was just a few days ago that I saw a new patient with fire ant anaphylaxis. The last time he tried to use an injectable epinephrine pen, he made two mistakes. First, he placed the wrong end against his thigh, and when it did not inject, he depressed it with his thumb — in other words, he injected his thumb with epinephrine. Of course, that cannot happen with neffy. 

I recall a few years ago, a child experienced anaphylaxis but the parent was hesitant to administer the EAI (epinephrine autoinjector). The parent drove to the emergency room but was delayed by traffic, and by the time they reached the ER, the patient had suffered a respiratory arrest and passed away. 

Patients are not the only ones who are hesitant to administer epinephrine. Some clinicians do not treat anaphylaxis appropriately. As an allergist, I see patients after-the-fact for diagnosis and management. Patients often tell me of systemic allergic reactions treated with IV antihistamines/corticosteroids and even sometimes with nebulized beta agonists, but not epinephrine. 

My opinion is that it’s not just needle phobia. As I mentioned, in my Medscape commentary “Injectable Epinephrine: An Epidemic of Misuse,” I believe it’s due to a misunderstanding of the guidelines and a sense that epinephrine is a potent medication to be used sparingly. Clinicians and patients must understand that epinephrine is a naturally occurring hormone and administration leads to serum levels seen under other natural circumstances (eg, stress — the fight-or-flight surge). The aforementioned article also includes a patient handout, “Don’t Fear Epinephrine,” which I encourage you to read and distribute. 

The potential benefits of neffy are clear: 

  • It should overcome fear of injection ergo being more likely to be used, and used earlier, by both patient/family member and clinicians.
  • It’s easier to carry than many larger devices (though not the AUVI-Q).
  • It cannot be injected incorrectly. 
  • Expiration is 8 months longer than the EAI.
  • There are no pharmacist substitutions (as there is no equivalent device).

Potential Problems With Neffy and Some Suggested Solutions

As promising and beneficial as it is, I wonder about a few training issues. In the office, patients can be trained with a (reusable) injectable epinephrine trainer but not with a nasal spray device trainer in the office (an important alternative is a small model of a nose in the office for patient education). A training device should also be included in the neffy prescription, as with the EAI.
 

 

 

Neffy and Patients With Nasal Polyps or Nasal Surgery

It’s more complicated than that neffy cannot be used with patients who have had nasal polyps or nasal surgery. It’s really about how much healthy nasal mucosa is required for absorption. Nasal surgery may be simple or complex. Nasal polyps may be obstructive or resolved with nasal steroid or biologic therapy. Nasal polyps affect 2% of the population, but 35% of pediatric food allergy (FA) patients develop allergic rhinitis (AR), and these AR symptoms present even when not triggered by FA. AR is present at baseline in patients with FA. How does this influence neffy absorption? For FA patients who have anaphylactic reactions with severe nasal reactions, neffy absorption could be further compromised, something that has not been studied. 

Insurance Coverage

As we don’t yet know the comparative efficacy of neffy in anaphylactic episodes, it’s likely that patients, especially with more severe food sensitivities, will be prescribed both the nasal and IM devices. The question remains whether insurance will cover both. 

In “mild cases,” I suspect that doctors might be more inclined to prescribe neffy.
 

Conclusion

Delay in epinephrine use is frequent despite the clear indication during anaphylactic episodes, which in turn increases risk for mortality. Neffy will probably save many lives. 

Dr. Stadtmauer serves on the advisory board of Medscape. He is in private practice in New York City and is affiliated with the Mount Sinai School of Medicine. 

A version of this article first appeared on Medscape.com.

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Longitudinal Depression on the Right Thumbnail

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Longitudinal Depression on the Right Thumbnail

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.1,2 It can be considered a variant of onychotillomania.1

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,1 which can be more prominent on the dominant hand.3 Patients typically note a long duration of nail deformity, often without insight into its etiology.2 Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.2 A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.4 Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.3 Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

References
  1. Rieder EA, Tosti A. Onychotillomania: an underrecognized disorder. J Am Acad Dermatol. 2016;75:1245-1250.doi:10.1016/j.jaad.2016
  2. Ring DS. Inexpensive solution for habit-tic deformity. Arch Dermatol. 2010;146:1222-1223. doi:10.1001/archdermatol.2010.287
  3. Horne MI, Utzig JB, Rieder EA, et al. Alopecia areata and habit tic deformities. Skin Appendage Disord. 2018;4:323-325. doi:10.1159/000486540
  4. Sonthalia S, Sharma P, Kapoor J, et al. Habit tic deformity: need fora comprehensive approach. Skin Appendage Disord. 2019;5:117-118.doi:10.1159/000489320 .05.036
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From the Department of Dermatology, University of Maryland School of Medicine, Baltimore.

The authors have no relevant financial disclosures to report.

Correspondence: Shealinna Ge, MD, University of Maryland School of Medicine, Department of Dermatology, 419 W Redwood St, Ste 235, Baltimore, MD 21201 (shealinnage@gmail.com).

Cutis. 2024 November;114(5):140,144. doi:10.12788/cutis.1120

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From the Department of Dermatology, University of Maryland School of Medicine, Baltimore.

The authors have no relevant financial disclosures to report.

Correspondence: Shealinna Ge, MD, University of Maryland School of Medicine, Department of Dermatology, 419 W Redwood St, Ste 235, Baltimore, MD 21201 (shealinnage@gmail.com).

Cutis. 2024 November;114(5):140,144. doi:10.12788/cutis.1120

Author and Disclosure Information

From the Department of Dermatology, University of Maryland School of Medicine, Baltimore.

The authors have no relevant financial disclosures to report.

Correspondence: Shealinna Ge, MD, University of Maryland School of Medicine, Department of Dermatology, 419 W Redwood St, Ste 235, Baltimore, MD 21201 (shealinnage@gmail.com).

Cutis. 2024 November;114(5):140,144. doi:10.12788/cutis.1120

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Related Articles

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.1,2 It can be considered a variant of onychotillomania.1

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,1 which can be more prominent on the dominant hand.3 Patients typically note a long duration of nail deformity, often without insight into its etiology.2 Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.2 A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.4 Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.3 Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

THE DIAGNOSIS: Habit-Tic Deformity

Habit-tic deformity is a cause of nail dystrophy that commonly arises in children and adults due to subconscious repetitive and self-injurious manipulation of the nail bed or cuticle, which ultimately damages the nail matrix.1,2 It can be considered a variant of onychotillomania.1

Characteristic features of habit-tic deformity include a longitudinal depression on the central nail plate with transverse ridges,1 which can be more prominent on the dominant hand.3 Patients typically note a long duration of nail deformity, often without insight into its etiology.2 Diagnosis relies on careful assessment of the clinical presentation and the patient’s history to rule out other differential diagnoses. Based on our patient’s clinical presentation and history, we excluded wart, squamous cell carcinoma, eczema, psoriasis, lichen planus, autoimmune connective tissue disease, onychomycosis, paronychia, pincer nail deformity, and Beau line as potential diagnoses. Biopsy also can be performed to exclude these diagnoses from the differential if the cause is unclear following clinical examination.

Treatment for habit-tic deformity involves identifying and addressing the underlying habit. Barrier methods such as bandages and cyanoacrylate adhesives that prevent further manipulation of the nail matrix are effective treatments for habit-tic deformity.2 A multidisciplinary approach with psychiatry may be optimal to identify underlying psychological comorbidities and break the habit through behavior interventions and medications.4 Nail dystrophy generally improves once the habit is disrupted; however, a younger age of onset may carry a worse prognosis.3 Patients should be counseled that the affected nail may never grow normally.

Our patient was advised to use fluocinonide ointment 0.05% to reduce inflammation of the proximal nail fold and to cover the thumbnail with a bandage to prevent picking. He also was counseled that the nail may show ongoing abnormal growth. Minimal improvement was noted after 6 months.

References
  1. Rieder EA, Tosti A. Onychotillomania: an underrecognized disorder. J Am Acad Dermatol. 2016;75:1245-1250.doi:10.1016/j.jaad.2016
  2. Ring DS. Inexpensive solution for habit-tic deformity. Arch Dermatol. 2010;146:1222-1223. doi:10.1001/archdermatol.2010.287
  3. Horne MI, Utzig JB, Rieder EA, et al. Alopecia areata and habit tic deformities. Skin Appendage Disord. 2018;4:323-325. doi:10.1159/000486540
  4. Sonthalia S, Sharma P, Kapoor J, et al. Habit tic deformity: need fora comprehensive approach. Skin Appendage Disord. 2019;5:117-118.doi:10.1159/000489320 .05.036
References
  1. Rieder EA, Tosti A. Onychotillomania: an underrecognized disorder. J Am Acad Dermatol. 2016;75:1245-1250.doi:10.1016/j.jaad.2016
  2. Ring DS. Inexpensive solution for habit-tic deformity. Arch Dermatol. 2010;146:1222-1223. doi:10.1001/archdermatol.2010.287
  3. Horne MI, Utzig JB, Rieder EA, et al. Alopecia areata and habit tic deformities. Skin Appendage Disord. 2018;4:323-325. doi:10.1159/000486540
  4. Sonthalia S, Sharma P, Kapoor J, et al. Habit tic deformity: need fora comprehensive approach. Skin Appendage Disord. 2019;5:117-118.doi:10.1159/000489320 .05.036
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A healthy 13-year-old boy presented to the dermatology department with dystrophy of the right thumbnail of 3 to 4 years’ duration. A 5-mm-wide, depressed median longitudinal groove with a fir tree pattern was noted on the central nail plate. The patient noted that the groove had been gradually deepening. There was erythema, edema, and lichenification of the proximal nailfold without vascular changes, and the lunula was enlarged. No hyperkeratosis, subungual debris, erythematous nail folds, or inward curvature of the lateral aspects of the nail were noted. The patient denied any pruritus, pain, discomfort, or bleeding; he also denied any recent illness or trauma to the nail. None of the other nails were affected, and no other lesions or rashes were observed elsewhere on the body. The patient was unsure if he picked at the nail but acknowledged that he may have done so subconsciously. He had no history of eczema, psoriasis, or autoimmune connective tissue disorders.

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On the Road to Care: Travel Nurses Still in Demand

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Thu, 11/07/2024 - 13:35

Ashly Doran has worked at seven hospitals in four states since she graduated from nursing school in 2020. No, she isn’t job-hopping. Her travel nursing assignments have ranged from level 1 trauma center emergency rooms in big cities to small medical-surgical units in the suburbs. After each 13-week assignment, Doran packs up her belongings and her cats and moves to a new post.

“Travel nursing is so flexible,” she said. “I decide where I want to go and how much I want to make and start looking for travel contracts in that area.”

Nationwide nursing shortages have forced hospitals to hire travel nurses to fill staffing gaps. During the COVID-19 pandemic, the demand for travel nurses increased by 35%. While there is still a demand for nurses to fill short-term contracts, data show that demand has declined 42% between January and July 2022 and has continued the downward trend.

“What we’re seeing now is a shift…to a pre-pandemic market,” said Rachel Neill, RN, senior clinician advocate at Vivian Health. “Travel [nursing] is not going away — there will always be a need for hospital systems and facilities to fill gaps — but hospitals have shifted more into a traditional ... operational environment.”
 

Traveling a Different Path

For some registered nurses (RNs), short-term assignments offer opportunities to gain experience in different facilities or explore new locations before settling into permanent positions. Even experienced RNs embrace travel nursing for the flexible schedules and opportunities to take longer breaks between contracts.

Burnout and turnover among nurses are high, and flexible schedules, including controlling when to work, are essential to sustaining a clinical nursing career. In fact, 34% of nurses called travel nursing an “ideal option” for their lifestyle, with 14% viewing it as an option for career progression.

Travel nursing is especially appealing to Millennials and Generation Z, according to Brian Weirich, RN, chief nurse innovation officer at Bon Secours Mercy Health in Cincinnati, Ohio. In fact, the average age of a travel nurse is 35 compared with an average age of 52 for all RNs.

These are generations that are more focused on reducing school loan debt and gaining experience, not 401(k) and health insurance, he said in an interview. Pay is also a factor. The average pay for travel nurses was $2588 per month, compared with $1375 for permanent staff nurses.

During the pandemic, Weirich recalls groups of nurses resigning to take travel assignments together. The RNs picked desirable locations, accepted short-term assignments, and moved together, “making top dollar in locations they wanted to explore with their best friends.”

It’s been more than a decade since Kelly Spurlock traded a permanent nursing role in Lake Placid, Florida, for short-term nursing contracts in intensive care units in 20 states.

Spurlock works with a recruiter at Ingenovis Health to secure new contracts and considers travel assignments “working vacations.” In the process of exploring new places and meeting new people, Spurlock believes that travel nursing allows her to prioritize patient care.

“I can be at the bedside and be an advocate for my patient but also keep out of the spotlight for the political part of what we do,” she explained.
 

 

 

The Road Ahead

The appeal of travel nursing is taking new nursing assignments in different cities and earning higher salaries, but there are downsides, too. Travel nurses often receive fewer benefits than staff nurses and end up with less favorable assignments; their levels of dissatisfaction and burnout are also higher, and their sense of work-life balance is lower than staff nurses.

Most travel contracts last between 4 and 13 weeks. Hospitals often put policies and practices in place that limit the number of back-to-back contracts that traveling nurses can accept, which means that RNs can either convert to core staff or move on to new assignments once their contract term is up.

Weirich noted that some hospitals devote considerable effort to recruiting traveling nurses to full-time roles, adding, “There are active initiatives ... to make it such a good experience that they want to stay.”

On the flip side, contracts can be terminated without notice, leaving traveling nurses scrambling to find a new assignment and a new place to live on short notice.

“You’re there as long as the hospital needs you,” said Neill. “You could sign a 12- or 15-week contract, and their needs change a month in, and ... there are budget cuts, and they can’t pay salaries anymore, so they are laying off their nurses.”

Declining demand for travel nurses has made it harder to line up back-to-back contracts. Despite being available for work, Doran once waited 6 weeks to secure a new assignment and had to live off her savings.

Spurlock believes increased competition and declining wages — pay for travel nurses declined more than 9% from January 2023 to January 2024 — have made travel nursing less attractive.

“There has been such an influx of travel nurses ... because of COVID,” said Spurlock. “The rates have now come down [and] everybody’s fighting for jobs, and ... it’s very difficult to get a job that’s paying decent money.”

Despite the challenges, Spurlock continues learning new things from each assignment and hopes to work as a travel nurse until retirement. Doran has worked at hospitals in Washington, Oregon, California, and Wisconsin and would like to add Montana, Utah, and Nevada to the list. The goal: Continue accepting assignments in different cities and states until she finds the place where she wants to put down roots.

“Nursing is a great job, but it’s a hard job [and] it can take its toll at times,” Neill said. It’s important that nurses know their goals and values to be able to find a good fitting position. “And the beauty of it is that travel can be a great way to explore and add some flexibility.”

A version of this article first appeared on Medscape.com.

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Ashly Doran has worked at seven hospitals in four states since she graduated from nursing school in 2020. No, she isn’t job-hopping. Her travel nursing assignments have ranged from level 1 trauma center emergency rooms in big cities to small medical-surgical units in the suburbs. After each 13-week assignment, Doran packs up her belongings and her cats and moves to a new post.

“Travel nursing is so flexible,” she said. “I decide where I want to go and how much I want to make and start looking for travel contracts in that area.”

Nationwide nursing shortages have forced hospitals to hire travel nurses to fill staffing gaps. During the COVID-19 pandemic, the demand for travel nurses increased by 35%. While there is still a demand for nurses to fill short-term contracts, data show that demand has declined 42% between January and July 2022 and has continued the downward trend.

“What we’re seeing now is a shift…to a pre-pandemic market,” said Rachel Neill, RN, senior clinician advocate at Vivian Health. “Travel [nursing] is not going away — there will always be a need for hospital systems and facilities to fill gaps — but hospitals have shifted more into a traditional ... operational environment.”
 

Traveling a Different Path

For some registered nurses (RNs), short-term assignments offer opportunities to gain experience in different facilities or explore new locations before settling into permanent positions. Even experienced RNs embrace travel nursing for the flexible schedules and opportunities to take longer breaks between contracts.

Burnout and turnover among nurses are high, and flexible schedules, including controlling when to work, are essential to sustaining a clinical nursing career. In fact, 34% of nurses called travel nursing an “ideal option” for their lifestyle, with 14% viewing it as an option for career progression.

Travel nursing is especially appealing to Millennials and Generation Z, according to Brian Weirich, RN, chief nurse innovation officer at Bon Secours Mercy Health in Cincinnati, Ohio. In fact, the average age of a travel nurse is 35 compared with an average age of 52 for all RNs.

These are generations that are more focused on reducing school loan debt and gaining experience, not 401(k) and health insurance, he said in an interview. Pay is also a factor. The average pay for travel nurses was $2588 per month, compared with $1375 for permanent staff nurses.

During the pandemic, Weirich recalls groups of nurses resigning to take travel assignments together. The RNs picked desirable locations, accepted short-term assignments, and moved together, “making top dollar in locations they wanted to explore with their best friends.”

It’s been more than a decade since Kelly Spurlock traded a permanent nursing role in Lake Placid, Florida, for short-term nursing contracts in intensive care units in 20 states.

Spurlock works with a recruiter at Ingenovis Health to secure new contracts and considers travel assignments “working vacations.” In the process of exploring new places and meeting new people, Spurlock believes that travel nursing allows her to prioritize patient care.

“I can be at the bedside and be an advocate for my patient but also keep out of the spotlight for the political part of what we do,” she explained.
 

 

 

The Road Ahead

The appeal of travel nursing is taking new nursing assignments in different cities and earning higher salaries, but there are downsides, too. Travel nurses often receive fewer benefits than staff nurses and end up with less favorable assignments; their levels of dissatisfaction and burnout are also higher, and their sense of work-life balance is lower than staff nurses.

Most travel contracts last between 4 and 13 weeks. Hospitals often put policies and practices in place that limit the number of back-to-back contracts that traveling nurses can accept, which means that RNs can either convert to core staff or move on to new assignments once their contract term is up.

Weirich noted that some hospitals devote considerable effort to recruiting traveling nurses to full-time roles, adding, “There are active initiatives ... to make it such a good experience that they want to stay.”

On the flip side, contracts can be terminated without notice, leaving traveling nurses scrambling to find a new assignment and a new place to live on short notice.

“You’re there as long as the hospital needs you,” said Neill. “You could sign a 12- or 15-week contract, and their needs change a month in, and ... there are budget cuts, and they can’t pay salaries anymore, so they are laying off their nurses.”

Declining demand for travel nurses has made it harder to line up back-to-back contracts. Despite being available for work, Doran once waited 6 weeks to secure a new assignment and had to live off her savings.

Spurlock believes increased competition and declining wages — pay for travel nurses declined more than 9% from January 2023 to January 2024 — have made travel nursing less attractive.

“There has been such an influx of travel nurses ... because of COVID,” said Spurlock. “The rates have now come down [and] everybody’s fighting for jobs, and ... it’s very difficult to get a job that’s paying decent money.”

Despite the challenges, Spurlock continues learning new things from each assignment and hopes to work as a travel nurse until retirement. Doran has worked at hospitals in Washington, Oregon, California, and Wisconsin and would like to add Montana, Utah, and Nevada to the list. The goal: Continue accepting assignments in different cities and states until she finds the place where she wants to put down roots.

“Nursing is a great job, but it’s a hard job [and] it can take its toll at times,” Neill said. It’s important that nurses know their goals and values to be able to find a good fitting position. “And the beauty of it is that travel can be a great way to explore and add some flexibility.”

A version of this article first appeared on Medscape.com.

Ashly Doran has worked at seven hospitals in four states since she graduated from nursing school in 2020. No, she isn’t job-hopping. Her travel nursing assignments have ranged from level 1 trauma center emergency rooms in big cities to small medical-surgical units in the suburbs. After each 13-week assignment, Doran packs up her belongings and her cats and moves to a new post.

“Travel nursing is so flexible,” she said. “I decide where I want to go and how much I want to make and start looking for travel contracts in that area.”

Nationwide nursing shortages have forced hospitals to hire travel nurses to fill staffing gaps. During the COVID-19 pandemic, the demand for travel nurses increased by 35%. While there is still a demand for nurses to fill short-term contracts, data show that demand has declined 42% between January and July 2022 and has continued the downward trend.

“What we’re seeing now is a shift…to a pre-pandemic market,” said Rachel Neill, RN, senior clinician advocate at Vivian Health. “Travel [nursing] is not going away — there will always be a need for hospital systems and facilities to fill gaps — but hospitals have shifted more into a traditional ... operational environment.”
 

Traveling a Different Path

For some registered nurses (RNs), short-term assignments offer opportunities to gain experience in different facilities or explore new locations before settling into permanent positions. Even experienced RNs embrace travel nursing for the flexible schedules and opportunities to take longer breaks between contracts.

Burnout and turnover among nurses are high, and flexible schedules, including controlling when to work, are essential to sustaining a clinical nursing career. In fact, 34% of nurses called travel nursing an “ideal option” for their lifestyle, with 14% viewing it as an option for career progression.

Travel nursing is especially appealing to Millennials and Generation Z, according to Brian Weirich, RN, chief nurse innovation officer at Bon Secours Mercy Health in Cincinnati, Ohio. In fact, the average age of a travel nurse is 35 compared with an average age of 52 for all RNs.

These are generations that are more focused on reducing school loan debt and gaining experience, not 401(k) and health insurance, he said in an interview. Pay is also a factor. The average pay for travel nurses was $2588 per month, compared with $1375 for permanent staff nurses.

During the pandemic, Weirich recalls groups of nurses resigning to take travel assignments together. The RNs picked desirable locations, accepted short-term assignments, and moved together, “making top dollar in locations they wanted to explore with their best friends.”

It’s been more than a decade since Kelly Spurlock traded a permanent nursing role in Lake Placid, Florida, for short-term nursing contracts in intensive care units in 20 states.

Spurlock works with a recruiter at Ingenovis Health to secure new contracts and considers travel assignments “working vacations.” In the process of exploring new places and meeting new people, Spurlock believes that travel nursing allows her to prioritize patient care.

“I can be at the bedside and be an advocate for my patient but also keep out of the spotlight for the political part of what we do,” she explained.
 

 

 

The Road Ahead

The appeal of travel nursing is taking new nursing assignments in different cities and earning higher salaries, but there are downsides, too. Travel nurses often receive fewer benefits than staff nurses and end up with less favorable assignments; their levels of dissatisfaction and burnout are also higher, and their sense of work-life balance is lower than staff nurses.

Most travel contracts last between 4 and 13 weeks. Hospitals often put policies and practices in place that limit the number of back-to-back contracts that traveling nurses can accept, which means that RNs can either convert to core staff or move on to new assignments once their contract term is up.

Weirich noted that some hospitals devote considerable effort to recruiting traveling nurses to full-time roles, adding, “There are active initiatives ... to make it such a good experience that they want to stay.”

On the flip side, contracts can be terminated without notice, leaving traveling nurses scrambling to find a new assignment and a new place to live on short notice.

“You’re there as long as the hospital needs you,” said Neill. “You could sign a 12- or 15-week contract, and their needs change a month in, and ... there are budget cuts, and they can’t pay salaries anymore, so they are laying off their nurses.”

Declining demand for travel nurses has made it harder to line up back-to-back contracts. Despite being available for work, Doran once waited 6 weeks to secure a new assignment and had to live off her savings.

Spurlock believes increased competition and declining wages — pay for travel nurses declined more than 9% from January 2023 to January 2024 — have made travel nursing less attractive.

“There has been such an influx of travel nurses ... because of COVID,” said Spurlock. “The rates have now come down [and] everybody’s fighting for jobs, and ... it’s very difficult to get a job that’s paying decent money.”

Despite the challenges, Spurlock continues learning new things from each assignment and hopes to work as a travel nurse until retirement. Doran has worked at hospitals in Washington, Oregon, California, and Wisconsin and would like to add Montana, Utah, and Nevada to the list. The goal: Continue accepting assignments in different cities and states until she finds the place where she wants to put down roots.

“Nursing is a great job, but it’s a hard job [and] it can take its toll at times,” Neill said. It’s important that nurses know their goals and values to be able to find a good fitting position. “And the beauty of it is that travel can be a great way to explore and add some flexibility.”

A version of this article first appeared on Medscape.com.

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The Bad News Behind the Rise in Locum Tenens

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Thu, 11/07/2024 - 13:24

I’ve worked locum tenens off and on since 1982. Flexible schedules allowed me to write several books, pursue a parallel career as a medical journalist, lead medical missions in the Philippines, and develop modest expertise as an underwater photographer.

But the recent rise in locum tenens practitioners signals trouble for medicine.
 

A Multibillion-Dollar Industry

Roughly 52,000 US doctors work locum tenens full or part time. In annual reports by CHG Healthcare, two thirds of healthcare facilities surveyed report using locums and more than half expect to maintain or increase their use in 2024.

Another measure of the industry’s growth is that membership of The National Association of Locum Tenens Organizations (NALTO), formed in 2001 to lead this fledgling industry, has doubled since 2019. Currently, NALTO has 148 member agencies.
 

Why Locums?

What used to be the preserve of older physicians transitioning to retirement is now becoming a career choice. According to the 2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals by AMN Healthcare, 81% of respondents said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. What entices doctors to move from place to place, repeatedly adapt to new facilities and electronic medical records, live in cheap hotels, and work without paid vacations, health insurance, or retirement benefits? 

Supplemental income is one reason. But the elephant in the room is clearly burnout. Rates of burnout in practicing doctors and physicians-in-training have exceeded 50%. Burnout results in medical errors, malpractice suits, and increased healthcare costs. 

A recent Doximity poll of 7590 physicians revealed that 63% would not want their children to pursue a medical career. And in a Medscape survey of 7000 physicians, a third of docs under 40 would not choose medicine again if they had a do-over. If a career in medicine brings high income and privileged status, why do so many physicians regret it and discourage their children from taking the same path?
 

Where Is Marcus Welby, MD?

Private practice is an endangered species that no one is trying to save. According to a 2022 AMA survey, 44% of physicians owned their practices compared with 76% of physicians in the 1980s. Even fewer younger physicians are choosing private practice. Among physicians under 45 years of age, only 32% owned their practices. Most physicians are now employees, not employers. They have lost control over their duties and work hours. 

In 2022, barely 13% of physicians were in solo practice. The iconic Dr Marcus Welby of the 1970s TV series has transmuted from an idealized physician to an implausible figure. (My medical students have never heard of him.)

Hospitals and health systems have purchased many private medical groups. Private-equity companies own close to 1000 physician practices and staff up to 40% of emergency rooms. For these firms, profits are paramount.
 

Canary in a Coal Mine

Locum tenens offers physicians unprecedented flexibility where they work, when they work, and how much they work. It provides an escape from overwhelming and unsatisfying clinical practice. While some physicians have fled to nonclinical careers, locums physicians can practice medicine without the burdens of administration, hospital politics, and ever-increasing overhead. 

The locum tenens paradox is that its successful growth indicates a deteriorating traditional healthcare model. Locum tenens is not the problem, but it’s also not the solution. At best, locums is a pair of crutches that helps the current system limp along.

Healthcare is increasingly controlled by those who prioritize profit, not patients. If physicians become nothing more than complicit cogs in a dysfunctional system, burnout will fester. The profession will fail to attract the best and the brightest, the doctor shortage will increase, and the quality of patient care will decline. Everyone will suffer. 

It’s already happening.

Andrew Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. He reported conflicts of interest from Accordant Health Services.
 

A version of this article first appeared on Medscape.com.

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I’ve worked locum tenens off and on since 1982. Flexible schedules allowed me to write several books, pursue a parallel career as a medical journalist, lead medical missions in the Philippines, and develop modest expertise as an underwater photographer.

But the recent rise in locum tenens practitioners signals trouble for medicine.
 

A Multibillion-Dollar Industry

Roughly 52,000 US doctors work locum tenens full or part time. In annual reports by CHG Healthcare, two thirds of healthcare facilities surveyed report using locums and more than half expect to maintain or increase their use in 2024.

Another measure of the industry’s growth is that membership of The National Association of Locum Tenens Organizations (NALTO), formed in 2001 to lead this fledgling industry, has doubled since 2019. Currently, NALTO has 148 member agencies.
 

Why Locums?

What used to be the preserve of older physicians transitioning to retirement is now becoming a career choice. According to the 2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals by AMN Healthcare, 81% of respondents said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. What entices doctors to move from place to place, repeatedly adapt to new facilities and electronic medical records, live in cheap hotels, and work without paid vacations, health insurance, or retirement benefits? 

Supplemental income is one reason. But the elephant in the room is clearly burnout. Rates of burnout in practicing doctors and physicians-in-training have exceeded 50%. Burnout results in medical errors, malpractice suits, and increased healthcare costs. 

A recent Doximity poll of 7590 physicians revealed that 63% would not want their children to pursue a medical career. And in a Medscape survey of 7000 physicians, a third of docs under 40 would not choose medicine again if they had a do-over. If a career in medicine brings high income and privileged status, why do so many physicians regret it and discourage their children from taking the same path?
 

Where Is Marcus Welby, MD?

Private practice is an endangered species that no one is trying to save. According to a 2022 AMA survey, 44% of physicians owned their practices compared with 76% of physicians in the 1980s. Even fewer younger physicians are choosing private practice. Among physicians under 45 years of age, only 32% owned their practices. Most physicians are now employees, not employers. They have lost control over their duties and work hours. 

In 2022, barely 13% of physicians were in solo practice. The iconic Dr Marcus Welby of the 1970s TV series has transmuted from an idealized physician to an implausible figure. (My medical students have never heard of him.)

Hospitals and health systems have purchased many private medical groups. Private-equity companies own close to 1000 physician practices and staff up to 40% of emergency rooms. For these firms, profits are paramount.
 

Canary in a Coal Mine

Locum tenens offers physicians unprecedented flexibility where they work, when they work, and how much they work. It provides an escape from overwhelming and unsatisfying clinical practice. While some physicians have fled to nonclinical careers, locums physicians can practice medicine without the burdens of administration, hospital politics, and ever-increasing overhead. 

The locum tenens paradox is that its successful growth indicates a deteriorating traditional healthcare model. Locum tenens is not the problem, but it’s also not the solution. At best, locums is a pair of crutches that helps the current system limp along.

Healthcare is increasingly controlled by those who prioritize profit, not patients. If physicians become nothing more than complicit cogs in a dysfunctional system, burnout will fester. The profession will fail to attract the best and the brightest, the doctor shortage will increase, and the quality of patient care will decline. Everyone will suffer. 

It’s already happening.

Andrew Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. He reported conflicts of interest from Accordant Health Services.
 

A version of this article first appeared on Medscape.com.

I’ve worked locum tenens off and on since 1982. Flexible schedules allowed me to write several books, pursue a parallel career as a medical journalist, lead medical missions in the Philippines, and develop modest expertise as an underwater photographer.

But the recent rise in locum tenens practitioners signals trouble for medicine.
 

A Multibillion-Dollar Industry

Roughly 52,000 US doctors work locum tenens full or part time. In annual reports by CHG Healthcare, two thirds of healthcare facilities surveyed report using locums and more than half expect to maintain or increase their use in 2024.

Another measure of the industry’s growth is that membership of The National Association of Locum Tenens Organizations (NALTO), formed in 2001 to lead this fledgling industry, has doubled since 2019. Currently, NALTO has 148 member agencies.
 

Why Locums?

What used to be the preserve of older physicians transitioning to retirement is now becoming a career choice. According to the 2024 Survey of Locum Tenens Physicians and Advanced Practice Professionals by AMN Healthcare, 81% of respondents said they started taking locum tenens assignments immediately after finishing medical training or in mid-career. What entices doctors to move from place to place, repeatedly adapt to new facilities and electronic medical records, live in cheap hotels, and work without paid vacations, health insurance, or retirement benefits? 

Supplemental income is one reason. But the elephant in the room is clearly burnout. Rates of burnout in practicing doctors and physicians-in-training have exceeded 50%. Burnout results in medical errors, malpractice suits, and increased healthcare costs. 

A recent Doximity poll of 7590 physicians revealed that 63% would not want their children to pursue a medical career. And in a Medscape survey of 7000 physicians, a third of docs under 40 would not choose medicine again if they had a do-over. If a career in medicine brings high income and privileged status, why do so many physicians regret it and discourage their children from taking the same path?
 

Where Is Marcus Welby, MD?

Private practice is an endangered species that no one is trying to save. According to a 2022 AMA survey, 44% of physicians owned their practices compared with 76% of physicians in the 1980s. Even fewer younger physicians are choosing private practice. Among physicians under 45 years of age, only 32% owned their practices. Most physicians are now employees, not employers. They have lost control over their duties and work hours. 

In 2022, barely 13% of physicians were in solo practice. The iconic Dr Marcus Welby of the 1970s TV series has transmuted from an idealized physician to an implausible figure. (My medical students have never heard of him.)

Hospitals and health systems have purchased many private medical groups. Private-equity companies own close to 1000 physician practices and staff up to 40% of emergency rooms. For these firms, profits are paramount.
 

Canary in a Coal Mine

Locum tenens offers physicians unprecedented flexibility where they work, when they work, and how much they work. It provides an escape from overwhelming and unsatisfying clinical practice. While some physicians have fled to nonclinical careers, locums physicians can practice medicine without the burdens of administration, hospital politics, and ever-increasing overhead. 

The locum tenens paradox is that its successful growth indicates a deteriorating traditional healthcare model. Locum tenens is not the problem, but it’s also not the solution. At best, locums is a pair of crutches that helps the current system limp along.

Healthcare is increasingly controlled by those who prioritize profit, not patients. If physicians become nothing more than complicit cogs in a dysfunctional system, burnout will fester. The profession will fail to attract the best and the brightest, the doctor shortage will increase, and the quality of patient care will decline. Everyone will suffer. 

It’s already happening.

Andrew Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. He reported conflicts of interest from Accordant Health Services.
 

A version of this article first appeared on Medscape.com.

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Myasthenia Gravis Highlights From AANEM 2024

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Fri, 11/08/2024 - 11:58
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Myasthenia Gravis Highlights From AANEM 2024

The latest data on myasthenia gravis (MG) research, reported at the American Association of Neuromuscular and Electrodiagnostic Medicine 2024 Annual Meeting, are presented by Dr Pushpa Narayanswami of Harvard Medical School in Boston, Massachusetts.  

Dr Narayanswami begins with a safety, tolerability, and efficacy study for subcutaneous efgartigimod. Results showed that the mean change in MG activities of daily living (MG-ADL) was no different between the fixed-dose and cyclic regimens, demonstrating another dosage option for patients.

Next, Dr Narayanswami discusses two separate complement C5 inhibitor therapy trials. The first was a global registry study looking at ravulizumab. Patient cohorts consisted of those who started and remained on ravulizumab vs another that switched from initial eculizumab to ravulizumab. In both groups, MG-ADL was improved. The other study investigated zilucoplan in acetylcholine receptor autoantibody–positive generalized MG patient populations; similarly, researchers found favorable results.

She then details a study looking at the safety outcomes in pregnant patients treated with eculizumab. Because of limited disease-specific data in the registry, further investigation is recommended.

Finally, Dr Narayanaswami examines results for inebilizumab, a first-in-class anti-CD19 B cell–depleting agent. The drug demonstrated safety and beneficial efficacy compared with placebo in seropositive generalized MG patients.

--

Pushpa Narayanaswami, MD, Associate Professor, Department of Neurology, Harvard Medical School; Vice Chair of Clinical Operations, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Pushpa Narayanaswami, MD, has disclosed the following relevant financial relationships:

Serve(d) as an advisor or consultant for: Alexion; Argenx; Janssen; Dianthus; UCB; GSK

Received research grant from: Alexion; UCB; Dianthus; Janssen

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The latest data on myasthenia gravis (MG) research, reported at the American Association of Neuromuscular and Electrodiagnostic Medicine 2024 Annual Meeting, are presented by Dr Pushpa Narayanswami of Harvard Medical School in Boston, Massachusetts.  

Dr Narayanswami begins with a safety, tolerability, and efficacy study for subcutaneous efgartigimod. Results showed that the mean change in MG activities of daily living (MG-ADL) was no different between the fixed-dose and cyclic regimens, demonstrating another dosage option for patients.

Next, Dr Narayanswami discusses two separate complement C5 inhibitor therapy trials. The first was a global registry study looking at ravulizumab. Patient cohorts consisted of those who started and remained on ravulizumab vs another that switched from initial eculizumab to ravulizumab. In both groups, MG-ADL was improved. The other study investigated zilucoplan in acetylcholine receptor autoantibody–positive generalized MG patient populations; similarly, researchers found favorable results.

She then details a study looking at the safety outcomes in pregnant patients treated with eculizumab. Because of limited disease-specific data in the registry, further investigation is recommended.

Finally, Dr Narayanaswami examines results for inebilizumab, a first-in-class anti-CD19 B cell–depleting agent. The drug demonstrated safety and beneficial efficacy compared with placebo in seropositive generalized MG patients.

--

Pushpa Narayanaswami, MD, Associate Professor, Department of Neurology, Harvard Medical School; Vice Chair of Clinical Operations, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Pushpa Narayanaswami, MD, has disclosed the following relevant financial relationships:

Serve(d) as an advisor or consultant for: Alexion; Argenx; Janssen; Dianthus; UCB; GSK

Received research grant from: Alexion; UCB; Dianthus; Janssen

The latest data on myasthenia gravis (MG) research, reported at the American Association of Neuromuscular and Electrodiagnostic Medicine 2024 Annual Meeting, are presented by Dr Pushpa Narayanswami of Harvard Medical School in Boston, Massachusetts.  

Dr Narayanswami begins with a safety, tolerability, and efficacy study for subcutaneous efgartigimod. Results showed that the mean change in MG activities of daily living (MG-ADL) was no different between the fixed-dose and cyclic regimens, demonstrating another dosage option for patients.

Next, Dr Narayanswami discusses two separate complement C5 inhibitor therapy trials. The first was a global registry study looking at ravulizumab. Patient cohorts consisted of those who started and remained on ravulizumab vs another that switched from initial eculizumab to ravulizumab. In both groups, MG-ADL was improved. The other study investigated zilucoplan in acetylcholine receptor autoantibody–positive generalized MG patient populations; similarly, researchers found favorable results.

She then details a study looking at the safety outcomes in pregnant patients treated with eculizumab. Because of limited disease-specific data in the registry, further investigation is recommended.

Finally, Dr Narayanaswami examines results for inebilizumab, a first-in-class anti-CD19 B cell–depleting agent. The drug demonstrated safety and beneficial efficacy compared with placebo in seropositive generalized MG patients.

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Pushpa Narayanaswami, MD, Associate Professor, Department of Neurology, Harvard Medical School; Vice Chair of Clinical Operations, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts

Pushpa Narayanaswami, MD, has disclosed the following relevant financial relationships:

Serve(d) as an advisor or consultant for: Alexion; Argenx; Janssen; Dianthus; UCB; GSK

Received research grant from: Alexion; UCB; Dianthus; Janssen

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