Cutis

Psoriasis, a chronic immune-mediated skin disease, is increasingly recognized for its systemic inflammation and associated cardiometabolic risk. The global rise of obesity has revealed a critical link between these 2 conditions. Current evidence confirms that obesity is an independent risk factor that can trigger psoriasis onset, drive more severe disease, and substantially impair treatment efficacy.^1,2 This review synthesizes the latest evidence on the shared pathophysiology, clinical consequences, and integrated management strategies for patients with both psoriasis and obesity.

Pathophysiologic Links Between Psoriasis and Obesity

Emerging evidence highlights a bidirectional relationship between psoriasis and obesity rooted in overlapping inflammatory pathways. Both conditions are characterized by chronic inflammation mediated by cytokines that sustain systemic immune activation and metabolic dysfunction. This interplay creates a reciprocal process in which psoriatic inflammation promotes metabolic disturbances while obesity amplifies systemic inflammation and disease severity.³

Psoriasis may contribute to obesity through cytokine-driven metabolic alterations in insulin signaling and adipocyte function. The psoriatic immune response is dominated by T helper (Th) 1, Th17, and Th22 cell activation, leading to elevated levels of interferon-γ, tumor necrosis factor (TNF) α, interleukin (IL) 6, IL-17, and IL-22 from keratinocytes.⁴ These cytokines contribute not only to cutaneous inflammation but also to insulin resistance and adipocyte dysfunction.⁵ Tumor necrosis factor α and IL-6 interfere with insulin signaling via activation of stress kinases (eg, IκB kinase and c-Jun N-terminal kinase), implicating these molecules in insulin resistance and weight gain.⁶ Moreover, IL-17, a central cytokine in psoriasis, has been implicated in vascular inflammation, insulin resistance, and type 2 diabetes, suggesting a mechanistic link between psoriatic inflammation and metabolic disease.⁵ Additionally, chronic systemic inflammation in psoriasis suppresses adiponectin, a protective adipokine that enhances insulin sensitivity and exerts anti-inflammatory effects by inhibiting TNF-α and IL-6 production while promoting IL-10 synthesis. Reduced adiponectin levels have consistently been observed in patients with psoriasis and concomitant obesity or metabolic syndrome.³ The resultant imbalance between proinflammatory and anti-inflammatory mediators creates a metabolic environment conducive to obesity.³

Conversely, obesity itself may intensify both the incidence and severity of psoriasis through shared inflammatory pathways. Leptin, whose expression rises proportionally with adipocyte mass, acts as a proinflammatory mediator linking obesity to psoriasis exacerbation. By promoting Th1 and Th17 cell differentiation and suppressing regulatory T-cell activity, leptin increases IL-17A, IL-6, and TNF-α production.⁷ These cytokines stimulate keratinocyte proliferation and perpetuate cutaneous inflammation, thereby intensifying disease activity. Similarly, resistin, another adipokine that is elevated in obesity, stimulates monocytes and macrophages to secrete TNF-α and IL-6, creating a proinflammatory state in the body that drives the relationship between excessive fat storage (adiposity) and the development and severity of psoriasis.⁸ In contrast, reduced adiponectin levels in obesity remove a key anti-inflammatory regulator that normally inhibits TNF-α and IL-6 synthesis and promotes IL-10 production. This deficiency provokes unrestrained cytokine activation within both adipose and cutaneous tissue, exacerbating psoriatic immune dysregulation.⁹

Free fatty acids derived from abundant adipocytes in obesity further activate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)–signaling and induce oxidative stress, augmenting systemic inflammation. Adipose tissue macrophages additionally secrete IL-1Β, IL-6, and TNF-α, which promote keratinocyte proliferation and amplify the psoriatic inflammatory cascade. Importantly, anti–TNF-α therapy has been shown to improve metabolic parameters, reducing low-density lipoprotein and total cholesterol levels and enhancing insulin sensitivity, highlighting the reciprocal benefits of dampening the inflammatory signaling from TNF-α.⁵

Together, these findings highlight that psoriasis and obesity are interconnected inflammatory disorders driven by overlapping cytokine networks, most notably TNF-α, IL-6, IL-17, and IL-23, and by imbalances in adipokines such as leptin, resistin, and adiponectin (Table).

Clinical Implications of Obesity-Related Comorbidities

Higher body mass index (BMI) has been associated with an increased and earlier incidence of psoriasis. When treated as continuous variables, both Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index scores were positively correlated with increases in BMI.^10,11 This close association suggests BMI may function as a practical indicator of disease severity and prognosis.^7,8,11

Psoriatic arthritis (PsA) is a major comorbidity of psoriasis that impacts disease severity and quality of life. Obesity is associated with an increased risk for PsA after accounting for traditional risk factors. Psoriatic arthritis can cause chronic mobility issues and complicate a patient’s ability to stay active. Early rheumatologist involvement may be warranted to prevent PsA development in patients with obesity and psoriasis.^11,12

Patients with psoriasis have an increased baseline risk for metabolic syndrome, including obesity, type 2 diabetes, hypertension, and dyslipidemia^11,13,14; therefore, the presence of obesity warrants regular metabolic evaluation. Unmanaged metabolic syndrome contributes to the increased prevalence of myocardial infarction, stroke, and heart failure seen with psoriasis.^13,14 Obesity also may cause obstructive sleep apnea, which can exacerbate hypertension and heart disease due to chronic hypoxia.¹¹ The interplay of these metabolic factors puts patients with psoriasis and obesity at heightened cardiovascular risk.^13,14

Both psoriasis and obesity present psychosocial challenges such as elevated rates of depression, anxiety, and body-image concerns, all of which become more pronounced when these conditions coexist. These psychological stressors may hinder a patient’s motivation for lifestyle changes or treatment adherence.¹³

Dermatology visits serve as an important opportunity to monitor obesity-related comorbidities.^13,15 Dermatologists are uniquely positioned to initiate metabolic screening while collaborating with primary care physicians for ongoing cardiometabolic management. Metabolic and cardiovascular baselines should be measured when care is established and should be followed longitudinally—these include BMI, waist circumference measurements, blood pressure, lipid panels, fasting glucose or A1C levels, and liver enzymes.^10,14,15 Regular screening for depression, suicidality, and disordered eating also is encouraged.¹³ Clinicians should follow established guidelines to identify and manage metabolic, cardiovascular, and psychological comorbidities.¹³

Impact of Obesity on Psoriasis Treatment

Obesity is a critical factor in clinical decision-making, as it consistently is associated with diminished response to numerous systemic psoriasis therapies. This reduced efficacy has been observed with conventional oral agents such as methotrexate and cyclosporine and is particularly well documented in the context of biologic therapies.^15,16 Several meta-analyses and large real-world studies have shown that higher BMI is associated with a suboptimal treatment response, with patients in higher BMI categories achieving lower rates of PASI 75 and PASI 90 than their nonobese counterparts receiving the same regimen.^15,17

This efficacy gap often is rooted in pharmacokinetic challenges. For many biologics administered via subcutaneous injection, increased BMI can lead to altered drug distribution, such as sequestration in adipose tissue. Altered distribution combined with potentially increased drug clearance can result in lower overall serum drug concentrations and subsequent underdosing for a patient’s inflammatory burden.¹⁵ This reality highlights the important distinction between fixed and weight-based dosing strategies. Therapies dosed by weight, such as infliximab, have demonstrated more consistent efficacy in populations with obesity, as the dose is escalated to match patient size.¹⁸ Despite the weight-dependent effect, recent real-world studies have suggested that fixed dosing of some IL-17A inhibitors (eg, ixekizumab) remains highly effective across BMI categories, while others (eg, secukinumab) show diminished efficacy in obese patients.^16,19 Furthermore, some real-world studies have reported an inverse relationship between elevated BMI and efficacy of IL-23 inhibitors, particularly guselkumab, while other studies reported no association.^20,21 These mixed observations support a nuanced interpretation of BMI’s role in treatment modification; consideration should be given to the specific medication and the dosing strategy over biologic class alone.

Whether obesity independently drives psoriasis severity or mainly diminishes treatment efficacy through pharmacokinetic effects remains debated. Observational studies show a dose-dependent relationship between BMI and disease severity even in untreated patients, supporting a proinflammatory role for obesity.¹⁰ Concurrently, higher BMI may predict lower responses to some fixed-dose biologics, likely due to altered distribution and sequestration in adipose tissue.^15,20 The precise contributions are challenging to delineate; both likely converge to heighten disease severity and reduce treatment response.

Beyond efficacy, obesity compounds the safety considerations of systemic treatments. Psoriasis and obesity are both strong independent risk factors for metabolic ­dysfunction–associated steatotic liver disease. This prevalent comorbidity creates a substantial clinical dilemma, as a first-line, cost-effective agent such as methotrexate carries a known risk for hepatotoxicity, which is amplified in patients with pre-existing liver steatosis.¹³ Consequently, the presence of obesity and metabolic dysfunction–associated steatotic liver disease often limits the use of methotrexate, forcing a change in therapy. Thorough baseline comorbidity screening in all patients with psoriasis and obesity is necessary to select a therapy that balances efficacy with safety.^13,14

Management Strategies

Weight management plays a pivotal role in improving psoriasis outcomes. Even modest weight loss of 5% to 10% has been shown in randomized and observational studies to substantially reduce disease severity, reflected by lower PASI and Dermatology Life Quality Index scores and enhance treatment responsiveness.^22,23 Dietary approaches emphasizing hypocaloric, Mediterranean, or ­anti-inflammatory patterns have demonstrated additional improvements in disease activity, likely through attenuation of systemic inflammation and metabolic dysregulation.²¹ Bariatric surgery provides more sustained benefits, with multiple studies reporting long-term remission or reduced psoriasis severity following substantial postoperative weight loss.^23,24

Pharmacologic weight-loss therapies, particularly glucagonlike peptide-1 receptor agonists, have emerged as potential adjuncts in psoriasis management. Although data remain limited, these agents may reduce systemic inflammation, improve insulin sensitivity, and indirectly enhance biologic response.²⁵

Conclusion

Psoriasis and obesity are interconnected chronic inflammatory conditions that share overlapping cytokine pathways and mutually exacerbate the clinical course. Systemic inflammation driven by cytokines such as TNF-α, IL-6, and IL-17 not only promotes psoriatic skin disease but also contributes to metabolic dysfunction and cardiovascular risk. In turn, excess adiposity amplifies inflammatory signaling and diminishes therapeutic response, creating a self-perpetuating cycle of disease.

Dermatologists should identify obesity-related risks early; counsel patients on lifestyle changes; initiate metabolic screening; and coordinate care across primary care, nutrition, and rheumatology. Regular screening for metabolic syndrome, cardiovascular comorbidities, and psychosocial distress should be integrated into psoriasis management. Future research should focus on personalized treatment strategies that integrate management of inflammatory skin disease with underlying metabolic health, such as optimizing biologic dosing and identifying novel targets that disrupt the pathophysiologic loop. By recognizing and addressing the shared inflammatory mechanisms of psoriasis and obesity, clinicians can improve both dermatologic and systemic outcomes for affected patients.

Psoriasis, a chronic immune-mediated skin disease, is increasingly recognized for its systemic inflammation and associated cardiometabolic risk. The global rise of obesity has revealed a critical link between these 2 conditions. Current evidence confirms that obesity is an independent risk factor that can trigger psoriasis onset, drive more severe disease, and substantially impair treatment efficacy.^1,2 This review synthesizes the latest evidence on the shared pathophysiology, clinical consequences, and integrated management strategies for patients with both psoriasis and obesity.

Pathophysiologic Links Between Psoriasis and Obesity

Emerging evidence highlights a bidirectional relationship between psoriasis and obesity rooted in overlapping inflammatory pathways. Both conditions are characterized by chronic inflammation mediated by cytokines that sustain systemic immune activation and metabolic dysfunction. This interplay creates a reciprocal process in which psoriatic inflammation promotes metabolic disturbances while obesity amplifies systemic inflammation and disease severity.³

Psoriasis may contribute to obesity through cytokine-driven metabolic alterations in insulin signaling and adipocyte function. The psoriatic immune response is dominated by T helper (Th) 1, Th17, and Th22 cell activation, leading to elevated levels of interferon-γ, tumor necrosis factor (TNF) α, interleukin (IL) 6, IL-17, and IL-22 from keratinocytes.⁴ These cytokines contribute not only to cutaneous inflammation but also to insulin resistance and adipocyte dysfunction.⁵ Tumor necrosis factor α and IL-6 interfere with insulin signaling via activation of stress kinases (eg, IκB kinase and c-Jun N-terminal kinase), implicating these molecules in insulin resistance and weight gain.⁶ Moreover, IL-17, a central cytokine in psoriasis, has been implicated in vascular inflammation, insulin resistance, and type 2 diabetes, suggesting a mechanistic link between psoriatic inflammation and metabolic disease.⁵ Additionally, chronic systemic inflammation in psoriasis suppresses adiponectin, a protective adipokine that enhances insulin sensitivity and exerts anti-inflammatory effects by inhibiting TNF-α and IL-6 production while promoting IL-10 synthesis. Reduced adiponectin levels have consistently been observed in patients with psoriasis and concomitant obesity or metabolic syndrome.³ The resultant imbalance between proinflammatory and anti-inflammatory mediators creates a metabolic environment conducive to obesity.³

Conversely, obesity itself may intensify both the incidence and severity of psoriasis through shared inflammatory pathways. Leptin, whose expression rises proportionally with adipocyte mass, acts as a proinflammatory mediator linking obesity to psoriasis exacerbation. By promoting Th1 and Th17 cell differentiation and suppressing regulatory T-cell activity, leptin increases IL-17A, IL-6, and TNF-α production.⁷ These cytokines stimulate keratinocyte proliferation and perpetuate cutaneous inflammation, thereby intensifying disease activity. Similarly, resistin, another adipokine that is elevated in obesity, stimulates monocytes and macrophages to secrete TNF-α and IL-6, creating a proinflammatory state in the body that drives the relationship between excessive fat storage (adiposity) and the development and severity of psoriasis.⁸ In contrast, reduced adiponectin levels in obesity remove a key anti-inflammatory regulator that normally inhibits TNF-α and IL-6 synthesis and promotes IL-10 production. This deficiency provokes unrestrained cytokine activation within both adipose and cutaneous tissue, exacerbating psoriatic immune dysregulation.⁹

Free fatty acids derived from abundant adipocytes in obesity further activate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)–signaling and induce oxidative stress, augmenting systemic inflammation. Adipose tissue macrophages additionally secrete IL-1Β, IL-6, and TNF-α, which promote keratinocyte proliferation and amplify the psoriatic inflammatory cascade. Importantly, anti–TNF-α therapy has been shown to improve metabolic parameters, reducing low-density lipoprotein and total cholesterol levels and enhancing insulin sensitivity, highlighting the reciprocal benefits of dampening the inflammatory signaling from TNF-α.⁵

Together, these findings highlight that psoriasis and obesity are interconnected inflammatory disorders driven by overlapping cytokine networks, most notably TNF-α, IL-6, IL-17, and IL-23, and by imbalances in adipokines such as leptin, resistin, and adiponectin (Table).

Clinical Implications of Obesity-Related Comorbidities

Higher body mass index (BMI) has been associated with an increased and earlier incidence of psoriasis. When treated as continuous variables, both Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index scores were positively correlated with increases in BMI.^10,11 This close association suggests BMI may function as a practical indicator of disease severity and prognosis.^7,8,11

Psoriatic arthritis (PsA) is a major comorbidity of psoriasis that impacts disease severity and quality of life. Obesity is associated with an increased risk for PsA after accounting for traditional risk factors. Psoriatic arthritis can cause chronic mobility issues and complicate a patient’s ability to stay active. Early rheumatologist involvement may be warranted to prevent PsA development in patients with obesity and psoriasis.^11,12

Patients with psoriasis have an increased baseline risk for metabolic syndrome, including obesity, type 2 diabetes, hypertension, and dyslipidemia^11,13,14; therefore, the presence of obesity warrants regular metabolic evaluation. Unmanaged metabolic syndrome contributes to the increased prevalence of myocardial infarction, stroke, and heart failure seen with psoriasis.^13,14 Obesity also may cause obstructive sleep apnea, which can exacerbate hypertension and heart disease due to chronic hypoxia.¹¹ The interplay of these metabolic factors puts patients with psoriasis and obesity at heightened cardiovascular risk.^13,14

Both psoriasis and obesity present psychosocial challenges such as elevated rates of depression, anxiety, and body-image concerns, all of which become more pronounced when these conditions coexist. These psychological stressors may hinder a patient’s motivation for lifestyle changes or treatment adherence.¹³

Dermatology visits serve as an important opportunity to monitor obesity-related comorbidities.^13,15 Dermatologists are uniquely positioned to initiate metabolic screening while collaborating with primary care physicians for ongoing cardiometabolic management. Metabolic and cardiovascular baselines should be measured when care is established and should be followed longitudinally—these include BMI, waist circumference measurements, blood pressure, lipid panels, fasting glucose or A1C levels, and liver enzymes.^10,14,15 Regular screening for depression, suicidality, and disordered eating also is encouraged.¹³ Clinicians should follow established guidelines to identify and manage metabolic, cardiovascular, and psychological comorbidities.¹³

Impact of Obesity on Psoriasis Treatment

Obesity is a critical factor in clinical decision-making, as it consistently is associated with diminished response to numerous systemic psoriasis therapies. This reduced efficacy has been observed with conventional oral agents such as methotrexate and cyclosporine and is particularly well documented in the context of biologic therapies.^15,16 Several meta-analyses and large real-world studies have shown that higher BMI is associated with a suboptimal treatment response, with patients in higher BMI categories achieving lower rates of PASI 75 and PASI 90 than their nonobese counterparts receiving the same regimen.^15,17

This efficacy gap often is rooted in pharmacokinetic challenges. For many biologics administered via subcutaneous injection, increased BMI can lead to altered drug distribution, such as sequestration in adipose tissue. Altered distribution combined with potentially increased drug clearance can result in lower overall serum drug concentrations and subsequent underdosing for a patient’s inflammatory burden.¹⁵ This reality highlights the important distinction between fixed and weight-based dosing strategies. Therapies dosed by weight, such as infliximab, have demonstrated more consistent efficacy in populations with obesity, as the dose is escalated to match patient size.¹⁸ Despite the weight-dependent effect, recent real-world studies have suggested that fixed dosing of some IL-17A inhibitors (eg, ixekizumab) remains highly effective across BMI categories, while others (eg, secukinumab) show diminished efficacy in obese patients.^16,19 Furthermore, some real-world studies have reported an inverse relationship between elevated BMI and efficacy of IL-23 inhibitors, particularly guselkumab, while other studies reported no association.^20,21 These mixed observations support a nuanced interpretation of BMI’s role in treatment modification; consideration should be given to the specific medication and the dosing strategy over biologic class alone.

Whether obesity independently drives psoriasis severity or mainly diminishes treatment efficacy through pharmacokinetic effects remains debated. Observational studies show a dose-dependent relationship between BMI and disease severity even in untreated patients, supporting a proinflammatory role for obesity.¹⁰ Concurrently, higher BMI may predict lower responses to some fixed-dose biologics, likely due to altered distribution and sequestration in adipose tissue.^15,20 The precise contributions are challenging to delineate; both likely converge to heighten disease severity and reduce treatment response.

Beyond efficacy, obesity compounds the safety considerations of systemic treatments. Psoriasis and obesity are both strong independent risk factors for metabolic ­dysfunction–associated steatotic liver disease. This prevalent comorbidity creates a substantial clinical dilemma, as a first-line, cost-effective agent such as methotrexate carries a known risk for hepatotoxicity, which is amplified in patients with pre-existing liver steatosis.¹³ Consequently, the presence of obesity and metabolic dysfunction–associated steatotic liver disease often limits the use of methotrexate, forcing a change in therapy. Thorough baseline comorbidity screening in all patients with psoriasis and obesity is necessary to select a therapy that balances efficacy with safety.^13,14

Management Strategies

Weight management plays a pivotal role in improving psoriasis outcomes. Even modest weight loss of 5% to 10% has been shown in randomized and observational studies to substantially reduce disease severity, reflected by lower PASI and Dermatology Life Quality Index scores and enhance treatment responsiveness.^22,23 Dietary approaches emphasizing hypocaloric, Mediterranean, or ­anti-inflammatory patterns have demonstrated additional improvements in disease activity, likely through attenuation of systemic inflammation and metabolic dysregulation.²¹ Bariatric surgery provides more sustained benefits, with multiple studies reporting long-term remission or reduced psoriasis severity following substantial postoperative weight loss.^23,24

Pharmacologic weight-loss therapies, particularly glucagonlike peptide-1 receptor agonists, have emerged as potential adjuncts in psoriasis management. Although data remain limited, these agents may reduce systemic inflammation, improve insulin sensitivity, and indirectly enhance biologic response.²⁵

Conclusion

Psoriasis and obesity are interconnected chronic inflammatory conditions that share overlapping cytokine pathways and mutually exacerbate the clinical course. Systemic inflammation driven by cytokines such as TNF-α, IL-6, and IL-17 not only promotes psoriatic skin disease but also contributes to metabolic dysfunction and cardiovascular risk. In turn, excess adiposity amplifies inflammatory signaling and diminishes therapeutic response, creating a self-perpetuating cycle of disease.

Dermatologists should identify obesity-related risks early; counsel patients on lifestyle changes; initiate metabolic screening; and coordinate care across primary care, nutrition, and rheumatology. Regular screening for metabolic syndrome, cardiovascular comorbidities, and psychosocial distress should be integrated into psoriasis management. Future research should focus on personalized treatment strategies that integrate management of inflammatory skin disease with underlying metabolic health, such as optimizing biologic dosing and identifying novel targets that disrupt the pathophysiologic loop. By recognizing and addressing the shared inflammatory mechanisms of psoriasis and obesity, clinicians can improve both dermatologic and systemic outcomes for affected patients.

Psoriasis, a chronic immune-mediated skin disease, is increasingly recognized for its systemic inflammation and associated cardiometabolic risk. The global rise of obesity has revealed a critical link between these 2 conditions. Current evidence confirms that obesity is an independent risk factor that can trigger psoriasis onset, drive more severe disease, and substantially impair treatment efficacy.^1,2 This review synthesizes the latest evidence on the shared pathophysiology, clinical consequences, and integrated management strategies for patients with both psoriasis and obesity.

Pathophysiologic Links Between Psoriasis and Obesity

Emerging evidence highlights a bidirectional relationship between psoriasis and obesity rooted in overlapping inflammatory pathways. Both conditions are characterized by chronic inflammation mediated by cytokines that sustain systemic immune activation and metabolic dysfunction. This interplay creates a reciprocal process in which psoriatic inflammation promotes metabolic disturbances while obesity amplifies systemic inflammation and disease severity.³

Psoriasis may contribute to obesity through cytokine-driven metabolic alterations in insulin signaling and adipocyte function. The psoriatic immune response is dominated by T helper (Th) 1, Th17, and Th22 cell activation, leading to elevated levels of interferon-γ, tumor necrosis factor (TNF) α, interleukin (IL) 6, IL-17, and IL-22 from keratinocytes.⁴ These cytokines contribute not only to cutaneous inflammation but also to insulin resistance and adipocyte dysfunction.⁵ Tumor necrosis factor α and IL-6 interfere with insulin signaling via activation of stress kinases (eg, IκB kinase and c-Jun N-terminal kinase), implicating these molecules in insulin resistance and weight gain.⁶ Moreover, IL-17, a central cytokine in psoriasis, has been implicated in vascular inflammation, insulin resistance, and type 2 diabetes, suggesting a mechanistic link between psoriatic inflammation and metabolic disease.⁵ Additionally, chronic systemic inflammation in psoriasis suppresses adiponectin, a protective adipokine that enhances insulin sensitivity and exerts anti-inflammatory effects by inhibiting TNF-α and IL-6 production while promoting IL-10 synthesis. Reduced adiponectin levels have consistently been observed in patients with psoriasis and concomitant obesity or metabolic syndrome.³ The resultant imbalance between proinflammatory and anti-inflammatory mediators creates a metabolic environment conducive to obesity.³

Conversely, obesity itself may intensify both the incidence and severity of psoriasis through shared inflammatory pathways. Leptin, whose expression rises proportionally with adipocyte mass, acts as a proinflammatory mediator linking obesity to psoriasis exacerbation. By promoting Th1 and Th17 cell differentiation and suppressing regulatory T-cell activity, leptin increases IL-17A, IL-6, and TNF-α production.⁷ These cytokines stimulate keratinocyte proliferation and perpetuate cutaneous inflammation, thereby intensifying disease activity. Similarly, resistin, another adipokine that is elevated in obesity, stimulates monocytes and macrophages to secrete TNF-α and IL-6, creating a proinflammatory state in the body that drives the relationship between excessive fat storage (adiposity) and the development and severity of psoriasis.⁸ In contrast, reduced adiponectin levels in obesity remove a key anti-inflammatory regulator that normally inhibits TNF-α and IL-6 synthesis and promotes IL-10 production. This deficiency provokes unrestrained cytokine activation within both adipose and cutaneous tissue, exacerbating psoriatic immune dysregulation.⁹

Free fatty acids derived from abundant adipocytes in obesity further activate nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)–signaling and induce oxidative stress, augmenting systemic inflammation. Adipose tissue macrophages additionally secrete IL-1Β, IL-6, and TNF-α, which promote keratinocyte proliferation and amplify the psoriatic inflammatory cascade. Importantly, anti–TNF-α therapy has been shown to improve metabolic parameters, reducing low-density lipoprotein and total cholesterol levels and enhancing insulin sensitivity, highlighting the reciprocal benefits of dampening the inflammatory signaling from TNF-α.⁵

Together, these findings highlight that psoriasis and obesity are interconnected inflammatory disorders driven by overlapping cytokine networks, most notably TNF-α, IL-6, IL-17, and IL-23, and by imbalances in adipokines such as leptin, resistin, and adiponectin (Table).

Clinical Implications of Obesity-Related Comorbidities

Higher body mass index (BMI) has been associated with an increased and earlier incidence of psoriasis. When treated as continuous variables, both Psoriasis Area and Severity Index (PASI) and Dermatology Life Quality Index scores were positively correlated with increases in BMI.^10,11 This close association suggests BMI may function as a practical indicator of disease severity and prognosis.^7,8,11

Psoriatic arthritis (PsA) is a major comorbidity of psoriasis that impacts disease severity and quality of life. Obesity is associated with an increased risk for PsA after accounting for traditional risk factors. Psoriatic arthritis can cause chronic mobility issues and complicate a patient’s ability to stay active. Early rheumatologist involvement may be warranted to prevent PsA development in patients with obesity and psoriasis.^11,12

Patients with psoriasis have an increased baseline risk for metabolic syndrome, including obesity, type 2 diabetes, hypertension, and dyslipidemia^11,13,14; therefore, the presence of obesity warrants regular metabolic evaluation. Unmanaged metabolic syndrome contributes to the increased prevalence of myocardial infarction, stroke, and heart failure seen with psoriasis.^13,14 Obesity also may cause obstructive sleep apnea, which can exacerbate hypertension and heart disease due to chronic hypoxia.¹¹ The interplay of these metabolic factors puts patients with psoriasis and obesity at heightened cardiovascular risk.^13,14

Both psoriasis and obesity present psychosocial challenges such as elevated rates of depression, anxiety, and body-image concerns, all of which become more pronounced when these conditions coexist. These psychological stressors may hinder a patient’s motivation for lifestyle changes or treatment adherence.¹³

Dermatology visits serve as an important opportunity to monitor obesity-related comorbidities.^13,15 Dermatologists are uniquely positioned to initiate metabolic screening while collaborating with primary care physicians for ongoing cardiometabolic management. Metabolic and cardiovascular baselines should be measured when care is established and should be followed longitudinally—these include BMI, waist circumference measurements, blood pressure, lipid panels, fasting glucose or A1C levels, and liver enzymes.^10,14,15 Regular screening for depression, suicidality, and disordered eating also is encouraged.¹³ Clinicians should follow established guidelines to identify and manage metabolic, cardiovascular, and psychological comorbidities.¹³

Impact of Obesity on Psoriasis Treatment

Obesity is a critical factor in clinical decision-making, as it consistently is associated with diminished response to numerous systemic psoriasis therapies. This reduced efficacy has been observed with conventional oral agents such as methotrexate and cyclosporine and is particularly well documented in the context of biologic therapies.^15,16 Several meta-analyses and large real-world studies have shown that higher BMI is associated with a suboptimal treatment response, with patients in higher BMI categories achieving lower rates of PASI 75 and PASI 90 than their nonobese counterparts receiving the same regimen.^15,17

This efficacy gap often is rooted in pharmacokinetic challenges. For many biologics administered via subcutaneous injection, increased BMI can lead to altered drug distribution, such as sequestration in adipose tissue. Altered distribution combined with potentially increased drug clearance can result in lower overall serum drug concentrations and subsequent underdosing for a patient’s inflammatory burden.¹⁵ This reality highlights the important distinction between fixed and weight-based dosing strategies. Therapies dosed by weight, such as infliximab, have demonstrated more consistent efficacy in populations with obesity, as the dose is escalated to match patient size.¹⁸ Despite the weight-dependent effect, recent real-world studies have suggested that fixed dosing of some IL-17A inhibitors (eg, ixekizumab) remains highly effective across BMI categories, while others (eg, secukinumab) show diminished efficacy in obese patients.^16,19 Furthermore, some real-world studies have reported an inverse relationship between elevated BMI and efficacy of IL-23 inhibitors, particularly guselkumab, while other studies reported no association.^20,21 These mixed observations support a nuanced interpretation of BMI’s role in treatment modification; consideration should be given to the specific medication and the dosing strategy over biologic class alone.

Whether obesity independently drives psoriasis severity or mainly diminishes treatment efficacy through pharmacokinetic effects remains debated. Observational studies show a dose-dependent relationship between BMI and disease severity even in untreated patients, supporting a proinflammatory role for obesity.¹⁰ Concurrently, higher BMI may predict lower responses to some fixed-dose biologics, likely due to altered distribution and sequestration in adipose tissue.^15,20 The precise contributions are challenging to delineate; both likely converge to heighten disease severity and reduce treatment response.

Beyond efficacy, obesity compounds the safety considerations of systemic treatments. Psoriasis and obesity are both strong independent risk factors for metabolic ­dysfunction–associated steatotic liver disease. This prevalent comorbidity creates a substantial clinical dilemma, as a first-line, cost-effective agent such as methotrexate carries a known risk for hepatotoxicity, which is amplified in patients with pre-existing liver steatosis.¹³ Consequently, the presence of obesity and metabolic dysfunction–associated steatotic liver disease often limits the use of methotrexate, forcing a change in therapy. Thorough baseline comorbidity screening in all patients with psoriasis and obesity is necessary to select a therapy that balances efficacy with safety.^13,14

Management Strategies

Weight management plays a pivotal role in improving psoriasis outcomes. Even modest weight loss of 5% to 10% has been shown in randomized and observational studies to substantially reduce disease severity, reflected by lower PASI and Dermatology Life Quality Index scores and enhance treatment responsiveness.^22,23 Dietary approaches emphasizing hypocaloric, Mediterranean, or ­anti-inflammatory patterns have demonstrated additional improvements in disease activity, likely through attenuation of systemic inflammation and metabolic dysregulation.²¹ Bariatric surgery provides more sustained benefits, with multiple studies reporting long-term remission or reduced psoriasis severity following substantial postoperative weight loss.^23,24

Pharmacologic weight-loss therapies, particularly glucagonlike peptide-1 receptor agonists, have emerged as potential adjuncts in psoriasis management. Although data remain limited, these agents may reduce systemic inflammation, improve insulin sensitivity, and indirectly enhance biologic response.²⁵

Conclusion

Psoriasis and obesity are interconnected chronic inflammatory conditions that share overlapping cytokine pathways and mutually exacerbate the clinical course. Systemic inflammation driven by cytokines such as TNF-α, IL-6, and IL-17 not only promotes psoriatic skin disease but also contributes to metabolic dysfunction and cardiovascular risk. In turn, excess adiposity amplifies inflammatory signaling and diminishes therapeutic response, creating a self-perpetuating cycle of disease.

Dermatologists should identify obesity-related risks early; counsel patients on lifestyle changes; initiate metabolic screening; and coordinate care across primary care, nutrition, and rheumatology. Regular screening for metabolic syndrome, cardiovascular comorbidities, and psychosocial distress should be integrated into psoriasis management. Future research should focus on personalized treatment strategies that integrate management of inflammatory skin disease with underlying metabolic health, such as optimizing biologic dosing and identifying novel targets that disrupt the pathophysiologic loop. By recognizing and addressing the shared inflammatory mechanisms of psoriasis and obesity, clinicians can improve both dermatologic and systemic outcomes for affected patients.

THE DIAGNOSIS: Terra Firma-Forme Dermatosis

During clinical examination, a 70% alcohol swab was utilized to gently rub several of the lesions, which were successfully removed. This confirmed a diagnosis of terra firma-forme dermatosis (TFFD)(also known as Duncan’s dirty dermatosis). The patient’s mother was counseled about the diagnosis and was instructed on how to use alcohol pads to remove the remaining lesions. Three days later, after several treatment sessions at home, the mother reported complete resolution of the lesions with no residual pigmentary changes, ulceration, or scarring (Figures 1 and 2).

Terra firma-forme dermatosis was first described in 1987 in a 12-year-old girl with hyperpigmented plaques on the neck that cleared when rubbing alcohol was applied before biopsy.^1,2 The term terra firma is Latin for “firm land” (or essentially “dirt”) in reference to what often is described as a characteristically “dirty” clinical appearance.² Terra firmaforme dermatosis can manifest anywhere on the body but shows a predilection for the neck, arms and legs, axillae, inguinal region, and umbilicus.³ Lesions typically are described as asymptomatic, smooth, well-circumscribed, reticular papules or patches that are brown or black. Terra firma-forme dermatosis also may demonstrate secondary features such as hyperkeratotic, scaly, velvety, or verrucous plaques and nodules.³

The etiology of this condition is theorized to be a result of abnormal or delayed keratinization and prolonged keratinocyte adhesion.^3,4 There are limited epidemiologic data, but TFFD has shown a predominance in children younger than 18 years (average age of onset, 10 years) with no known predilection for sex or race and no recognized pattern of inheritance.^3-5

Histopathology typically demonstrates epidermal atrophy, hyperkeratosis, and often a component of trapping and compaction of melanin, sebum, microorganisms, and environmental debris.⁵

Management of TFFD is straightforward and generally consists of rubbing with 70% isopropyl alcohol to remove the lesions. For more adherent lesions or for extensive involvement, other keratolytics such as salicylic acid or alpha-hydroxy acids may be used.⁵ For TFFD manifesting in infants and young children, widespread involvement, or lesions involving the face or genitals, a urea-based keratolytic with or without a topical anti-inflammatory is suggested.⁵ Other treatment options include other alpha-hydroxy acids, topical retinoids, and nonpolar solvents such as acetone or CO2 laser for recalcitrant cases.^4,5 Fortunately, most TFFD lesions respond well to conservative therapies, with recurrence reported only in 6.3% (5/79) of patients in one study.³

Dermatosis neglecta is clinically similar to TFFD and often is considered on the same spectrum of disease⁶; however, this entity is associated with decreased bathing or limited hygiene, which could be related to child or elder abuse/neglect or comorbid psychiatric disorders. These conditions can be distinguished by attempting to remove the lesions using soap and water; lesions of dermatosis neglecta will clear, whereas those of TFFD will not.

Metastatic melanoma in pediatric patients has a polymorphous appearance and may or may not be pigmented. Lesions often may be associated with lymphadenopathy of the draining lymph node basins, and nodules and lesions may be firm on palpation.⁷ Linear configurations of metastatic melanoma may represent a satellite or in-transit metastasis. Fortunately, melanoma is extraordinarily rare in children, with an estimated incidence of 2.1 per million for individuals younger than 20 years.⁸

Acanthosis nigricans is characterized by velvety plaques most commonly affecting the posterior neck, axillae, and flexor extremities. These lesions commonly are associated with obesity and insulin resistance but occasionally can be associated with underlying malignancy. In the latter association, acanthosis nigricans lesions tend to manifest more abruptly, often are pruritic, and can involve the mucous membranes. Fortunately, acanthosis nigricans related to malignancy in the pediatric population is rare.⁹

Epidermal nevi may exhibit clinical similarities to TFFD, particularly in lesions with brown/black pigment or with a reticulated or verrucous appearance; however, epidermal nevi often are congenital or manifest within the first few years of life. They commonly are distributed over the lines of Blaschko and have a linear appearance; they also enlarge and thicken as the patient ages.¹⁰

Black-dot tinea capitis, a classic manifestation of endothrix infection, manifests as alopecia with broken hairs and is most commonly caused by Tinea tonsurans.¹¹ The black dots refer to the appearance of the infected hair shafts, which have been weakened and broken off at the follicular ostia. As such, lesions typically are monomorphic and may be interspersed with uninvolved hair shafts. There often is associated scale and a lack of inflammation.^11,12

Additional differential diagnoses to consider include seborrheic keratoses and confluent and reticulated papillomatosis. Further workup (eg, potassium hydroxide preparation of skin scrapings or skin biopsy) may help elucidate the diagnosis.⁵ A simple and cost-effective initial diagnostic tool involves wiping suspicious lesions with a 70% isopropyl alcohol pad to confirm this diagnosis.

THE DIAGNOSIS: Terra Firma-Forme Dermatosis

During clinical examination, a 70% alcohol swab was utilized to gently rub several of the lesions, which were successfully removed. This confirmed a diagnosis of terra firma-forme dermatosis (TFFD)(also known as Duncan’s dirty dermatosis). The patient’s mother was counseled about the diagnosis and was instructed on how to use alcohol pads to remove the remaining lesions. Three days later, after several treatment sessions at home, the mother reported complete resolution of the lesions with no residual pigmentary changes, ulceration, or scarring (Figures 1 and 2).

Terra firma-forme dermatosis was first described in 1987 in a 12-year-old girl with hyperpigmented plaques on the neck that cleared when rubbing alcohol was applied before biopsy.^1,2 The term terra firma is Latin for “firm land” (or essentially “dirt”) in reference to what often is described as a characteristically “dirty” clinical appearance.² Terra firmaforme dermatosis can manifest anywhere on the body but shows a predilection for the neck, arms and legs, axillae, inguinal region, and umbilicus.³ Lesions typically are described as asymptomatic, smooth, well-circumscribed, reticular papules or patches that are brown or black. Terra firma-forme dermatosis also may demonstrate secondary features such as hyperkeratotic, scaly, velvety, or verrucous plaques and nodules.³

The etiology of this condition is theorized to be a result of abnormal or delayed keratinization and prolonged keratinocyte adhesion.^3,4 There are limited epidemiologic data, but TFFD has shown a predominance in children younger than 18 years (average age of onset, 10 years) with no known predilection for sex or race and no recognized pattern of inheritance.^3-5

Histopathology typically demonstrates epidermal atrophy, hyperkeratosis, and often a component of trapping and compaction of melanin, sebum, microorganisms, and environmental debris.⁵

Management of TFFD is straightforward and generally consists of rubbing with 70% isopropyl alcohol to remove the lesions. For more adherent lesions or for extensive involvement, other keratolytics such as salicylic acid or alpha-hydroxy acids may be used.⁵ For TFFD manifesting in infants and young children, widespread involvement, or lesions involving the face or genitals, a urea-based keratolytic with or without a topical anti-inflammatory is suggested.⁵ Other treatment options include other alpha-hydroxy acids, topical retinoids, and nonpolar solvents such as acetone or CO2 laser for recalcitrant cases.^4,5 Fortunately, most TFFD lesions respond well to conservative therapies, with recurrence reported only in 6.3% (5/79) of patients in one study.³

Dermatosis neglecta is clinically similar to TFFD and often is considered on the same spectrum of disease⁶; however, this entity is associated with decreased bathing or limited hygiene, which could be related to child or elder abuse/neglect or comorbid psychiatric disorders. These conditions can be distinguished by attempting to remove the lesions using soap and water; lesions of dermatosis neglecta will clear, whereas those of TFFD will not.

Metastatic melanoma in pediatric patients has a polymorphous appearance and may or may not be pigmented. Lesions often may be associated with lymphadenopathy of the draining lymph node basins, and nodules and lesions may be firm on palpation.⁷ Linear configurations of metastatic melanoma may represent a satellite or in-transit metastasis. Fortunately, melanoma is extraordinarily rare in children, with an estimated incidence of 2.1 per million for individuals younger than 20 years.⁸

Acanthosis nigricans is characterized by velvety plaques most commonly affecting the posterior neck, axillae, and flexor extremities. These lesions commonly are associated with obesity and insulin resistance but occasionally can be associated with underlying malignancy. In the latter association, acanthosis nigricans lesions tend to manifest more abruptly, often are pruritic, and can involve the mucous membranes. Fortunately, acanthosis nigricans related to malignancy in the pediatric population is rare.⁹

Epidermal nevi may exhibit clinical similarities to TFFD, particularly in lesions with brown/black pigment or with a reticulated or verrucous appearance; however, epidermal nevi often are congenital or manifest within the first few years of life. They commonly are distributed over the lines of Blaschko and have a linear appearance; they also enlarge and thicken as the patient ages.¹⁰

Black-dot tinea capitis, a classic manifestation of endothrix infection, manifests as alopecia with broken hairs and is most commonly caused by Tinea tonsurans.¹¹ The black dots refer to the appearance of the infected hair shafts, which have been weakened and broken off at the follicular ostia. As such, lesions typically are monomorphic and may be interspersed with uninvolved hair shafts. There often is associated scale and a lack of inflammation.^11,12

Additional differential diagnoses to consider include seborrheic keratoses and confluent and reticulated papillomatosis. Further workup (eg, potassium hydroxide preparation of skin scrapings or skin biopsy) may help elucidate the diagnosis.⁵ A simple and cost-effective initial diagnostic tool involves wiping suspicious lesions with a 70% isopropyl alcohol pad to confirm this diagnosis.

THE DIAGNOSIS: Terra Firma-Forme Dermatosis

During clinical examination, a 70% alcohol swab was utilized to gently rub several of the lesions, which were successfully removed. This confirmed a diagnosis of terra firma-forme dermatosis (TFFD)(also known as Duncan’s dirty dermatosis). The patient’s mother was counseled about the diagnosis and was instructed on how to use alcohol pads to remove the remaining lesions. Three days later, after several treatment sessions at home, the mother reported complete resolution of the lesions with no residual pigmentary changes, ulceration, or scarring (Figures 1 and 2).

Terra firma-forme dermatosis was first described in 1987 in a 12-year-old girl with hyperpigmented plaques on the neck that cleared when rubbing alcohol was applied before biopsy.^1,2 The term terra firma is Latin for “firm land” (or essentially “dirt”) in reference to what often is described as a characteristically “dirty” clinical appearance.² Terra firmaforme dermatosis can manifest anywhere on the body but shows a predilection for the neck, arms and legs, axillae, inguinal region, and umbilicus.³ Lesions typically are described as asymptomatic, smooth, well-circumscribed, reticular papules or patches that are brown or black. Terra firma-forme dermatosis also may demonstrate secondary features such as hyperkeratotic, scaly, velvety, or verrucous plaques and nodules.³

The etiology of this condition is theorized to be a result of abnormal or delayed keratinization and prolonged keratinocyte adhesion.^3,4 There are limited epidemiologic data, but TFFD has shown a predominance in children younger than 18 years (average age of onset, 10 years) with no known predilection for sex or race and no recognized pattern of inheritance.^3-5

Histopathology typically demonstrates epidermal atrophy, hyperkeratosis, and often a component of trapping and compaction of melanin, sebum, microorganisms, and environmental debris.⁵

Management of TFFD is straightforward and generally consists of rubbing with 70% isopropyl alcohol to remove the lesions. For more adherent lesions or for extensive involvement, other keratolytics such as salicylic acid or alpha-hydroxy acids may be used.⁵ For TFFD manifesting in infants and young children, widespread involvement, or lesions involving the face or genitals, a urea-based keratolytic with or without a topical anti-inflammatory is suggested.⁵ Other treatment options include other alpha-hydroxy acids, topical retinoids, and nonpolar solvents such as acetone or CO2 laser for recalcitrant cases.^4,5 Fortunately, most TFFD lesions respond well to conservative therapies, with recurrence reported only in 6.3% (5/79) of patients in one study.³

Dermatosis neglecta is clinically similar to TFFD and often is considered on the same spectrum of disease⁶; however, this entity is associated with decreased bathing or limited hygiene, which could be related to child or elder abuse/neglect or comorbid psychiatric disorders. These conditions can be distinguished by attempting to remove the lesions using soap and water; lesions of dermatosis neglecta will clear, whereas those of TFFD will not.

Metastatic melanoma in pediatric patients has a polymorphous appearance and may or may not be pigmented. Lesions often may be associated with lymphadenopathy of the draining lymph node basins, and nodules and lesions may be firm on palpation.⁷ Linear configurations of metastatic melanoma may represent a satellite or in-transit metastasis. Fortunately, melanoma is extraordinarily rare in children, with an estimated incidence of 2.1 per million for individuals younger than 20 years.⁸

Acanthosis nigricans is characterized by velvety plaques most commonly affecting the posterior neck, axillae, and flexor extremities. These lesions commonly are associated with obesity and insulin resistance but occasionally can be associated with underlying malignancy. In the latter association, acanthosis nigricans lesions tend to manifest more abruptly, often are pruritic, and can involve the mucous membranes. Fortunately, acanthosis nigricans related to malignancy in the pediatric population is rare.⁹

Epidermal nevi may exhibit clinical similarities to TFFD, particularly in lesions with brown/black pigment or with a reticulated or verrucous appearance; however, epidermal nevi often are congenital or manifest within the first few years of life. They commonly are distributed over the lines of Blaschko and have a linear appearance; they also enlarge and thicken as the patient ages.¹⁰

Black-dot tinea capitis, a classic manifestation of endothrix infection, manifests as alopecia with broken hairs and is most commonly caused by Tinea tonsurans.¹¹ The black dots refer to the appearance of the infected hair shafts, which have been weakened and broken off at the follicular ostia. As such, lesions typically are monomorphic and may be interspersed with uninvolved hair shafts. There often is associated scale and a lack of inflammation.^11,12

Additional differential diagnoses to consider include seborrheic keratoses and confluent and reticulated papillomatosis. Further workup (eg, potassium hydroxide preparation of skin scrapings or skin biopsy) may help elucidate the diagnosis.⁵ A simple and cost-effective initial diagnostic tool involves wiping suspicious lesions with a 70% isopropyl alcohol pad to confirm this diagnosis.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

To the Editor:

It is known that dermatologist evaluation of skin conditions in hospitalized patients confers enhanced diagnostic accuracy, timely and appropriate treatment, and an overall reduction in readmissions compared to assessments by nondermatology hospitalists.¹ Dermatology consultations have been shown to alter diagnoses in up to 50% of cases and lead to changes in management in nearly 75% of cases, even for prevalent dermatologic conditions such as drug rashes, cellulitis, and stasis dermatitis.^1,2 Previous studies have observed a multiday reduction in length of hospital stay, a 10-fold reduction in readmission rate, and lower 30-day mortality, all leading to a reduction in patient morbidity and costs to both the patient and the health care system.^3,4 Despite these benefits, there has been a decrease in the number of dermatologists providing inpatient services and a reduction in medical centers offering dermatology consultations over the past several years.⁵ To better appreciate current trends of declining dermatology inpatient and consultative services within our region, we evaluated the availability of dermatology care at hospitals across Virginia.

A simple telephone survey was conducted across community hospitals in Virginia wherein medical staff administrators were asked to provide details regarding their dermatology staffing. The following figures were collected: number of dermatologists on staff, number of dermatologists with consulting privileges, number of affiliated dermatologists, and number of advanced-practice dermatology providers. Follow-up calls were carried out to elaborate on how dermatologists (when available) were integrated into inpatient care workflow and made accessible to hospitalists and emergency medicine departments. Academic centers, military hospitals, and specialty hospitals were excluded from the survey.

To better appreciate the relationships between hospital and population characteristics and the availability of dermatology care, publicly available data were collected on hospital bed counts and regional population density for each facility.^6-9 Spearman rank correlation analyses were conducted in Microsoft Excel to evaluate the association between the number of dermatologists on staff, number of consulting dermatologists, staffed inpatient beds, and population size.

Sixty-four hospitals—more than 70% of the 90 eligible community hospitals—responded to the survey between May and August 2024 and were included in the study. On-staff dermatologists were present at 8 (12.5%) of the hospitals surveyed; of these, 4 (50.0%) hospitals had between 1 and 5 dermatologists, 3 (37.5%) had between 6 and 10 dermatologists, and 1 (12.5%) had between 11 and 15 dermatologists. An additional 4 (6.3%) hospitals provided consultative dermatology services from outside dermatology clinics. Urban hospitals accounted for 9 of 12 (75%) hospitals offering in-house dermatology services, either through on-staff physicians or consultations with clinic-based providers.

Based on Spearman rank correlation analysis, there was a positive correlation between the number of dermatologists on staff and the number of staffed hospital beds (r=0.61; P <.001). Similarly, there was a positive correlation between the number of dermatologists on staff and the population density of the affiliated region (r=0.58; P <.001). Finally, there was a positive correlation between the number of dermatologists on staff and the number of available consulting dermatologists (r=0.89; P <.001).

At facilities with only consultative dermatology services accessible, there often was no formal dermatology team or department present. Rather, the hospitals relied on a loosely affiliated network of dermatology providers or navigated inpatient dermatology needs almost exclusively via internal medicine hospitalists or emergency medicine physicians. When available, dermatology support from dermatology physicians often was provided through teledermatology platforms. Although teledermatology has a large role in increasing access to care within underserved areas, its reliance on images and second-hand case descriptions can limit the provider’s ability to perform a comprehensive examination and assessment. Moreover, it was noted that few hospital representatives could offer clarity on how dermatologists were integrated into the inpatient setting. It remained unclear whether dermatologists were practically accessible to the inpatient care teams in a structured manner.

The uneven distribution and limited availability of dermatology inpatient care in Virginia reflect national trends and underscore ongoing access issues for patients. Without intentional intervention, these trends are expected to continue, contributing to a glaring gap in hospital services as well as to patient morbidity and mortality. The correlation data obtained in our study further qualify these disparities. The positive correlations between dermatologist availability and hospital size and population density suggest that larger, more urban facilities are more likely to offer inpatient dermatology care, whether through staffing or consultation. This relationship is not unexpected, given the greater financial resources and specialist networks available to facilities with large patient volumes. This suggests that dermatology care is shaped by institutional capacity and geographic leverage rather than clinical need, reinforcing existing disparities.

Importantly, it should be noted that the data may overestimate the true availability of dermatologists to these patients. As revealed via follow-up survey calls, respondent facilities that provided dermatology via consultative services often did not have a defined structure for integrating this care into the inpatient workflow. In some instances, dermatologists were technically affiliated with the hospital but had varying levels of practical interaction with the hospital providers and their patients. Administrative staff's differing awareness regarding dermatology interaction with the hospital facility may reveal systemic underutilization and opportunities to improve coordination to achieve the greatest benefit from dermatology services. These observations are further informed by the scope of our study, which focused specifically on community hospitals. The exclusion of academic and military institutions—and the tendency of these to exist in more densely populated areas—may have limited how broadly our findings reflect nationwide dermatology access by omitting more established dermatology departments and specialty care. As a result, regional variations in predominant facility type should be considered when interpreting the implications of these results beyond Virginia’s community hospital system.

In response to access limitations and differences in availability, facilities are turning to integrated teledermatology as a valuable tool to expand the reach of specialist care, particularly in rural or resource-limited settings. This modality acts as an important step toward improving equity in care by beginning to bridge geographic gaps; however, along with these logistical advantages, teledermatology also confers diagnostic limitations and clinical trade-offs that should be thoughtfully considered. Our findings highlight the need to expand access in a way that integrates technological advances with in-person care to build a sustainable and effective path forward without compromising the quality of care patients receive. We present these outcomes to emphasize the importance of increasing dermatology involvement in the care of hospitalized patients, which is a promising strategy to improve patient outcomes and reduce existing disparities in Virginia and nationwide.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

THE DIAGNOSIS: Follicular Mucinosis

Histologic examination of the hematoxylin and eosin–stained sections of the biopsy revealed an overall moderately dense, perivascular, and perifollicular lymphocytic infiltrate with follicular intraepidermal mucin (Figure). Immunohistochemical staining showed that the lymphocytic infiltrate was predominantly CD4+ over CD8+, with moderate loss of CD7 and absence of CD20 expression. Positive T-cell receptor (TCR) gene rearrangements were detected for both TCRγ and TCRΒ. The clinical features along with the histopathologic findings suggested a diagnosis of follicular mucinosis (FM) with concern in the differential for folliculotropic mycosis fungoides.

Follicular mucinosis, also known as alopecia mucinosa, is an uncommon inflammatory disorder characterized by follicular degeneration due to the accumulation of mucin within the pilosebaceous unit.¹ This condition manifests clinically as indurated plaques and/or follicular papules most often on the face, neck, and scalp.² It is further categorized as primary vs secondary FM. Primary idiopathic FM, which can further be subdivided into acute or chronic, tends to follow a more benign course, whereas secondary FM usually is associated with underlying inflammatory or neoplastic conditions, most commonly mycosis fungoides, a cutaneous T-cell lymphoma.^1,2 In cases of secondary FM, treatment of the underlying cause often leads to resolution of symptoms. Regular follow-up is warranted in either classification.^1,3

The initial differential diagnosis for this patient included contact dermatitis associated with mask use, with possible underlying seborrheic dermatitis or rosacea; however, the rash persisted and worsened after treatment with topical triamcinolone and ketoconazole. After the diagnosis of FM was made, the patient was started on topical betamethasone and tacrolimus with good response.

A referral to hematology/oncology revealed that the patient had primary FM and possible stage 1A folliculotropic mycosis fungoides with limited skin involvement (<10% body surface area). On physical examination, no palpable cervical or axillary lymphadenopathy were noted. Flow cytometry for lymphoma was negative with no lymphoid or blast population detected. Laboratory workup and positron emission tomography/computed tomography were unremarkable. The patient had rapid improvement with a more potent topical steroid but also was given tacrolimus ointment 0.1% for residual findings. His disease remained stable without progression at 1-year follow-up.

Contact dermatitis typically manifests as an eczematous eruption that appears on an anatomic location that was exposed to or came into contact with allergens or irritants.⁴ Contact dermatitis was less likely in our patient due to the lack of acute or subacute spongiosis and lymphocyte exocytosis. Rosacea is a chronic inflammatory dermatosis that presents as recurrent episodes of flushing or transient erythema, persistent erythema, phyphymatous changes, papules, pustules, and telangiectasia⁵; however, rosacea was less likely in our patient due to the histopathologic and immunohistochemical findings that were suggestive of FM on punch biopsy. Cutaneous lupus generally is associated with photosensitivity and manifests as erythema over the malar eminences and bridge of the nose with sparing of the nasolabial folds.⁶ Seborrheic dermatitis manifests as erythematous macules or patches with scale and associated pruritis on the scalp, eyebrows, eyelids, and nasolabial folds.⁷ This condition was less likely in our patient due to the persistence and worsening of the facial erythematous dermatitis despite the use of ketoconazole cream as well as no evidence of spongiosis, shoulder parakeratosis, vascular changes, or presence of microorganisms such as Malassezia species.

Due to the relatively rare nature of this condition as well as a wide variety of other more common etiologies for an erythematous dermatitis of the cheeks, the diagnosis of FM may be delayed or missed entirely. Physicians must have a high index of suspicion to diagnose properly and biopsy if necessary. This photoquiz serves as an important reminder to physicians to keep uncommon diseases on their differential, especially when the patient’s symptoms do not respond to treatment.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

To the Editor:

A 22-year-old man presented to our clinic with a history of longstanding widespread recalcitrant atopic dermatitis (AD) since early childhood. He had been treated by an outside physician with topical steroids and nonsteroidal medications without notable improvement as well as with dupilumab, which was discontinued due to the development of severe head and neck dermatitis. Given the severity of his AD on presentation, we initiated treatment with upadacitinib 15 mg/d, which resulted in partial improvement. The dose was increased to 30 mg/d at 3 months with further clinical improvement.

Ten months after the patient was started on upadacitinib, he presented for a follow-up evaluation and reported a new nontender nodule on the scalp. A punch biopsy revealed a dense dermal and subcutaneous lymphoid infiltrate (Figure 1) composed of many large atypical CD2+/CD5+/CD45+ T cells with partial loss of CD3 expression (Figure 2). The atypical cells demonstrated diffuse CD30+ expression (Figure 3) and a CD4:CD8 ratio of greater than 50:1 (Figures 4 and 5). He was diagnosed with anaplastic large cell lymphoma (ALCL), and the upadacitinib was discontinued. No additional therapies directed toward ALCL were initiated.

Over the next 2 weeks, the patient developed additional nodules on the postauricular skin and trunk that demonstrated similar histopathology and immunophenotype to the original scalp nodule. T-cell receptor gene rearrangement studies demonstrated shared clonal peaks in these subsequent nodules. A concurrent biopsy of an eczematous plaque on the back showed spongiotic dermatitis without evidence of cutaneous T-cell lymphoma; gene rearrangement studies from this site were negative. A positron emission tomography–computed tomography scan showed mildly hypermetabolic cervical, axillary, and inguinal lymph nodes, which were favored to be reactive. Narrow-band UVB phototherapy was initiated for management of the AD, and no additional nodules developed over the subsequent months.

Janus kinase (JAK) inhibitors are immunomodulatory small molecules that interfere with JAK–signal transducer and activator of transcription signaling involving 1 or more isoforms (eg, JAK1, JAK2, JAK3, tyrosine kinase 2) and have been used to treat various inflammatory conditions, including rheumatoid arthritis, psoriatic arthritis, psoriasis, axial spondyloarthritis, inflammatory bowel disease, and AD.¹ Upadacitinib is an oral selective JAK1 inhibitor approved by the US Food and Drug Administration for treatment of moderate to severe AD in adults and children aged 12 years and older.² A search of PubMed using the terms upadacitinib or Rinvoq and anaplastic large cell lymphoma did not identify any cases of cutaneous ALCL arising after treatment with upadacitinib. However, a case of lymphomatoid papulosis after initiation of upadacitinib for the treatment of rheumatoid arthritis in a 74-year-old Japanese woman has been described,³ and the JAK/signal transducer and activator of transcription pathway has been implicated in the development of other CD30+ lymphoproliferative disorders.^4,5

An association between JAK inhibitors and aggressive B-cell lymphomas has been described. In an observational study of 626 patients with myeloproliferative neoplasia by Porpaczy et al,⁶ 4 of 69 (5.8%) patients treated with JAK inhibitors developed an aggressive B-cell lymphoma, whereas only 2 of 557 (0.36%) patients who did not receive JAK-inhibitor therapy developed an aggressive B-cell lymphoma. In contrast, a retrospective analysis of 2583 patients with myeloproliferative neoplasia by Pemmaraju et al⁷ found no significant increase in lymphoma rates in the JAK inhibitor–treated population as compared with the non-JAK inhibitor–treated group; 9 (0.56%) cases of lymphoma occurred in 1617 patients with myelofibrosis, of which 6 had exposure to JAK inhibitor therapy and 3 had no exposure to JAK inhibitor therapy (P=.082) and 5 (0.52%) cases of lymphoma occurred in 966 patients with essential thrombocythemia or polycythemia vera, none of whom had exposure to JAK inhibitor therapy.Finally, some evidence suggests the use of JAK inhibitors may be associated with an elevated risk of malignancies overall. The ORAL Surveillance study found the incidence of all cancers, excluding nonmelanoma skin cancer (NMSC), in patients treated with tofacitinib to be 4.2% (122/2911) compared with 2.9% (42/1451) in patients treated with tumor necrosis factor α inhibitors; it should be noted that the patients in this study were restricted to adults aged 50 years and older who were undergoing treatment for rheumatoid arthritis.⁸ In a safety profile study for upadacitinib, a higher rate of malignancies, excluding NMSC, was found in patients with AD treated with upadacitinib 30 mg/d than in patients treated with 15 mg/d; however, the overall rates of malignancies, excluding NMSC, in patients treated with upadacitinib were comparable to the standard incidence rates of malignancies in the general population derived from Surveillance, Epidemiology, and End Results data.⁹

In summary, we present a case of cutaneous ALCL arising after treatment with upadacitinib for AD. While some literature suggests AD may independently predispose patients to the development of CD30+ lymphoproliferative disorders, the onset of our patient’s cutaneous ALCL 10 months after initiation of upadacitinib is suggestive of an association between his lymphoproliferative disorder and JAK inhibition. Further studies are needed to better characterize the risk of lymphoproliferative disorders and other malignancies in patients treated with JAK inhibitors.

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

THE DIAGNOSIS: Neutrophilic Dermatosis of the Dorsal Hands

Histopathology showed a unilocular pustule with a dense neutrophilic infiltrate of the superficial dermis. Minimal vascular alterations also were observed. These findings were consistent with a diagnosis of neutrophilic dermatosis of the dorsal hands (NDDH). Our patient was treated successfully with systemic corticosteroids (1 mg/kg/d) with rapid improvement after 10 days of treatment.

Neutrophilic dermatosis of the dorsal hands is an evolving disease concept that was first described as pustular vasculitis by Strutton et al¹ in 1995. Galaria et al² subsequently identified NDDH as a clinical entity associating tender erythematous plaques, pustules, bullae, and/or ulcers on the dorsal hands with histologic features of Sweet syndrome (SS). After reviewing 9 cases of NDDH—all of which demonstrated clinical, laboratory, and histologic characteristics of SS—Walling et al³ concluded that NDDH was best understood as a distributional variant of SS.

Our patient presented with vascular alterations described as a reactive response to the neutrophilic infiltration. The presence of vasculitis in SS and NDDH biopsies is considered as an occasional epiphenomenon and should not rule out the diagnosis of NDDH.³ A literature review of 123 cases of NDDH revealed the presence of vasculitis in 36 (29.5%) patients.⁴ With regard to other clinical findings, it has been suggested that an increased white blood cell count and elevated C-reactive protein level, as was seen in our patient, may be observed in NDDH, albeit less frequently than in classical SS.⁴

While palmar involvement of NDDH is considered rare, the recent review of 123 cases of NDDH identified palmar lesions in 5 patients (4.1%).⁴ Earlier reviews had identified 12 historical cases.⁵ Palmar manifestations of NDDH have been shown to be associated with erythematous nonulcerated lesions (as opposed to the classical ulcerative or pustular plaques) and a lower association with hematologic malignancies.⁵

In our patient’s case, dyshidrosis was excluded due to the presence of painful ulcerative plaques rather than pruritic, deep-seated vesicles. Pustular psoriasis typically manifests with sterile pustules on the palms and soles; however, the rapid onset of ulcerative, necrotic plaques and substantial edema are more specific to NDDH. Poststreptococcal pustulosis generally follows a streptococcal infection and lacks the violaceous undermined borders seen in NDDH. Reactive arthritis manifests with hyperkeratotic plaques and is associated with the clinical triad of urethritis, conjunctivitis, and arthritis, which were absent in our patient.

The histologic differential diagnosis of NDDH includes infection, pyoderma gangrenosum, bowel-associated dermatosis-arthritis syndrome, rheumatoid neutrophilic dermatitis, and erythema elevatum diutinum^3,4; however, these conditions typically manifest with distinct clinical features that allow for differentiation, despite histologic similarities. The wide histologic spectrum of neutrophilic dermatosis may contribute to variable clinical manifestations and an evolving disease concept, as the classification of NDDH has changed from a primary vasculitis to a variant of SS. However, this evolution does not affect the appropriate management, as they all have shown good response to corticosteroid treatment.^4,6

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

To the Editor:

Primary cutaneous B-cell lymphomas (pcBCLs) can clinically mimic basal cell carcinomas (BCCs); however, histopathologic examination typically demonstrates features of lymphoma without evidence of an epithelial tumor. We present the case of a patient who demonstrated histologic features of both pcBCL and BCC in the same lesion, which was discovered during Mohs micrographic surgery.

An 84-year-old man presented for Mohs surgery for a biopsy-proven nodular and infiltrative BCC on the right superior helix of the ear of 1 year’s duration. Physical examination of the ear revealed a 1.0×1.3–cm ulcerated indurated plaque with rolled borders and a central hyperkeratotic crust (Figure 1). Frozen sections from the first Mohs stage demonstrated residual superficial, infiltrative, and basosquamous BCC (Figure 2). In addition, there was a brisk inflammatory infiltrate throughout the deep margins. The second stage showed no residual BCC, but there still was a brisk atypical lymphocytic infiltrate, with some areas showing lymphocytes in a linear cordlike distribution (Figure 3). Permanent sections demonstrated infiltration of small to medium lymphoid cells. Immunohistochemistry stains were positive for CD20 and BCL2 and negative for CD5, CD10, BCL6, and CD43; a low Ki-67 proliferation fraction also was observed. B-cell clonality studies and polymerase chain reaction demonstrated rearrangements of the IgH and IgK genes, consistent with primary cutaneous marginal zone lymphoma (pcMZL). Positron emission tomography showed no spread of malignancy; therefore, medical oncology recommended observation and close monitoring.

Primary cutaneous B-cell lymphoma accounts for approximately 25% of all cutaneous lymphomas.¹ Three main cutaneous subtypes exist: pcMZL; primary cutaneous follicular center lymphoma; and primary cutaneous diffuse large B-cell lymphoma, leg type. The second most common type of cutaneous lymphoma, pcMZL, accounts for 25% of cases of pcBCL.¹ Primary cutaneous follicular center lymphoma makes up 60% of cutaneous lymphomas, and the remainder are primary cutaneous diffuse large B-cell lymphoma, leg type. All share a notable male predominance and onset most commonly in the sixth through eighth decades of life, although they also can occur in younger patients.¹

Histologically, pcMZL has 2 distinct subtypes: one resembling mucosal-associated lymphoid tissue lymphomas and a more clinically aggressive subtype with heavy chain class switching, although intermediate forms also exist. Both are characterized by diffuse and/or nodular infiltrates in the subcutis and dermis with sparing of the epidermis. Often, these infiltrates are more prominent in the deeper sections examined, and occasionally they may be accompanied by germinal center follicles. Immunohistochemical stains are key in determining the pcBCL subtype. Primary cutaneous marginal zone lymphoma will most commonly show a BCL2+, BCL6–, CD20+, and CD10– immunophenotype, as in our case. If a majority of cells have undergone plasmacytoid differentiation, loss of CD20 can occur, but retention of other B-cell markers, such as CD79a and CD19, will be seen. Proliferation fraction via Ki-67 commonly is low, reflecting the indolence of this subtype of lymphoma.¹

Monoclonal rearrangement of immunoglobulins also can occur, with IgH rearrangements detected in 60% to 80% of cases of pcMZL. Translocations are not a reliable method of diagnosis for pcMZL but can be present in a variable manner, with t(14;18), t(3;14), and t(11;18) reported in a subset of cases.² Leukemic infiltrates encountered on frozen sections should prompt the Mohs surgeon to consider the possibility of a concomitant leukemia or lymphoma. In one study, 36% (20/55) of patients with chronic lymphocytic leukemia (CLL) were found to have predominantly leukemic B-cell infiltrates on frozen sections.³ Numerous reports also exist of asymptomatic patients being diagnosed with CLL due to leukemic infiltrates identified during Mohs surgery.^4,5 Patients with systemic hematologic malignancies, including CLL and non-Hodgkin lymphoma, also are known to be at an increased risk for skin cancers, including keratinocyte cancers, melanoma, and Merkel cell carcinoma. This can be attributed partially to immunosuppression, a well-known risk factor for development of cutaneous malignancies.⁵ Padgett et al⁵ speculated that local immune suppression due to underlying pcBCL and reaction of lymphocytes to tumor antigens could have played a role in the development of BCC at this site. If a leukemic infiltrate is demonstrated, the surgeon should consider sending tissue for permanent section and immunostaining. This can be helpful to determine if it is a reactive or neoplastic process and aid in characterizing the leukemic infiltrate if it is suspected to be neoplastic in nature.

There are numerous reports of pcBCL imitating the cutaneous findings of BCC clinically, but this is quite uncommon on histopathology. As in our case, findings of sheets of dense, monomorphic lymphocytes; inability to clear inflammation on deeper Mohs sections; presence of primordial follicles; and atypical cytology, including predominance of blastic forms, plasmacytoid cells, or cleaved lymphocytes, should give the clinician pause to consider further evaluation through permanent sections as well as genetic and immunoglobulin studies by a dermatopathologist. This case highlights the importance of further evaluation when an atypical finding is encountered during Mohs surgery.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

Photosensitivity refers to clinical manifestations arising from exposure to sunlight. Photodermatoses encompass a group of skin diseases caused by varying degrees of radiation exposure, including UV radiation and visible light. Photodermatoses can be categorized into 5 main types: primary, exogenous, photoexacerbated, metabolic, and genetic.¹ The clinical features of photodermatoses vary depending on the underlying cause but often include pruritic flares, wheals, or dermatitis on sun-exposed areas of the skin.² While photodermatoses typically are not life threatening, they can greatly impact patients’ quality of life. It is crucial to emphasize the importance of photoprotection and sunlight avoidance to patients as preventive measures against the manifestations of these skin diseases. Furthermore, we present a case of photocontact dermatitis (PCD) and discuss common causative agents, diagnostic mimickers, and treatment options.

Case Report

A 51-year-old woman with no relevant medical history presented to the dermatology clinic with a rash on the neck and under the eyes of 6 days’ duration. The rash was intermittently pruritic but otherwise asymptomatic. The patient reported that she had spent extensive time on the golf course the day of the rash onset and noted that a similar rash had occurred one other time 2 to 3 months prior, also following a prolonged period on the golf course. She had been using over-the-counter fexofenadine 180 mg and over-the-counter lidocaine spray for symptom relief.

Upon physical examination, erythematous patches were appreciated in a photodistributed pattern on the arms, legs, neck, face, and chest—areas that were not covered by clothing (Figures 1-3). Due to the distribution and morphology of the erythematous patches along with clinical course of onset following exposure to various environmental agents including pesticides, herbicides, oak, and pollen, a diagnosis of PCD was made. The patient was prescribed hydrocortisone cream 2.5%, fluticasone propionate cream 0.05%, and methylprednisolone in addition to the antihistamine. Improvement was noted after 3 days with complete resolution of the skin manifestations. She was counseled on wearing clothing with a universal protection factor rating of 50+ when on the golf course and when sun exposure is expected for an extended period of time.

Causative Agents

Photodermatoses are caused by antigenic substances that lead to photosensitization acquired by either contact or oral ingestion with subsequent sensitization to UV radiation. Halogenated salicylanilide, fenticlor, hexachlorophene, bithionol and, in rare cases, sunscreens, have been reported as triggers.³ In a study performed in 2010, sunscreens, antimicrobial agents, medications, fragrances, plants/plant derivatives, and pesticides were the most commonly reported offending agents listed from highest to lowest frequency. Of the antimicrobial agents, fenticlor, a topical antimicrobial and antifungal that is now mostly used in veterinary medicine, was the most common culprit, causing 60% of cases.^4,5

Clinical Manifestations

Clinical manifestations of photodermatoses vary depending upon the specific type of reaction. Examples of primary photodermatoses include polymorphous light eruption (PMLE) and solar urticaria. The cardinal symptoms of PMLE consist of severely pruritic skin lesions that can have macular, papular, papulovesicular, urticarial, multiformelike, and plaquelike variants that develop hours to days after sun exposure.³ Conversely, solar urticaria commonly develops more abruptly, with indurated plaques and wheals appearing on the arms and neck within 30 minutes of sun exposure. The lesions typically resolve within 24 hours.¹

Examples of the exogenous subtype include drug-induced photosensitivity, PCD, and pseudoporphyria, with the common clinical presentation of eruption following contact with the causative agent. Drug-induced photosensitivity primarily manifests as a severe sunburnlike rash commonly caused by systemic drugs such as tetracyclines. Photocontact dermatitis is limited to sun-exposed areas of the skin and is caused by a reactive irritant such as chemicals or topical creams. Pseudoporphyria, usually caused by nonsteroidal anti-inflammatory drugs, can manifest with skin fragility and subepidermal blisters.⁶

Photoexacerbated photodermatoses encompass a variety of conditions ranging from hyperpigmentation disorders such as melasma to autoimmune conditions such as systemic lupus erythematosus (SLE) and dermatomyositis (DM). Common clinical features of these diseases include photodistributed erythema, often involving the cheeks, upper back, and anterior neck. Photo-exposed areas of the dorsal hands also are commonplace for both SLE and DM. Clinical manifestations of PCD are limited to sun-exposed areas of the body, specifically those that come into contact with photoallergic triggers.³ Manifestations of PCD can include pruritic eczematous eruptions resembling those of contact dermatitis 1 to 2 days after sun exposure.¹

Photocontact dermatitis represents a specific sensitization via contact or oral ingestion acquired prior to sunlight exposure. It can be broken down into 2 distinct subtypes: photoallergic and photoirritant dermatitis, dependent on whether an allergic or irritant reaction is invoked.² Plants are known to be a common trigger of photoirritant reactions, while extrinsic triggers include psoralens and medications such as tetracycline antibiotics or sulfonamides. Photoallergic reactions commonly can be caused by topical application of sunscreen or medications, namely nonsteroidal anti-inflammatory drugs.² Clinical manifestations that may point to photoirritant dermatitis include a photodistributed eruption and classic morphology showing erythema and edema with bullae present in severe cases. These can be contrasted with the clinical manifestations of photoallergic reactions, which usually do not correlate to sun-exposed areas and consist of a monomorphous distribution pattern similar to that of eczema. Although there are distinguishing features of both subtypes of PCD, the overlapping clinical features can mimic those of solar urticaria, PMLE, cutaneous lupus erythematosus, and more systemic conditions such as SLE and DM.⁷

Systemic lupus erythematosus is associated with a broad range of cutaneous manifestations.⁸ Exposure to UV radiation is a common trigger for lupus and has the propensity to cause a malar (butterfly) rash that covers the cheeks and nasal bridge but classically spares the nasolabial folds. The rash may display confluent reddish-purple discoloration with papules and/or edema and typically is present at diagnosis in 40% to 52% of patients with SLE.⁸ Discoid lupus erythematosus, one of the most common cutaneous forms of lupus, manifests with various-sized coin-shaped plaques with adherent follicular hyperkeratosis and plugging. These lesions usually develop on the face, scalp, and ears but also may appear in non–sun-exposed areas.⁸ Dermatomyositis can manifest with photodistributed erythema affecting classic areas such as the upper back (shawl sign), anterior neck and upper chest (V-sign), and a malar rash similar to that seen in lupus, though DM classically does not spare the nasolabial folds.^8,9

Because SLE and DM manifest with photodistributed rashes, it can be difficult to distinguish them from the classic symptoms of photoirritant dermatitis.⁹ Thus, it is imperative that providers have a high clinical index of suspicion when dealing with patients of similar presentations, as the treatment regimens vastly differ. Approaching the patient with a thorough medical history review, review of systems, biopsy (including immunofluorescence), and appropriate laboratory workup may aid in excluding more complex differential diagnoses such as SLE and DM.

Metabolic and genetic photodermatoses are more rare but can include conditions such as porphyria cutanea tarda and xeroderma pigmentosum, both of which demonstrate fragile skin, slow wound healing, and bullae on photo-exposed skin.¹ Although the manifestations can be similar in these systemic conditions, they are caused by very different mechanisms. Porphyria cutanea tarda is caused by deficiencies in enzymes involved in the heme synthesis pathway, whereas xeroderma pigmentosum is caused by an alteration in DNA repair mechanisms.⁷

Prevalence and the Need for Standardized Testing

Most practicing dermatologists see cases of PCD due to its multiple causative agents; however, little is known about its overall prevalence. The incidence of PCD is fairly low in the general population, but this may be due to its clinical diagnosis, which excludes diagnostic testing such as phototesting and photopatch testing.¹⁰ While the incidence of photoallergic contact dermatitis also is fairly unknown, the inception of testing modalities has allowed statistics to be drawn. Research conducted in the United States has disclosed that the incidence of photoallergic contact dermatitis in individuals with a history of a prior photosensitivity eruption is approximately 10% to 20%.¹⁰ The development of guidelines and a registry for photopatch testing would aid in a greater understanding of the incidence of PCD and overall consistency of diagnosis.⁷ Regardless of this lack of consensus, these conditions can be properly managed and prevented if recognized clinically, while newer testing modalities would allow for confirmation of the diagnosis. It is important that any patient presenting with a history of photosensitivity be seen as a candidate for photopatch testing, especially today, as the general population is increasingly exposed to new chemicals entering the market and new social trends.^7,10

Diagnosis and Treatment

It is important to consider a detailed history, including the timing, location, duration, family history, and seasonal variation of suspected photodermatoses. A thorough skin examination that takes note of the specific areas affected, morphology, and involvement of the rash or lesions can be helpful.¹ Further diagnostic testing such as phototesting and photopatch testing can be employed and is especially important when distinguishing photoallergy from phototoxicity.¹¹ Phototesting involves exposing the patient’s skin to different doses of UVA, UVB, and visible light, followed by an immediate clinical reading of the results and then a delayed reading conducted after 24 hours.¹ Photopatch testing involves the application of 2 sets of identical photoallergens to prepped skin (typically cleansed with isopropyl alcohol), with one being irradiated with UVA after 24 hours and one serving as the control. A clinical assessment is conducted at 24 hours and repeated 7 days later.¹ In photodermatoses, a visible reaction can be appreciated on the treatment arm while the control arm remains clear. When both sides reveal a visible reaction, this is more indicative of a ­light-independent allergic contact dermatitis.¹

Photodermatoses occur only if there has been a specific sensitization, and therefore it is important to work with the patient to discover any new products that have been introduced into their regimen. Though many photosensitizers in personal care products (eg, antiseptics in soap and topical creams) have been discontinued, certain allergenic ingredients may remain.¹² It also is important to note that sensitization to a substance that previously was not a known allergen for a particular patient can occur later in life. Avoiding further sun exposure can rapidly improve the dermatitis, and it is possible for spontaneous remission without further intervention; however, as photoallergic reactions can cause severely pruritic skin lesions, the mainstay of symptomatic treatment consists of topical corticosteroids. Oral and topical antihistamines may help alleviate the pruritus but should not be heavily relied on as this can lead to medication resistance and diminishing efficacy.³ Use of short-term oral steroids also may be considered for rapid improvement of symptoms when the patient is in moderate distress and there are no contraindications. By identifying a temporal association between the introduction of new products and the emergence of dermatitis, it may be possible to identify the causative agent. The patient should promptly discontinue the suspected agent and remain under close observation by the clinician for any further eruptions, especially following additional sun exposure.

Prevention Strategies

In the case of PCD, prevention is key. As PCD indicates a photoallergy, it is important to inform patients that the allergy will persist for a lifetime, much like in contact dermatitis; therefore, the causative agent should be avoided indefinitely.³ Patients with PCD should make intentional efforts to read ingredient lists when purchasing new personal care products to ensure they do not contain the specific causative allergen if one has been identified. Further steps should be taken to ensure proper photoprotection, including use of dense clothing and sunscreen with UVA and UVB filters (broad spectrum).³ It has also been suggested that utilizing sunscreen with ectoin, an amino acid–derived molecule, may result in increased protection against UVA-induced photodermatoses.¹³

Final Thoughts

Photodermatoses are a group of skin diseases caused by exposure to UV radiation. Photocontact dermatitis/photoallergy is a form of allergic contact dermatitis that results from exposure to an allergen, whether topical, oral, or environmental. The allergen is activated by exposure to UV radiation to sensitize the allergic response, resulting in a rash characterized by confluent erythematous patches or plaques, papular vesicles, and rarely blisters.³ Photocontact dermatitis, although rare, is an important differential diagnosis to consider when the presenting rash is restricted to sun-exposed areas of the skin such as the arms, legs, neck, and face. Diagnosis remains a challenge; however, new testing modalities such as photopatch testing may open the door for further confirmation and aid in proper diagnosis leading to earlier treatment times for patients. It is recommended that the clinician and patient work together to identify the possible causative agent to prevent further eruptions.

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²

THE DIAGNOSIS: Cutaneous Leishmaniasis

The biopsy results revealed amastigotes at the periphery of parasitized histiocytes, consistent with a diagnosis of cutaneous leishmaniasis. Polymerase chain reaction analysis revealed Leishmania guyanensis species complex, which includes both L guyanensis and Leishmania panamensis. In this case of disseminated cutaneous leishmaniasis (Figure 1), our patient received a prolonged course of systemic therapy with oral miltefosine 50 mg 3 times daily. At the most recent follow-up appointment, she showed ongoing resolution of ulcerations, subcutaneous plaques, and lymphadenopathy on the trunk and face, but development of subcutaneous nodules continued on the arms and legs. At the next follow-up, physical examination revealed that the lesions slowly started to fade.

Leishmania species are parasites transmitted by bites of female sand flies, which belong to the genera Phlebotomus (Old World, Eastern Hemisphere) and Lutzomyia (New World, Western Hemisphere) genera.¹ Leishmania species have a complex life cycle, propagating within human macrophages, ultimately leading to cutaneous, mucocutaneous, and visceral disease manifestations.² Cutaneous leishmaniasis manifests classically as scattered, painless, slow-healing ulcers.³ A biopsy taken from the edge of a cutaneous ulcer for hematoxylin and eosin processing is recommended for initial diagnosis, and subsequent polymerase chain reaction of the sample is required for speciation, which guides therapeutic options.^4,5 Classic hematoxylin and eosin and Giemsa stain findings include amastigotes lining the edges of parasitized histiocytes (Figure 2).

Systemic treatment options include sodium stibogluconate, amphotericin B, pentamidine, paromomycin, miltefosine, and azole antifungals.^2,5 Geography often plays a critical role in selecting treatment options due to resistance rates of individual Leishmania species; for example, paromomycin compounds are more effective for cutaneous disease caused by Leishmania major than Leishmania tropica. Miltefosine is not effective for treating Leishmania braziliensis which can be acquired outside Guatemala, and higher doses of amphotericin B are recommended for visceral disease from East Africa.^2,5 In patients with cutaneous leishmaniasis caused by L guyanensis, miltefosine remains a first-line option due to its oral formulation and long half-life within organisms, though there is a risk for teratogenicity.² Amphotericin B remains the most effective treatment for visceral leishmaniasis and can be used off label to treat mucocutaneous disease or when cutaneous disease is refractory to other treatment options.³

Given the potential of L guyanensis to progress to mucocutaneous disease, monitoring for mucosal involvement should be performed at regular intervals for 6 months to 1 year.² Treatment may be considered efficacious if no new skin lesions occur after 4 to 6 weeks of therapy; existing skin lesions should be re-epithelializing and reduced by 50% in size, with most cutaneous disease adequately controlled after 3 months of therapy.²