Dermatology

IN THIS ARTICLE

• Diagnosis
• Management
• Outcome for the case patient

An 18-year-old woman presents to urgent care with a one-day history of sudden-onset sore throat, chills, malaise, and fever (102.5°F). On physical examination, the tonsils and pharynx are erythematous, and anterior cervical lymph nodes are tender on palpation. A rapid strep test is negative. The patient is instructed to use throat lozenges and take ibuprofen (400 mg every 8 h) as needed for pain.

On day 2, the patient’s fever resolves, but a painful rash develops on her palms and soles. Clinical examination reveals multiple erythematous plaques on the hands and feet (see Figure 1). The patient is diagnosed with hand-foot-and-mouth disease (HFMD).

DISCUSSION

HFMD is caused by enteroviruses, most commonly coxsackievirus A16 (CV-A16) or enterovirus 71 (EV71).¹ However, a newly recognized strain, CV-A6, has caused worldwide outbreaks of HFMD in both children and adults. Although less common than CV-A16 or EV71, CV-A6 is associated with a more severe disease course.¹ The CV-A6 strain was first identified in Finland in 2008 during a major outbreak of HFMD; it reached the United States in 2011.^2,3 Accurate statistics on the prevalence of CV-A6 in the US are difficult to obtain because HFMD is not a reportable condition.

Clinical presentation

HFMD typically manifests with painful oral lesions, with or without a macular, maculopapular, or vesicular exanthema. If a fever is present, it is usually below 101°F. The oral lesions are typically benign and manifest as erythematous macules that progress to vesicles with an erythematous halo. These lesions tend to be painful and may interfere with eating or drinking. Signs and symptoms associated with the more virulent form, CV-A6, may include

• Higher fever
• Wider distribution of lesions
• More extensive skin involvement
• Longer duration
• Palmar and plantar desquamation
• Nail dystrophy.^4,5

Laboratory diagnosis

Most symptomatic enterovirus infections are diagnosed based on clinical findings alone, reducing the need for laboratory testing. Laboratory confirmation may be warranted for more severe infections and during outbreaks. Molecular methods, such as reverse transcriptase polymerase chain reaction, are typically used for identifying enteroviruses, as they are rapid, sensitive, and widely available in hospital and commercial laboratories.⁶ Viral culture methods are labor-intensive, expensive, and reserved for typing the isolate. Serology is not useful in the diagnosis of acute infection.

Continue to: Differential diagnosis

The differential diagnosis of HFMD includes conditions with oral lesions and maculopapular, vesicular lesions involving the palms and/or soles, as well as erythroderma.

Oral lesions. Aphthous ulcers are shallow, painful oral lesions not accompanied by skin rashes. Herpes gingivostomatitis, caused by herpes simplex virus (HSV), is often preceded by a prodrome of fever. The associated lesions manifest as vesicular clusters on a red base that evolve into large, painful ulcers. HSV mouth lesions can populate the gingivae, pharynx, hard palate, lips, and perioral skin. Skin lesions may occur unilaterally.

Rashes involving palms and soles. A number of conditions manifest with skin lesions similar to those of HFMD. An autoeczematization reaction consisting of a pruritic, papulovesicular eruption secondary to dermatophyte infection (eg, tinea pedis, tinea manuum, tinea cruris, tinea corporis, tinea capitis) should be ruled out. This type of reaction is thought to be a delayed hypersensitivity response to fungal antigens. Pruritus and the absence of mouth sores distinguishes this reaction from HFMD.⁷

Secondary syphilis can manifest with a short-lived macular rash involving the palm and soles, as well as oral mucous patches and generalized lymphad­enopathy. Syphilis testing, including rapid plasma reagin or Venereal Disease Research Laboratory test with fluorescent treponemal antibody absorption, can rule out this diagnosis.

Erythema multiforme, which is more common in young adults, is characterized by target lesions on the palms and soles and erosions and/or bullae in the mouth and mucous membranes. It is usually preceded by a trigger, such as HSV infection.

Continue to: Erythroderma

Erythroderma. In addition to a rash, erythema multiforme can cause desquamation later in the disease course. Toxic shock syndrome (TSS), a life-threatening condition caused by Streptococcus or Staphylococcus, has an abrupt onset that is associated with high fever and hypotension. TSS causes a sunburn-like rash on the palms and soles that desquamates weeks after onset. Scarlet fever, caused by group A Streptococcus, can cause an erythematous rash with desquamation in children and adolescents. Scalded skin syndrome is a desquamative condition caused by Staphylococcus that occurs primarily in infants and young children.

Management

There is no specific antiviral treatment for HFMD, and thus management is mainly supportive. Fever and pain can be managed with ibuprofen or acetaminophen. Children who are unable to maintain oral hydration may require hospitalization for IV fluids.

Prevention of HFMD requires strict hand hygiene—washing with soap and water—as well as thoroughly cleaning and disinfecting surfaces that come in contact with infected oral secretions or feces.⁸

OUTCOME FOR THE CASE PATIENT

The patient was discharged and instructed to take ibuprofen as needed.

About three weeks later, the patient’s palms and soles began to peel. Clinical examination at follow-up revealed painful, diffuse, scaly desquamation of the hands and feet (see Figure 2). The patient also experienced loosening and shedding of the proximal nails (see Figure 3). She was diagnosed with postviral shedding.

Continue to: About eight weeks after the desquamatory rash manifested...

About eight weeks after the desquamatory rash manifested, complete resolution was seen. The patient experienced continued onychomadesis three months after the initial presentation.

CONCLUSION

Clinicians should be mindful of the increasing incidence of HFMD in the adult population, since it may mimic other disease states. The extent and chronicity of this patient’s clinical manifestations were unusual and may have been caused by CV-A6.

IN THIS ARTICLE

• Diagnosis
• Management
• Outcome for the case patient

An 18-year-old woman presents to urgent care with a one-day history of sudden-onset sore throat, chills, malaise, and fever (102.5°F). On physical examination, the tonsils and pharynx are erythematous, and anterior cervical lymph nodes are tender on palpation. A rapid strep test is negative. The patient is instructed to use throat lozenges and take ibuprofen (400 mg every 8 h) as needed for pain.

On day 2, the patient’s fever resolves, but a painful rash develops on her palms and soles. Clinical examination reveals multiple erythematous plaques on the hands and feet (see Figure 1). The patient is diagnosed with hand-foot-and-mouth disease (HFMD).

DISCUSSION

HFMD is caused by enteroviruses, most commonly coxsackievirus A16 (CV-A16) or enterovirus 71 (EV71).¹ However, a newly recognized strain, CV-A6, has caused worldwide outbreaks of HFMD in both children and adults. Although less common than CV-A16 or EV71, CV-A6 is associated with a more severe disease course.¹ The CV-A6 strain was first identified in Finland in 2008 during a major outbreak of HFMD; it reached the United States in 2011.^2,3 Accurate statistics on the prevalence of CV-A6 in the US are difficult to obtain because HFMD is not a reportable condition.

Clinical presentation

HFMD typically manifests with painful oral lesions, with or without a macular, maculopapular, or vesicular exanthema. If a fever is present, it is usually below 101°F. The oral lesions are typically benign and manifest as erythematous macules that progress to vesicles with an erythematous halo. These lesions tend to be painful and may interfere with eating or drinking. Signs and symptoms associated with the more virulent form, CV-A6, may include

• Higher fever
• Wider distribution of lesions
• More extensive skin involvement
• Longer duration
• Palmar and plantar desquamation
• Nail dystrophy.^4,5

Laboratory diagnosis

Most symptomatic enterovirus infections are diagnosed based on clinical findings alone, reducing the need for laboratory testing. Laboratory confirmation may be warranted for more severe infections and during outbreaks. Molecular methods, such as reverse transcriptase polymerase chain reaction, are typically used for identifying enteroviruses, as they are rapid, sensitive, and widely available in hospital and commercial laboratories.⁶ Viral culture methods are labor-intensive, expensive, and reserved for typing the isolate. Serology is not useful in the diagnosis of acute infection.

Continue to: Differential diagnosis

The differential diagnosis of HFMD includes conditions with oral lesions and maculopapular, vesicular lesions involving the palms and/or soles, as well as erythroderma.

Oral lesions. Aphthous ulcers are shallow, painful oral lesions not accompanied by skin rashes. Herpes gingivostomatitis, caused by herpes simplex virus (HSV), is often preceded by a prodrome of fever. The associated lesions manifest as vesicular clusters on a red base that evolve into large, painful ulcers. HSV mouth lesions can populate the gingivae, pharynx, hard palate, lips, and perioral skin. Skin lesions may occur unilaterally.

Rashes involving palms and soles. A number of conditions manifest with skin lesions similar to those of HFMD. An autoeczematization reaction consisting of a pruritic, papulovesicular eruption secondary to dermatophyte infection (eg, tinea pedis, tinea manuum, tinea cruris, tinea corporis, tinea capitis) should be ruled out. This type of reaction is thought to be a delayed hypersensitivity response to fungal antigens. Pruritus and the absence of mouth sores distinguishes this reaction from HFMD.⁷

Secondary syphilis can manifest with a short-lived macular rash involving the palm and soles, as well as oral mucous patches and generalized lymphad­enopathy. Syphilis testing, including rapid plasma reagin or Venereal Disease Research Laboratory test with fluorescent treponemal antibody absorption, can rule out this diagnosis.

Erythema multiforme, which is more common in young adults, is characterized by target lesions on the palms and soles and erosions and/or bullae in the mouth and mucous membranes. It is usually preceded by a trigger, such as HSV infection.

Continue to: Erythroderma

Erythroderma. In addition to a rash, erythema multiforme can cause desquamation later in the disease course. Toxic shock syndrome (TSS), a life-threatening condition caused by Streptococcus or Staphylococcus, has an abrupt onset that is associated with high fever and hypotension. TSS causes a sunburn-like rash on the palms and soles that desquamates weeks after onset. Scarlet fever, caused by group A Streptococcus, can cause an erythematous rash with desquamation in children and adolescents. Scalded skin syndrome is a desquamative condition caused by Staphylococcus that occurs primarily in infants and young children.

Management

There is no specific antiviral treatment for HFMD, and thus management is mainly supportive. Fever and pain can be managed with ibuprofen or acetaminophen. Children who are unable to maintain oral hydration may require hospitalization for IV fluids.

Prevention of HFMD requires strict hand hygiene—washing with soap and water—as well as thoroughly cleaning and disinfecting surfaces that come in contact with infected oral secretions or feces.⁸

OUTCOME FOR THE CASE PATIENT

The patient was discharged and instructed to take ibuprofen as needed.

About three weeks later, the patient’s palms and soles began to peel. Clinical examination at follow-up revealed painful, diffuse, scaly desquamation of the hands and feet (see Figure 2). The patient also experienced loosening and shedding of the proximal nails (see Figure 3). She was diagnosed with postviral shedding.

Continue to: About eight weeks after the desquamatory rash manifested...

About eight weeks after the desquamatory rash manifested, complete resolution was seen. The patient experienced continued onychomadesis three months after the initial presentation.

CONCLUSION

Clinicians should be mindful of the increasing incidence of HFMD in the adult population, since it may mimic other disease states. The extent and chronicity of this patient’s clinical manifestations were unusual and may have been caused by CV-A6.

IN THIS ARTICLE

• Diagnosis
• Management
• Outcome for the case patient

An 18-year-old woman presents to urgent care with a one-day history of sudden-onset sore throat, chills, malaise, and fever (102.5°F). On physical examination, the tonsils and pharynx are erythematous, and anterior cervical lymph nodes are tender on palpation. A rapid strep test is negative. The patient is instructed to use throat lozenges and take ibuprofen (400 mg every 8 h) as needed for pain.

On day 2, the patient’s fever resolves, but a painful rash develops on her palms and soles. Clinical examination reveals multiple erythematous plaques on the hands and feet (see Figure 1). The patient is diagnosed with hand-foot-and-mouth disease (HFMD).

DISCUSSION

HFMD is caused by enteroviruses, most commonly coxsackievirus A16 (CV-A16) or enterovirus 71 (EV71).¹ However, a newly recognized strain, CV-A6, has caused worldwide outbreaks of HFMD in both children and adults. Although less common than CV-A16 or EV71, CV-A6 is associated with a more severe disease course.¹ The CV-A6 strain was first identified in Finland in 2008 during a major outbreak of HFMD; it reached the United States in 2011.^2,3 Accurate statistics on the prevalence of CV-A6 in the US are difficult to obtain because HFMD is not a reportable condition.

Clinical presentation

HFMD typically manifests with painful oral lesions, with or without a macular, maculopapular, or vesicular exanthema. If a fever is present, it is usually below 101°F. The oral lesions are typically benign and manifest as erythematous macules that progress to vesicles with an erythematous halo. These lesions tend to be painful and may interfere with eating or drinking. Signs and symptoms associated with the more virulent form, CV-A6, may include

• Higher fever
• Wider distribution of lesions
• More extensive skin involvement
• Longer duration
• Palmar and plantar desquamation
• Nail dystrophy.^4,5

Laboratory diagnosis

Most symptomatic enterovirus infections are diagnosed based on clinical findings alone, reducing the need for laboratory testing. Laboratory confirmation may be warranted for more severe infections and during outbreaks. Molecular methods, such as reverse transcriptase polymerase chain reaction, are typically used for identifying enteroviruses, as they are rapid, sensitive, and widely available in hospital and commercial laboratories.⁶ Viral culture methods are labor-intensive, expensive, and reserved for typing the isolate. Serology is not useful in the diagnosis of acute infection.

Continue to: Differential diagnosis

The differential diagnosis of HFMD includes conditions with oral lesions and maculopapular, vesicular lesions involving the palms and/or soles, as well as erythroderma.

Oral lesions. Aphthous ulcers are shallow, painful oral lesions not accompanied by skin rashes. Herpes gingivostomatitis, caused by herpes simplex virus (HSV), is often preceded by a prodrome of fever. The associated lesions manifest as vesicular clusters on a red base that evolve into large, painful ulcers. HSV mouth lesions can populate the gingivae, pharynx, hard palate, lips, and perioral skin. Skin lesions may occur unilaterally.

Rashes involving palms and soles. A number of conditions manifest with skin lesions similar to those of HFMD. An autoeczematization reaction consisting of a pruritic, papulovesicular eruption secondary to dermatophyte infection (eg, tinea pedis, tinea manuum, tinea cruris, tinea corporis, tinea capitis) should be ruled out. This type of reaction is thought to be a delayed hypersensitivity response to fungal antigens. Pruritus and the absence of mouth sores distinguishes this reaction from HFMD.⁷

Secondary syphilis can manifest with a short-lived macular rash involving the palm and soles, as well as oral mucous patches and generalized lymphad­enopathy. Syphilis testing, including rapid plasma reagin or Venereal Disease Research Laboratory test with fluorescent treponemal antibody absorption, can rule out this diagnosis.

Erythema multiforme, which is more common in young adults, is characterized by target lesions on the palms and soles and erosions and/or bullae in the mouth and mucous membranes. It is usually preceded by a trigger, such as HSV infection.

Continue to: Erythroderma

Erythroderma. In addition to a rash, erythema multiforme can cause desquamation later in the disease course. Toxic shock syndrome (TSS), a life-threatening condition caused by Streptococcus or Staphylococcus, has an abrupt onset that is associated with high fever and hypotension. TSS causes a sunburn-like rash on the palms and soles that desquamates weeks after onset. Scarlet fever, caused by group A Streptococcus, can cause an erythematous rash with desquamation in children and adolescents. Scalded skin syndrome is a desquamative condition caused by Staphylococcus that occurs primarily in infants and young children.

Management

There is no specific antiviral treatment for HFMD, and thus management is mainly supportive. Fever and pain can be managed with ibuprofen or acetaminophen. Children who are unable to maintain oral hydration may require hospitalization for IV fluids.

Prevention of HFMD requires strict hand hygiene—washing with soap and water—as well as thoroughly cleaning and disinfecting surfaces that come in contact with infected oral secretions or feces.⁸

OUTCOME FOR THE CASE PATIENT

The patient was discharged and instructed to take ibuprofen as needed.

About three weeks later, the patient’s palms and soles began to peel. Clinical examination at follow-up revealed painful, diffuse, scaly desquamation of the hands and feet (see Figure 2). The patient also experienced loosening and shedding of the proximal nails (see Figure 3). She was diagnosed with postviral shedding.

Continue to: About eight weeks after the desquamatory rash manifested...

About eight weeks after the desquamatory rash manifested, complete resolution was seen. The patient experienced continued onychomadesis three months after the initial presentation.

CONCLUSION

Clinicians should be mindful of the increasing incidence of HFMD in the adult population, since it may mimic other disease states. The extent and chronicity of this patient’s clinical manifestations were unusual and may have been caused by CV-A6.

Based on the clinical findings, the patient was diagnosed with flagellate shiitake mushroom dermatitis.  (Subsequent treponemal and nontreponemal tests were negative for syphilis.)

Shiitake dermatitis is a rare disease that appears in susceptible patients after the consumption of large amounts of raw or undercooked shiitake mushrooms. The eruption is believed to be attributable to either a toxic or hypersensitivity reaction to lentinan, a polysaccharide component found within the mushroom cell wall.¹ Shiitake dermatitis is self-limiting and treatment focuses on symptomatic management.

Early recognition and proper counseling should ensure symptomatic relief and prevent future episodes. In addition, anyone preparing shiitake mushrooms should make sure that they are fully cooked before serving or eating them.²

In the case described here, the patient was advised to avoid eating undercooked shiitake mushrooms in the future and he was prescribed topical steroids (mometasone furoate 0.1% cream). The eruption resolved 2 weeks later.

References

1. Nguyen AH, Gonzaga MI, Lim VM, et al. Clinical features of shiitake dermatitis: a systematic review. Int J Dermatol. 2017;56:610-616.

2. Stephany MP, Chung S, Handler MZ, et al. Shiitake mushroom dermatitis: a review. Am J Clin Dermatol. 2016;17:485-489.

Based on the clinical findings, the patient was diagnosed with flagellate shiitake mushroom dermatitis.  (Subsequent treponemal and nontreponemal tests were negative for syphilis.)

Shiitake dermatitis is a rare disease that appears in susceptible patients after the consumption of large amounts of raw or undercooked shiitake mushrooms. The eruption is believed to be attributable to either a toxic or hypersensitivity reaction to lentinan, a polysaccharide component found within the mushroom cell wall.¹ Shiitake dermatitis is self-limiting and treatment focuses on symptomatic management.

Early recognition and proper counseling should ensure symptomatic relief and prevent future episodes. In addition, anyone preparing shiitake mushrooms should make sure that they are fully cooked before serving or eating them.²

In the case described here, the patient was advised to avoid eating undercooked shiitake mushrooms in the future and he was prescribed topical steroids (mometasone furoate 0.1% cream). The eruption resolved 2 weeks later.

References

1. Nguyen AH, Gonzaga MI, Lim VM, et al. Clinical features of shiitake dermatitis: a systematic review. Int J Dermatol. 2017;56:610-616.

2. Stephany MP, Chung S, Handler MZ, et al. Shiitake mushroom dermatitis: a review. Am J Clin Dermatol. 2016;17:485-489.

Based on the clinical findings, the patient was diagnosed with flagellate shiitake mushroom dermatitis.  (Subsequent treponemal and nontreponemal tests were negative for syphilis.)

Shiitake dermatitis is a rare disease that appears in susceptible patients after the consumption of large amounts of raw or undercooked shiitake mushrooms. The eruption is believed to be attributable to either a toxic or hypersensitivity reaction to lentinan, a polysaccharide component found within the mushroom cell wall.¹ Shiitake dermatitis is self-limiting and treatment focuses on symptomatic management.

Early recognition and proper counseling should ensure symptomatic relief and prevent future episodes. In addition, anyone preparing shiitake mushrooms should make sure that they are fully cooked before serving or eating them.²

In the case described here, the patient was advised to avoid eating undercooked shiitake mushrooms in the future and he was prescribed topical steroids (mometasone furoate 0.1% cream). The eruption resolved 2 weeks later.

References

1. Nguyen AH, Gonzaga MI, Lim VM, et al. Clinical features of shiitake dermatitis: a systematic review. Int J Dermatol. 2017;56:610-616.

2. Stephany MP, Chung S, Handler MZ, et al. Shiitake mushroom dermatitis: a review. Am J Clin Dermatol. 2016;17:485-489.

LAKE TAHOE, CALIF. – Several years ago, David H. Darrow, MD, DDS, began to notice a pattern in the conversation threads on websites dedicated to support for parents of children with facial port-wine stains (PWS).

Parents were reporting that dental problems arose earlier on their child’s side of face with the PWS, and that the alveolar ridge was lower on the side of the face that harbored the lesion. “Most importantly, parents were concerned that dentists were not touching their children because they were concerned about bleeding,” Dr. Darrow said at the annual meeting of the Society for Pediatric Dermatology. A search in the medical literature for port-wine stains and oral cavity changes, did not turn up much except for a few articles on bleeding. “One said that port-wine stains or capillary malformations rarely present major problems for the oral and maxillofacial surgeon. The other said that periodontal probing should not be done, as even gentle probing can result in uncontrolled bleeding,” he noted.

This prompted Dr. Darrow, who directs the Center for Hemangiomas and Vascular Birthmarks at the Eastern Virginia Medical School, Norfolk, and coinvestigators, Megan B. Dowling, MD, and Yueqin Zhao, PhD, to characterize manifestations of PWS in the oral cavity via an anonymous paired survey of volunteers with facial PWS and their dentists who were recruited from birthmarks.com and 10 collaborating physician practices (J Am Acad Dermatol 2012;67:687-93). Volunteers ranged in age from 1 to 62 years; mean age was 29 years. A total of 30 patients participated, and most (67%) were female.

The five most common oral manifestations reported by the patients were lip hyperplasia (53%), stained gingiva (47%), malocclusion (30%), bleeding gingiva (27%), and spacing between teeth (23%). Only 3% reported bleeding from dental procedures. When the researchers evaluated the orodental findings in the paired patient-physician responses, “most of the time there was good agreement between the patient and the dentist,” Dr. Darrow said. “The only one that fell out of agreement was lip hyperplasia. That’s probably because most dentists look right past the lips and into the oral cavity.”

When the researchers examined patients who had stained gingiva versus those who did not, they found that early-stage lesions demonstrated a reddish blush of the oral mucosa and gingiva, while late-stage lesions demonstrated increased blush of the oral tissues, as well as hyperplasia of the soft tissue or bone in the affected area. “Based on our review of the literature, bleeding of gums is rarely prolonged and dental procedures are safe,” Dr. Darrow said.

The findings are important, he continued, because capillary malformations of the oral cavity may result in periodontal disease associated with gingival overgrowth. The depth of the gingival pocket should be no more than 2-3 mm. “When you have areas of inflammation and deep-pocket formation, plaque and bacteria slowly erode the connection between the tooth and the soft tissue,” he explained. “At some point, that pocket becomes so deep that it reaches down into the bone in which the tooth is anchored. As that bone is eroded, the teeth loosen and begin to fall out. The goals of therapy are prevention of periodontal disease with meticulous oral hygiene.”

Soft tissue hyperplasia may be exacerbated by medications such as calcium channel blockers, cyclosporine, and phenytoin and phenobarbital, which are sometimes used by patients with Sturge-Weber syndrome, he said.

Dr. Darrow reported having no financial disclosures.

dbrunk@mdedge.com

LAKE TAHOE, CALIF. – Several years ago, David H. Darrow, MD, DDS, began to notice a pattern in the conversation threads on websites dedicated to support for parents of children with facial port-wine stains (PWS).

Parents were reporting that dental problems arose earlier on their child’s side of face with the PWS, and that the alveolar ridge was lower on the side of the face that harbored the lesion. “Most importantly, parents were concerned that dentists were not touching their children because they were concerned about bleeding,” Dr. Darrow said at the annual meeting of the Society for Pediatric Dermatology. A search in the medical literature for port-wine stains and oral cavity changes, did not turn up much except for a few articles on bleeding. “One said that port-wine stains or capillary malformations rarely present major problems for the oral and maxillofacial surgeon. The other said that periodontal probing should not be done, as even gentle probing can result in uncontrolled bleeding,” he noted.

This prompted Dr. Darrow, who directs the Center for Hemangiomas and Vascular Birthmarks at the Eastern Virginia Medical School, Norfolk, and coinvestigators, Megan B. Dowling, MD, and Yueqin Zhao, PhD, to characterize manifestations of PWS in the oral cavity via an anonymous paired survey of volunteers with facial PWS and their dentists who were recruited from birthmarks.com and 10 collaborating physician practices (J Am Acad Dermatol 2012;67:687-93). Volunteers ranged in age from 1 to 62 years; mean age was 29 years. A total of 30 patients participated, and most (67%) were female.

The five most common oral manifestations reported by the patients were lip hyperplasia (53%), stained gingiva (47%), malocclusion (30%), bleeding gingiva (27%), and spacing between teeth (23%). Only 3% reported bleeding from dental procedures. When the researchers evaluated the orodental findings in the paired patient-physician responses, “most of the time there was good agreement between the patient and the dentist,” Dr. Darrow said. “The only one that fell out of agreement was lip hyperplasia. That’s probably because most dentists look right past the lips and into the oral cavity.”

When the researchers examined patients who had stained gingiva versus those who did not, they found that early-stage lesions demonstrated a reddish blush of the oral mucosa and gingiva, while late-stage lesions demonstrated increased blush of the oral tissues, as well as hyperplasia of the soft tissue or bone in the affected area. “Based on our review of the literature, bleeding of gums is rarely prolonged and dental procedures are safe,” Dr. Darrow said.

The findings are important, he continued, because capillary malformations of the oral cavity may result in periodontal disease associated with gingival overgrowth. The depth of the gingival pocket should be no more than 2-3 mm. “When you have areas of inflammation and deep-pocket formation, plaque and bacteria slowly erode the connection between the tooth and the soft tissue,” he explained. “At some point, that pocket becomes so deep that it reaches down into the bone in which the tooth is anchored. As that bone is eroded, the teeth loosen and begin to fall out. The goals of therapy are prevention of periodontal disease with meticulous oral hygiene.”

Soft tissue hyperplasia may be exacerbated by medications such as calcium channel blockers, cyclosporine, and phenytoin and phenobarbital, which are sometimes used by patients with Sturge-Weber syndrome, he said.

Dr. Darrow reported having no financial disclosures.

dbrunk@mdedge.com

LAKE TAHOE, CALIF. – Several years ago, David H. Darrow, MD, DDS, began to notice a pattern in the conversation threads on websites dedicated to support for parents of children with facial port-wine stains (PWS).

Parents were reporting that dental problems arose earlier on their child’s side of face with the PWS, and that the alveolar ridge was lower on the side of the face that harbored the lesion. “Most importantly, parents were concerned that dentists were not touching their children because they were concerned about bleeding,” Dr. Darrow said at the annual meeting of the Society for Pediatric Dermatology. A search in the medical literature for port-wine stains and oral cavity changes, did not turn up much except for a few articles on bleeding. “One said that port-wine stains or capillary malformations rarely present major problems for the oral and maxillofacial surgeon. The other said that periodontal probing should not be done, as even gentle probing can result in uncontrolled bleeding,” he noted.

This prompted Dr. Darrow, who directs the Center for Hemangiomas and Vascular Birthmarks at the Eastern Virginia Medical School, Norfolk, and coinvestigators, Megan B. Dowling, MD, and Yueqin Zhao, PhD, to characterize manifestations of PWS in the oral cavity via an anonymous paired survey of volunteers with facial PWS and their dentists who were recruited from birthmarks.com and 10 collaborating physician practices (J Am Acad Dermatol 2012;67:687-93). Volunteers ranged in age from 1 to 62 years; mean age was 29 years. A total of 30 patients participated, and most (67%) were female.

The five most common oral manifestations reported by the patients were lip hyperplasia (53%), stained gingiva (47%), malocclusion (30%), bleeding gingiva (27%), and spacing between teeth (23%). Only 3% reported bleeding from dental procedures. When the researchers evaluated the orodental findings in the paired patient-physician responses, “most of the time there was good agreement between the patient and the dentist,” Dr. Darrow said. “The only one that fell out of agreement was lip hyperplasia. That’s probably because most dentists look right past the lips and into the oral cavity.”

When the researchers examined patients who had stained gingiva versus those who did not, they found that early-stage lesions demonstrated a reddish blush of the oral mucosa and gingiva, while late-stage lesions demonstrated increased blush of the oral tissues, as well as hyperplasia of the soft tissue or bone in the affected area. “Based on our review of the literature, bleeding of gums is rarely prolonged and dental procedures are safe,” Dr. Darrow said.

The findings are important, he continued, because capillary malformations of the oral cavity may result in periodontal disease associated with gingival overgrowth. The depth of the gingival pocket should be no more than 2-3 mm. “When you have areas of inflammation and deep-pocket formation, plaque and bacteria slowly erode the connection between the tooth and the soft tissue,” he explained. “At some point, that pocket becomes so deep that it reaches down into the bone in which the tooth is anchored. As that bone is eroded, the teeth loosen and begin to fall out. The goals of therapy are prevention of periodontal disease with meticulous oral hygiene.”

Soft tissue hyperplasia may be exacerbated by medications such as calcium channel blockers, cyclosporine, and phenytoin and phenobarbital, which are sometimes used by patients with Sturge-Weber syndrome, he said.

Dr. Darrow reported having no financial disclosures.

dbrunk@mdedge.com

A 7-year-old boy was brought to his family physician for evaluation of a mildly pruritic spreading rash. Ten days earlier, the skin eruption had appeared, and he was given a diagnosis of streptococcal pharyngitis, which was confirmed by a throat swab and a positive antistreptolysin O titer. The child had no personal or family history of skin disorders, including eczema or psoriasis. He hadn’t used any topical agents or new medications recently, nor had he been exposed to triggering plants, animals, or chemicals. There was no history of trauma, friction, or rubbing in the area.

Physical examination revealed multiple erythematous, scaly papules and plaques of varying size on the patient’s trunk, arms, and legs (FIGURE). His palms and soles were spared.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

A diagnosis of guttate psoriasis was made based on the physical exam findings and the preceding group A beta-hemolytic streptococcal infection.

This condition affects approximately 2% of all patients with psoriasis; it is characterized by the acute onset of multiple erythematosquamous papules and small plaques that look like droplets (“gutta”).¹ It tends to affect children and young adults and typically occurs following an acute infection (eg, streptococcal pharyngitis).^2,3 In this case, a rapid strep test and throat culture positive for group A Streptococcus supported the diagnosis.

One-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.

Although this particular phenotype of psoriasis is usually associated with streptococcal infection and mainly occurs in patients with the HLA-Cw6+ allele, the specific immunologic response that causes these skin lesions is poorly understood.⁴ Antigenic similarities between streptococcal proteins and keratinocyte antigens might explain why the condition is triggered by streptococcal infections.⁵

Pityriasis rosea and tinea corporis are part of the differential

The differential includes skin conditions such as pityriasis rosea, tinea corporis, varicella, and insect bites.

Pityriasis rosea can manifest as a papulosquamous eruption, but it has an inward-facing scale, called a collarette. The “Christmas tree” pattern on the back that is preceded by a solitary 2- to 10-cm oval, pink, scaly herald patch (in 17%-50% of cases) is key to the diagnosis.⁶ (For more information, see “Rash on trunk and upper arms.”)

Continue to: Tinea corporis...

Tinea corporis is a dermatophyte infection that causes flat, red, scaly lesions that progress into annular lesions with central clearing or brown discoloration. The plaques can range from a few centimeters to several inches in size, but are always characterized by the slowly advancing border.⁶

Varicella also affects the trunk and extremities, but a key clinical finding is crops of characteristic lesions, including papules, vesicles, pustules, and crusted lesions in different stages that manifest simultaneously.⁶

Insect bites usually appear as urticarial papules and plaques associated with outdoor exposure. The lesions are distributed where insects are likely to bite.⁶

Treat the infection, control the psoriasis

The first-line treatment for streptococcal infection is amoxicillin (50 mg/kg/d [maximum: 1000 mg/d] orally for 10 d) or penicillin G benzathine (for children < 60 lb, 6 × 10⁵ units intramuscularly; children ≥ 60 lb, 1.2 × 10⁶ units intramuscularly).⁷ For the psoriasis lesions, treatment options include topical glucocorticosteroids, vitamin D derivatives, or combinations of both.⁵ In most cases, guttate psoriasis completely resolves. However, one-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.⁸

Our patient was treated with penicillin G benzathine (1.2 × 10⁶ units intramuscularly) and a calcipotriol/betamethasone combination gel. The streptococcal infection and skin lesions completely resolved. No adverse events were reported, and no relapse was observed after 3 months.

CORRESPONDENCE
Rita Matos, MD, Rua Actor Mário Viegas SN Rio Tinto, Portugal; anasotam@gmail.com

A 7-year-old boy was brought to his family physician for evaluation of a mildly pruritic spreading rash. Ten days earlier, the skin eruption had appeared, and he was given a diagnosis of streptococcal pharyngitis, which was confirmed by a throat swab and a positive antistreptolysin O titer. The child had no personal or family history of skin disorders, including eczema or psoriasis. He hadn’t used any topical agents or new medications recently, nor had he been exposed to triggering plants, animals, or chemicals. There was no history of trauma, friction, or rubbing in the area.

Physical examination revealed multiple erythematous, scaly papules and plaques of varying size on the patient’s trunk, arms, and legs (FIGURE). His palms and soles were spared.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

A diagnosis of guttate psoriasis was made based on the physical exam findings and the preceding group A beta-hemolytic streptococcal infection.

This condition affects approximately 2% of all patients with psoriasis; it is characterized by the acute onset of multiple erythematosquamous papules and small plaques that look like droplets (“gutta”).¹ It tends to affect children and young adults and typically occurs following an acute infection (eg, streptococcal pharyngitis).^2,3 In this case, a rapid strep test and throat culture positive for group A Streptococcus supported the diagnosis.

One-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.

Although this particular phenotype of psoriasis is usually associated with streptococcal infection and mainly occurs in patients with the HLA-Cw6+ allele, the specific immunologic response that causes these skin lesions is poorly understood.⁴ Antigenic similarities between streptococcal proteins and keratinocyte antigens might explain why the condition is triggered by streptococcal infections.⁵

Pityriasis rosea and tinea corporis are part of the differential

The differential includes skin conditions such as pityriasis rosea, tinea corporis, varicella, and insect bites.

Pityriasis rosea can manifest as a papulosquamous eruption, but it has an inward-facing scale, called a collarette. The “Christmas tree” pattern on the back that is preceded by a solitary 2- to 10-cm oval, pink, scaly herald patch (in 17%-50% of cases) is key to the diagnosis.⁶ (For more information, see “Rash on trunk and upper arms.”)

Continue to: Tinea corporis...

Tinea corporis is a dermatophyte infection that causes flat, red, scaly lesions that progress into annular lesions with central clearing or brown discoloration. The plaques can range from a few centimeters to several inches in size, but are always characterized by the slowly advancing border.⁶

Varicella also affects the trunk and extremities, but a key clinical finding is crops of characteristic lesions, including papules, vesicles, pustules, and crusted lesions in different stages that manifest simultaneously.⁶

Insect bites usually appear as urticarial papules and plaques associated with outdoor exposure. The lesions are distributed where insects are likely to bite.⁶

Treat the infection, control the psoriasis

The first-line treatment for streptococcal infection is amoxicillin (50 mg/kg/d [maximum: 1000 mg/d] orally for 10 d) or penicillin G benzathine (for children < 60 lb, 6 × 10⁵ units intramuscularly; children ≥ 60 lb, 1.2 × 10⁶ units intramuscularly).⁷ For the psoriasis lesions, treatment options include topical glucocorticosteroids, vitamin D derivatives, or combinations of both.⁵ In most cases, guttate psoriasis completely resolves. However, one-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.⁸

Our patient was treated with penicillin G benzathine (1.2 × 10⁶ units intramuscularly) and a calcipotriol/betamethasone combination gel. The streptococcal infection and skin lesions completely resolved. No adverse events were reported, and no relapse was observed after 3 months.

CORRESPONDENCE
Rita Matos, MD, Rua Actor Mário Viegas SN Rio Tinto, Portugal; anasotam@gmail.com

A 7-year-old boy was brought to his family physician for evaluation of a mildly pruritic spreading rash. Ten days earlier, the skin eruption had appeared, and he was given a diagnosis of streptococcal pharyngitis, which was confirmed by a throat swab and a positive antistreptolysin O titer. The child had no personal or family history of skin disorders, including eczema or psoriasis. He hadn’t used any topical agents or new medications recently, nor had he been exposed to triggering plants, animals, or chemicals. There was no history of trauma, friction, or rubbing in the area.

Physical examination revealed multiple erythematous, scaly papules and plaques of varying size on the patient’s trunk, arms, and legs (FIGURE). His palms and soles were spared.

WHAT IS YOUR DIAGNOSIS?
HOW WOULD YOU TREAT THIS PATIENT?

A diagnosis of guttate psoriasis was made based on the physical exam findings and the preceding group A beta-hemolytic streptococcal infection.

This condition affects approximately 2% of all patients with psoriasis; it is characterized by the acute onset of multiple erythematosquamous papules and small plaques that look like droplets (“gutta”).¹ It tends to affect children and young adults and typically occurs following an acute infection (eg, streptococcal pharyngitis).^2,3 In this case, a rapid strep test and throat culture positive for group A Streptococcus supported the diagnosis.

One-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.

Although this particular phenotype of psoriasis is usually associated with streptococcal infection and mainly occurs in patients with the HLA-Cw6+ allele, the specific immunologic response that causes these skin lesions is poorly understood.⁴ Antigenic similarities between streptococcal proteins and keratinocyte antigens might explain why the condition is triggered by streptococcal infections.⁵

Pityriasis rosea and tinea corporis are part of the differential

The differential includes skin conditions such as pityriasis rosea, tinea corporis, varicella, and insect bites.

Pityriasis rosea can manifest as a papulosquamous eruption, but it has an inward-facing scale, called a collarette. The “Christmas tree” pattern on the back that is preceded by a solitary 2- to 10-cm oval, pink, scaly herald patch (in 17%-50% of cases) is key to the diagnosis.⁶ (For more information, see “Rash on trunk and upper arms.”)

Continue to: Tinea corporis...

Tinea corporis is a dermatophyte infection that causes flat, red, scaly lesions that progress into annular lesions with central clearing or brown discoloration. The plaques can range from a few centimeters to several inches in size, but are always characterized by the slowly advancing border.⁶

Varicella also affects the trunk and extremities, but a key clinical finding is crops of characteristic lesions, including papules, vesicles, pustules, and crusted lesions in different stages that manifest simultaneously.⁶

Insect bites usually appear as urticarial papules and plaques associated with outdoor exposure. The lesions are distributed where insects are likely to bite.⁶

Treat the infection, control the psoriasis

The first-line treatment for streptococcal infection is amoxicillin (50 mg/kg/d [maximum: 1000 mg/d] orally for 10 d) or penicillin G benzathine (for children < 60 lb, 6 × 10⁵ units intramuscularly; children ≥ 60 lb, 1.2 × 10⁶ units intramuscularly).⁷ For the psoriasis lesions, treatment options include topical glucocorticosteroids, vitamin D derivatives, or combinations of both.⁵ In most cases, guttate psoriasis completely resolves. However, one-third of children with guttate psoriasis go on to develop plaque psoriasis later in life.⁸

Our patient was treated with penicillin G benzathine (1.2 × 10⁶ units intramuscularly) and a calcipotriol/betamethasone combination gel. The streptococcal infection and skin lesions completely resolved. No adverse events were reported, and no relapse was observed after 3 months.

CORRESPONDENCE
Rita Matos, MD, Rua Actor Mário Viegas SN Rio Tinto, Portugal; anasotam@gmail.com

Diabetic foot ulcers and infections can lead to osteomyelitis, a potentially devastating infection in the bone.

WILLSIE/Getty Images

How much of a difference can osteomyelitis make to a patient’s prognosis? A 2014 commentary by Benjamin A. Lipsky, MD, a prominent expert in problems associated with diabetic patients’ feet who’s with the University of Washington, Seattle, hints at the potential toll: “Overall, about 20% of patients with a diabetic foot infection (and over 60% of those with severe infections) have underlying osteomyelitis, which dramatically increases the risk of lower-extremity amputation” (Diabetes Care. 2014 Mar;37[3]:593-5).

Diagnosis of osteomyelitis, which relies on a bone biopsy, is clearly important. But there’s a big gap in diagnostic findings depending on whether doctors request culture or histology results, according to a new study released at the 2018 scientific meeting of the American Diabetes Association (Diabetes. 2018 Jul. doi: 10.2337/db18-110-OR).

In an interview, lead author and podiatrist Peter A. Crisologo, DPM, of University of Texas Southwestern Medical Center, Dallas, explained the study findings and offered guidance for requesting bone biopsies in possible cases of osteomyelitis.

Q: What makes diagnosis and treatment of osteomyelitis unique?

A: In the foot, there’s not a lot of soft tissue between the outside world and your bone. If the wounds on the feet go deep enough, they can spread a bacterial infection to the bone. This changes how foot infections are treated.
 

If you have a skin infection, it requires 11-12 days of antibiotics. Things start ramping up once you start getting into the bone. You’re talking potential surgery and 6 weeks of antibiotics through IV treatments. This is why it’s really important that you get your diagnosis right.

A lot of people say “I’m going to do the safe thing” and treat a bone infection with an extended course of antibiotics.

That’s not necessarily safe. If you’re overdiagnosing – for example, you identify bacteria that’s just a contaminant – you could put a patient through 6 weeks of IV treatment along with the risks of a PICC (peripherally inserted central catheter ) line infection, complications from IV placement, and complications from the antibiotic.

Also, acute kidney injury develops in at least a third of the patients who undergo 6 weeks of antibiotics. That’s not to mention the cost of the visits and the labs you have to draw. But we don’t want to underdiagnose either. If osteomyelitis is underdiagnosed and then not treated, the infection can smolder and continue to progress and worsen.

Q: Your study looks at the bone biopsy. How does it fit into care of osteomyelitis in the diabetic foot?

A: A bone biopsy is the standard for diagnosis under the guidelines of the Infectious Diseases Society of America/International Working Group on the Diabetic Foot (Clin Infect Dis. 2012;54[12]:e132-73 ).
 

But beyond that, nobody says anything. Everyone has an operational definition of how a bone biopsy is interpreted, and there’s a need for a consensus on how a bone biopsy can be used to diagnose osteomyelitis.

You’ll get different percentages of your patients diagnosed with osteomyelitis. For example, someone may say the biopsy is only positive if the histology is positive, while another says the histology doesn’t matter if the culture is positive.

Q: Your study looks at histology and culture analyses. What do these reveal?

A: A traditional culture helps you identify the bacteria, as well as guide your treatment when it’s tested against antibiotics.
 

A traditional histology allows the pathologist to look under a microscope for signs of osteomyelitis: Do they see the right inflammatory cells, white cells, lymphocytes, combinations of cells? Does this look like an acute or chronic osteomyelitis?

Q: Why might it be wise to combine culture and histology analyses?

A: If you have bacteria that’s difficult to culture via traditional methods, it may be a bacteria that doesn’t grow well or easily. If you combine culture with histology, pathologists can look and say, “Your culture was negative but we see these other signs, so we feel this is osteomyelitis.”



Q: Your study examined 35 consecutive patients aged at least 21 years who had moderate or severe infections bone infections in the foot linked with type 1 diabetes (n = 4) or type 2 diabetes (n = 31).

The samples were analyzed via culture, histology, and culture/histology examinations. You also performed genetic sequencing (quantitative polymerase chain reaction targeting 16S rRNA). How does this test fit in to bone biopsies in the clinic?

A: That’s a newer method and not a standard of care treatment for the diabetic foot. This analysis looks at DNA that’s present, bypassing the analysis of difficult-to-grow bacteria.



Q: What did you discover?

A: In this study, histology had the lowest incidence of positively detecting osteomyelitis. (45.7%). The level increases when a culture is taken (68.6% vs. histology; P = .02).
 

Then it goes up when DNA is used because it’s catching everything (82.9%, P = .001 vs. histology and P = .31 vs. culture).

[The study also found that adding histology to culture or to genetic sequencing did not change positive findings.]

Q: Does the study suggest one approach is better than the others?

A: This paper doesn’t provide enough evidence to use one method over another. The main purpose was to raise the concern that diagnosis can change dramatically depending on how the gold standard of bone biopsy is interpreted.



Q: What were the pros and cons of the genetic sequencing approach?

A: When we use this approach, our positive diagnostic rate significantly increases. But there are also downsides. We don’t know whether the bacteria we see is alive or dead. We just know it was there. So are the patients truly positive? That’s a question we can’t answer.
 

Genetic sequencing also doesn’t tell us about susceptibilities to antibiotics.

Q: What is the take-home message here for physicians who may order bone biopsies?

A: The thing to do is request both traditional culture and traditional histology.
 

As far as DNA sequencing, that not something I’d recommend as a standard of care.

Q: Can you comment on cost and insurance coverage for these approaches?

A: As far as I know, genetic sequencing is not covered as it is not standard of care in the diabetic foot and is used mainly for research at this time.
 

Pathology and culture are standard of care when evaluating for osteomyelitis and should be a covered service. However, a patient should call their insurance company first prior to having the procedure done to see whether it is covered.

Q: What’s next for research in this area?

A: From here, the next step is bigger numbers: Increase the study size and look at this again. Also, we may be able to identify susceptibilities by identifying resistance within the DNA.



Dr. Crisologo and two other study authors report no relevant disclosures. One study author reported various disclosures including research support, consulting, and service on speakers' bureaus.
 

Diabetic foot ulcers and infections can lead to osteomyelitis, a potentially devastating infection in the bone.

WILLSIE/Getty Images

How much of a difference can osteomyelitis make to a patient’s prognosis? A 2014 commentary by Benjamin A. Lipsky, MD, a prominent expert in problems associated with diabetic patients’ feet who’s with the University of Washington, Seattle, hints at the potential toll: “Overall, about 20% of patients with a diabetic foot infection (and over 60% of those with severe infections) have underlying osteomyelitis, which dramatically increases the risk of lower-extremity amputation” (Diabetes Care. 2014 Mar;37[3]:593-5).

Diagnosis of osteomyelitis, which relies on a bone biopsy, is clearly important. But there’s a big gap in diagnostic findings depending on whether doctors request culture or histology results, according to a new study released at the 2018 scientific meeting of the American Diabetes Association (Diabetes. 2018 Jul. doi: 10.2337/db18-110-OR).

In an interview, lead author and podiatrist Peter A. Crisologo, DPM, of University of Texas Southwestern Medical Center, Dallas, explained the study findings and offered guidance for requesting bone biopsies in possible cases of osteomyelitis.

Q: What makes diagnosis and treatment of osteomyelitis unique?

A: In the foot, there’s not a lot of soft tissue between the outside world and your bone. If the wounds on the feet go deep enough, they can spread a bacterial infection to the bone. This changes how foot infections are treated.
 

If you have a skin infection, it requires 11-12 days of antibiotics. Things start ramping up once you start getting into the bone. You’re talking potential surgery and 6 weeks of antibiotics through IV treatments. This is why it’s really important that you get your diagnosis right.

A lot of people say “I’m going to do the safe thing” and treat a bone infection with an extended course of antibiotics.

That’s not necessarily safe. If you’re overdiagnosing – for example, you identify bacteria that’s just a contaminant – you could put a patient through 6 weeks of IV treatment along with the risks of a PICC (peripherally inserted central catheter ) line infection, complications from IV placement, and complications from the antibiotic.

Also, acute kidney injury develops in at least a third of the patients who undergo 6 weeks of antibiotics. That’s not to mention the cost of the visits and the labs you have to draw. But we don’t want to underdiagnose either. If osteomyelitis is underdiagnosed and then not treated, the infection can smolder and continue to progress and worsen.

Q: Your study looks at the bone biopsy. How does it fit into care of osteomyelitis in the diabetic foot?

A: A bone biopsy is the standard for diagnosis under the guidelines of the Infectious Diseases Society of America/International Working Group on the Diabetic Foot (Clin Infect Dis. 2012;54[12]:e132-73 ).
 

But beyond that, nobody says anything. Everyone has an operational definition of how a bone biopsy is interpreted, and there’s a need for a consensus on how a bone biopsy can be used to diagnose osteomyelitis.

You’ll get different percentages of your patients diagnosed with osteomyelitis. For example, someone may say the biopsy is only positive if the histology is positive, while another says the histology doesn’t matter if the culture is positive.

Q: Your study looks at histology and culture analyses. What do these reveal?

A: A traditional culture helps you identify the bacteria, as well as guide your treatment when it’s tested against antibiotics.
 

A traditional histology allows the pathologist to look under a microscope for signs of osteomyelitis: Do they see the right inflammatory cells, white cells, lymphocytes, combinations of cells? Does this look like an acute or chronic osteomyelitis?

Q: Why might it be wise to combine culture and histology analyses?

A: If you have bacteria that’s difficult to culture via traditional methods, it may be a bacteria that doesn’t grow well or easily. If you combine culture with histology, pathologists can look and say, “Your culture was negative but we see these other signs, so we feel this is osteomyelitis.”



Q: Your study examined 35 consecutive patients aged at least 21 years who had moderate or severe infections bone infections in the foot linked with type 1 diabetes (n = 4) or type 2 diabetes (n = 31).

The samples were analyzed via culture, histology, and culture/histology examinations. You also performed genetic sequencing (quantitative polymerase chain reaction targeting 16S rRNA). How does this test fit in to bone biopsies in the clinic?

A: That’s a newer method and not a standard of care treatment for the diabetic foot. This analysis looks at DNA that’s present, bypassing the analysis of difficult-to-grow bacteria.



Q: What did you discover?

A: In this study, histology had the lowest incidence of positively detecting osteomyelitis. (45.7%). The level increases when a culture is taken (68.6% vs. histology; P = .02).
 

Then it goes up when DNA is used because it’s catching everything (82.9%, P = .001 vs. histology and P = .31 vs. culture).

[The study also found that adding histology to culture or to genetic sequencing did not change positive findings.]

Q: Does the study suggest one approach is better than the others?

A: This paper doesn’t provide enough evidence to use one method over another. The main purpose was to raise the concern that diagnosis can change dramatically depending on how the gold standard of bone biopsy is interpreted.



Q: What were the pros and cons of the genetic sequencing approach?

A: When we use this approach, our positive diagnostic rate significantly increases. But there are also downsides. We don’t know whether the bacteria we see is alive or dead. We just know it was there. So are the patients truly positive? That’s a question we can’t answer.
 

Genetic sequencing also doesn’t tell us about susceptibilities to antibiotics.

Q: What is the take-home message here for physicians who may order bone biopsies?

A: The thing to do is request both traditional culture and traditional histology.
 

As far as DNA sequencing, that not something I’d recommend as a standard of care.

Q: Can you comment on cost and insurance coverage for these approaches?

A: As far as I know, genetic sequencing is not covered as it is not standard of care in the diabetic foot and is used mainly for research at this time.
 

Pathology and culture are standard of care when evaluating for osteomyelitis and should be a covered service. However, a patient should call their insurance company first prior to having the procedure done to see whether it is covered.

Q: What’s next for research in this area?

A: From here, the next step is bigger numbers: Increase the study size and look at this again. Also, we may be able to identify susceptibilities by identifying resistance within the DNA.



Dr. Crisologo and two other study authors report no relevant disclosures. One study author reported various disclosures including research support, consulting, and service on speakers' bureaus.
 

Diabetic foot ulcers and infections can lead to osteomyelitis, a potentially devastating infection in the bone.

WILLSIE/Getty Images

How much of a difference can osteomyelitis make to a patient’s prognosis? A 2014 commentary by Benjamin A. Lipsky, MD, a prominent expert in problems associated with diabetic patients’ feet who’s with the University of Washington, Seattle, hints at the potential toll: “Overall, about 20% of patients with a diabetic foot infection (and over 60% of those with severe infections) have underlying osteomyelitis, which dramatically increases the risk of lower-extremity amputation” (Diabetes Care. 2014 Mar;37[3]:593-5).

Diagnosis of osteomyelitis, which relies on a bone biopsy, is clearly important. But there’s a big gap in diagnostic findings depending on whether doctors request culture or histology results, according to a new study released at the 2018 scientific meeting of the American Diabetes Association (Diabetes. 2018 Jul. doi: 10.2337/db18-110-OR).

In an interview, lead author and podiatrist Peter A. Crisologo, DPM, of University of Texas Southwestern Medical Center, Dallas, explained the study findings and offered guidance for requesting bone biopsies in possible cases of osteomyelitis.

Q: What makes diagnosis and treatment of osteomyelitis unique?

A: In the foot, there’s not a lot of soft tissue between the outside world and your bone. If the wounds on the feet go deep enough, they can spread a bacterial infection to the bone. This changes how foot infections are treated.
 

If you have a skin infection, it requires 11-12 days of antibiotics. Things start ramping up once you start getting into the bone. You’re talking potential surgery and 6 weeks of antibiotics through IV treatments. This is why it’s really important that you get your diagnosis right.

A lot of people say “I’m going to do the safe thing” and treat a bone infection with an extended course of antibiotics.

That’s not necessarily safe. If you’re overdiagnosing – for example, you identify bacteria that’s just a contaminant – you could put a patient through 6 weeks of IV treatment along with the risks of a PICC (peripherally inserted central catheter ) line infection, complications from IV placement, and complications from the antibiotic.

Also, acute kidney injury develops in at least a third of the patients who undergo 6 weeks of antibiotics. That’s not to mention the cost of the visits and the labs you have to draw. But we don’t want to underdiagnose either. If osteomyelitis is underdiagnosed and then not treated, the infection can smolder and continue to progress and worsen.

Q: Your study looks at the bone biopsy. How does it fit into care of osteomyelitis in the diabetic foot?

A: A bone biopsy is the standard for diagnosis under the guidelines of the Infectious Diseases Society of America/International Working Group on the Diabetic Foot (Clin Infect Dis. 2012;54[12]:e132-73 ).
 

But beyond that, nobody says anything. Everyone has an operational definition of how a bone biopsy is interpreted, and there’s a need for a consensus on how a bone biopsy can be used to diagnose osteomyelitis.

You’ll get different percentages of your patients diagnosed with osteomyelitis. For example, someone may say the biopsy is only positive if the histology is positive, while another says the histology doesn’t matter if the culture is positive.

Q: Your study looks at histology and culture analyses. What do these reveal?

A: A traditional culture helps you identify the bacteria, as well as guide your treatment when it’s tested against antibiotics.
 

A traditional histology allows the pathologist to look under a microscope for signs of osteomyelitis: Do they see the right inflammatory cells, white cells, lymphocytes, combinations of cells? Does this look like an acute or chronic osteomyelitis?

Q: Why might it be wise to combine culture and histology analyses?

A: If you have bacteria that’s difficult to culture via traditional methods, it may be a bacteria that doesn’t grow well or easily. If you combine culture with histology, pathologists can look and say, “Your culture was negative but we see these other signs, so we feel this is osteomyelitis.”



Q: Your study examined 35 consecutive patients aged at least 21 years who had moderate or severe infections bone infections in the foot linked with type 1 diabetes (n = 4) or type 2 diabetes (n = 31).

The samples were analyzed via culture, histology, and culture/histology examinations. You also performed genetic sequencing (quantitative polymerase chain reaction targeting 16S rRNA). How does this test fit in to bone biopsies in the clinic?

A: That’s a newer method and not a standard of care treatment for the diabetic foot. This analysis looks at DNA that’s present, bypassing the analysis of difficult-to-grow bacteria.



Q: What did you discover?

A: In this study, histology had the lowest incidence of positively detecting osteomyelitis. (45.7%). The level increases when a culture is taken (68.6% vs. histology; P = .02).
 

Then it goes up when DNA is used because it’s catching everything (82.9%, P = .001 vs. histology and P = .31 vs. culture).

[The study also found that adding histology to culture or to genetic sequencing did not change positive findings.]

Q: Does the study suggest one approach is better than the others?

A: This paper doesn’t provide enough evidence to use one method over another. The main purpose was to raise the concern that diagnosis can change dramatically depending on how the gold standard of bone biopsy is interpreted.



Q: What were the pros and cons of the genetic sequencing approach?

A: When we use this approach, our positive diagnostic rate significantly increases. But there are also downsides. We don’t know whether the bacteria we see is alive or dead. We just know it was there. So are the patients truly positive? That’s a question we can’t answer.
 

Genetic sequencing also doesn’t tell us about susceptibilities to antibiotics.

Q: What is the take-home message here for physicians who may order bone biopsies?

A: The thing to do is request both traditional culture and traditional histology.
 

As far as DNA sequencing, that not something I’d recommend as a standard of care.

Q: Can you comment on cost and insurance coverage for these approaches?

A: As far as I know, genetic sequencing is not covered as it is not standard of care in the diabetic foot and is used mainly for research at this time.
 

Pathology and culture are standard of care when evaluating for osteomyelitis and should be a covered service. However, a patient should call their insurance company first prior to having the procedure done to see whether it is covered.

Q: What’s next for research in this area?

A: From here, the next step is bigger numbers: Increase the study size and look at this again. Also, we may be able to identify susceptibilities by identifying resistance within the DNA.



Dr. Crisologo and two other study authors report no relevant disclosures. One study author reported various disclosures including research support, consulting, and service on speakers' bureaus.
 

Risankizumab showed better efficacy than ustekinumab in treating patients with moderate to severe plaque psoriasis but with similar safety, according to results of a pair of head-to-head trials published in the Lancet.

Courtesy National Psoriasis Foundation

The replicate phase 3, randomized, double-blind, placebo- and active comparator–controlled trials, UltIMMa-1 (NCT02684370) and UltIMMa-2 (NCT02684375) altogether randomized 997 patients to risankizumab, ustekinumab, or placebo. The coprimary endpoints were the proportions of patients achieving 90% reduction in Psoriasis Area and Severity Index (PASI 90) at 16 weeks and a static Physician Global Assessment (sPGA) score of 0 or 1, and the 15 ranked secondary endpoints included proportions of those achieving PASI 100 or sPGA 0, both of which demonstrate total clearance of psoriasis, as well as measures of quality of life improvement.

Compared with those receiving either ustekinumab or placebo, a significantly higher proportion of patients receiving risankizumab achieved the coprimary endpoints, and all secondary endpoints were met. In UltIMMA-1, 75.3% of risankizumab patients achieved PASI 90, compared with 4.9% of placebo patients and 42% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab); sPGA of 0 or 1 was achieved by 87.8% of risankizumab patients and only 7.8% of placebo patients and 63% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab). Results were similar in UltIMMA-2: 74.8% of risankizumab patients achieved PASI 90, and 83.7% of them achieved sPGA 0 or 1 (P less than .0001 when comparing them with placebo and ustekinumab). According to results of the secondary endpoints, both studies also showed greater rates of clearance and improvements in quality of life among patients receiving risankizumab than among those receiving either placebo or ustekinumab.

The safety profiles across treatment groups were similar in both studies, with the most common adverse events including upper respiratory tract infection, headache, and diarrhea.

Risankizumab is a humanized IgG1 monoclonal antibody that targets the p19 subunit of only interleukin-23, unlike the studies’ active comparator, ustekinumab, which targets both interleukin-23 and interleukin-12. “Selectively blocking interleukin 23 with a p19 inhibitor appears to be one of the best ways to treat psoriasis,” commented Abigail Cline, MD, and Steven R. Feldman, MD, PhD, both of Wake Forest University, Winston-Salem, N.C., in an accompanying editorial (Lancet. 2018 Aug 7;392:616-71.).

The authors of the study reported relationships with various industry entities, including AbbVie, which sponsored the studies and developed risankizumab, and Boehringer Ingelheim, which collaborated in the studies. The authors of the editorial also disclosed relationships with entities, including AbbVie.

cpalmer@mdedge.com

SOURCE: Gordon KB et al. Lancet. 2018 Aug 7;392:650-61.

Risankizumab showed better efficacy than ustekinumab in treating patients with moderate to severe plaque psoriasis but with similar safety, according to results of a pair of head-to-head trials published in the Lancet.

Courtesy National Psoriasis Foundation

The replicate phase 3, randomized, double-blind, placebo- and active comparator–controlled trials, UltIMMa-1 (NCT02684370) and UltIMMa-2 (NCT02684375) altogether randomized 997 patients to risankizumab, ustekinumab, or placebo. The coprimary endpoints were the proportions of patients achieving 90% reduction in Psoriasis Area and Severity Index (PASI 90) at 16 weeks and a static Physician Global Assessment (sPGA) score of 0 or 1, and the 15 ranked secondary endpoints included proportions of those achieving PASI 100 or sPGA 0, both of which demonstrate total clearance of psoriasis, as well as measures of quality of life improvement.

Compared with those receiving either ustekinumab or placebo, a significantly higher proportion of patients receiving risankizumab achieved the coprimary endpoints, and all secondary endpoints were met. In UltIMMA-1, 75.3% of risankizumab patients achieved PASI 90, compared with 4.9% of placebo patients and 42% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab); sPGA of 0 or 1 was achieved by 87.8% of risankizumab patients and only 7.8% of placebo patients and 63% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab). Results were similar in UltIMMA-2: 74.8% of risankizumab patients achieved PASI 90, and 83.7% of them achieved sPGA 0 or 1 (P less than .0001 when comparing them with placebo and ustekinumab). According to results of the secondary endpoints, both studies also showed greater rates of clearance and improvements in quality of life among patients receiving risankizumab than among those receiving either placebo or ustekinumab.

The safety profiles across treatment groups were similar in both studies, with the most common adverse events including upper respiratory tract infection, headache, and diarrhea.

Risankizumab is a humanized IgG1 monoclonal antibody that targets the p19 subunit of only interleukin-23, unlike the studies’ active comparator, ustekinumab, which targets both interleukin-23 and interleukin-12. “Selectively blocking interleukin 23 with a p19 inhibitor appears to be one of the best ways to treat psoriasis,” commented Abigail Cline, MD, and Steven R. Feldman, MD, PhD, both of Wake Forest University, Winston-Salem, N.C., in an accompanying editorial (Lancet. 2018 Aug 7;392:616-71.).

The authors of the study reported relationships with various industry entities, including AbbVie, which sponsored the studies and developed risankizumab, and Boehringer Ingelheim, which collaborated in the studies. The authors of the editorial also disclosed relationships with entities, including AbbVie.

cpalmer@mdedge.com

SOURCE: Gordon KB et al. Lancet. 2018 Aug 7;392:650-61.

Risankizumab showed better efficacy than ustekinumab in treating patients with moderate to severe plaque psoriasis but with similar safety, according to results of a pair of head-to-head trials published in the Lancet.

Courtesy National Psoriasis Foundation

The replicate phase 3, randomized, double-blind, placebo- and active comparator–controlled trials, UltIMMa-1 (NCT02684370) and UltIMMa-2 (NCT02684375) altogether randomized 997 patients to risankizumab, ustekinumab, or placebo. The coprimary endpoints were the proportions of patients achieving 90% reduction in Psoriasis Area and Severity Index (PASI 90) at 16 weeks and a static Physician Global Assessment (sPGA) score of 0 or 1, and the 15 ranked secondary endpoints included proportions of those achieving PASI 100 or sPGA 0, both of which demonstrate total clearance of psoriasis, as well as measures of quality of life improvement.

Compared with those receiving either ustekinumab or placebo, a significantly higher proportion of patients receiving risankizumab achieved the coprimary endpoints, and all secondary endpoints were met. In UltIMMA-1, 75.3% of risankizumab patients achieved PASI 90, compared with 4.9% of placebo patients and 42% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab); sPGA of 0 or 1 was achieved by 87.8% of risankizumab patients and only 7.8% of placebo patients and 63% of ustekinumab patients (P less than .0001 when comparing it with both placebo and ustekinumab). Results were similar in UltIMMA-2: 74.8% of risankizumab patients achieved PASI 90, and 83.7% of them achieved sPGA 0 or 1 (P less than .0001 when comparing them with placebo and ustekinumab). According to results of the secondary endpoints, both studies also showed greater rates of clearance and improvements in quality of life among patients receiving risankizumab than among those receiving either placebo or ustekinumab.

The safety profiles across treatment groups were similar in both studies, with the most common adverse events including upper respiratory tract infection, headache, and diarrhea.

Risankizumab is a humanized IgG1 monoclonal antibody that targets the p19 subunit of only interleukin-23, unlike the studies’ active comparator, ustekinumab, which targets both interleukin-23 and interleukin-12. “Selectively blocking interleukin 23 with a p19 inhibitor appears to be one of the best ways to treat psoriasis,” commented Abigail Cline, MD, and Steven R. Feldman, MD, PhD, both of Wake Forest University, Winston-Salem, N.C., in an accompanying editorial (Lancet. 2018 Aug 7;392:616-71.).

The authors of the study reported relationships with various industry entities, including AbbVie, which sponsored the studies and developed risankizumab, and Boehringer Ingelheim, which collaborated in the studies. The authors of the editorial also disclosed relationships with entities, including AbbVie.

cpalmer@mdedge.com

SOURCE: Gordon KB et al. Lancet. 2018 Aug 7;392:650-61.

CHICAGO – Oral itraconazole shows potential for treatment of locally advanced or metastatic basal cell carcinoma (BCC) as well as Gorlin syndrome, Justin J. Leitenberger, MD, declared at the annual meeting of the American College of Mohs Surgery.

Bruce Jancin/MDedge News

The oral antifungal inhibits the hedgehog signaling pathway, a key driver of BCC. And while itraconazole is not as potent an inhibitor of hedgehog pathway expression as, say vismodegib (Erivedge), the antifungal acts at a separate site on the pathway, making it an attractive candidate for combination therapy, explained Dr. Leitenberger of Oregon Health & Science University, Portland.

Dermatologists at Stanford University have led the way in exploring oral itraconazole as a treatment for BCC. Among a series of 29 patients with one or more large but nonadvanced BCCs, 19 were treated using oral itraconazole at 200 mg b.i.d. for 1 month or 100 mg b.i.d. for an average of 2.3 months. Hedgehog pathway expression was reduced by 65% in the itraconazole-treated patients, as compared with the 90% reduction which is achieved with vismodegib.

Of more direct clinical relevance, however, itraconazole also reduced tumor area by 24%. Four of eight patients with 57 tumors achieved a partial response, and the other four had stable disease (J Clin Oncol. 2014 Mar 10;32[8]:745-51).

The Stanford group has also shown that combination therapy with oral itraconazole and intravenous arsenic trioxide reduces hedgehog pathway expression by 75%, up by an absolute 10% from itraconazole alone. The two agents inhibit the pathway at different sites.

Five patients with metastatic BCC who relapsed after treatment with vismodegib received intravenous arsenic trioxide for the first 5 days of every month, followed by oral itraconazole at 200 mg b.i.d. on days 6-28. Three patients completed three such cycles, while two discontinued early because of progressive disease or adverse events including a grade 3 infection and grade 2 transaminitis. All three patients who completed three treatment cycles achieved stable disease. The Stanford investigators speculated that concurrent continuous dosing might be required to obtain tumor shrinkage (JAMA Dermatol. 2016 Apr;152[4]:452-6).

Lots more work remains to be done in order to optimize combination therapy utilizing oral itraconazole for advanced BCC. Different dosing regimens and combinations of hedgehog pathway inhibitors need to be studied. Another important question is how effective itraconazole-based combinations will be in vismodegib-naive as compared with vismodegib-resistant patients, Dr. Leitenberger observed.

He reported having no financial conflicts regarding his presentation.

bjancin@mdedge.com

CHICAGO – Oral itraconazole shows potential for treatment of locally advanced or metastatic basal cell carcinoma (BCC) as well as Gorlin syndrome, Justin J. Leitenberger, MD, declared at the annual meeting of the American College of Mohs Surgery.

Bruce Jancin/MDedge News

The oral antifungal inhibits the hedgehog signaling pathway, a key driver of BCC. And while itraconazole is not as potent an inhibitor of hedgehog pathway expression as, say vismodegib (Erivedge), the antifungal acts at a separate site on the pathway, making it an attractive candidate for combination therapy, explained Dr. Leitenberger of Oregon Health & Science University, Portland.

Dermatologists at Stanford University have led the way in exploring oral itraconazole as a treatment for BCC. Among a series of 29 patients with one or more large but nonadvanced BCCs, 19 were treated using oral itraconazole at 200 mg b.i.d. for 1 month or 100 mg b.i.d. for an average of 2.3 months. Hedgehog pathway expression was reduced by 65% in the itraconazole-treated patients, as compared with the 90% reduction which is achieved with vismodegib.

Of more direct clinical relevance, however, itraconazole also reduced tumor area by 24%. Four of eight patients with 57 tumors achieved a partial response, and the other four had stable disease (J Clin Oncol. 2014 Mar 10;32[8]:745-51).

The Stanford group has also shown that combination therapy with oral itraconazole and intravenous arsenic trioxide reduces hedgehog pathway expression by 75%, up by an absolute 10% from itraconazole alone. The two agents inhibit the pathway at different sites.

Five patients with metastatic BCC who relapsed after treatment with vismodegib received intravenous arsenic trioxide for the first 5 days of every month, followed by oral itraconazole at 200 mg b.i.d. on days 6-28. Three patients completed three such cycles, while two discontinued early because of progressive disease or adverse events including a grade 3 infection and grade 2 transaminitis. All three patients who completed three treatment cycles achieved stable disease. The Stanford investigators speculated that concurrent continuous dosing might be required to obtain tumor shrinkage (JAMA Dermatol. 2016 Apr;152[4]:452-6).

Lots more work remains to be done in order to optimize combination therapy utilizing oral itraconazole for advanced BCC. Different dosing regimens and combinations of hedgehog pathway inhibitors need to be studied. Another important question is how effective itraconazole-based combinations will be in vismodegib-naive as compared with vismodegib-resistant patients, Dr. Leitenberger observed.

He reported having no financial conflicts regarding his presentation.

bjancin@mdedge.com

CHICAGO – Oral itraconazole shows potential for treatment of locally advanced or metastatic basal cell carcinoma (BCC) as well as Gorlin syndrome, Justin J. Leitenberger, MD, declared at the annual meeting of the American College of Mohs Surgery.

Bruce Jancin/MDedge News

The oral antifungal inhibits the hedgehog signaling pathway, a key driver of BCC. And while itraconazole is not as potent an inhibitor of hedgehog pathway expression as, say vismodegib (Erivedge), the antifungal acts at a separate site on the pathway, making it an attractive candidate for combination therapy, explained Dr. Leitenberger of Oregon Health & Science University, Portland.

Dermatologists at Stanford University have led the way in exploring oral itraconazole as a treatment for BCC. Among a series of 29 patients with one or more large but nonadvanced BCCs, 19 were treated using oral itraconazole at 200 mg b.i.d. for 1 month or 100 mg b.i.d. for an average of 2.3 months. Hedgehog pathway expression was reduced by 65% in the itraconazole-treated patients, as compared with the 90% reduction which is achieved with vismodegib.

Of more direct clinical relevance, however, itraconazole also reduced tumor area by 24%. Four of eight patients with 57 tumors achieved a partial response, and the other four had stable disease (J Clin Oncol. 2014 Mar 10;32[8]:745-51).

The Stanford group has also shown that combination therapy with oral itraconazole and intravenous arsenic trioxide reduces hedgehog pathway expression by 75%, up by an absolute 10% from itraconazole alone. The two agents inhibit the pathway at different sites.

Five patients with metastatic BCC who relapsed after treatment with vismodegib received intravenous arsenic trioxide for the first 5 days of every month, followed by oral itraconazole at 200 mg b.i.d. on days 6-28. Three patients completed three such cycles, while two discontinued early because of progressive disease or adverse events including a grade 3 infection and grade 2 transaminitis. All three patients who completed three treatment cycles achieved stable disease. The Stanford investigators speculated that concurrent continuous dosing might be required to obtain tumor shrinkage (JAMA Dermatol. 2016 Apr;152[4]:452-6).

Lots more work remains to be done in order to optimize combination therapy utilizing oral itraconazole for advanced BCC. Different dosing regimens and combinations of hedgehog pathway inhibitors need to be studied. Another important question is how effective itraconazole-based combinations will be in vismodegib-naive as compared with vismodegib-resistant patients, Dr. Leitenberger observed.

He reported having no financial conflicts regarding his presentation.

bjancin@mdedge.com

The itchy patch of skin on this 60-year-old man’s forearm, beneath his watch, has troubled him intermittently for a year. It is unresponsive to topical medications, including tolnaftate cream and 1% hydrocortisone cream; the latter seemed to improve the condition initially, but with time, the patch grew larger and itchier.

The patient’s primary care provider believed the rash might be precancerous and prescribed 5-fluorouracil cream, which showed no benefit. The patient was then referred to a dermatologist, who performed a KOH examination. No fungal elements were found.

At that point, the patient decided to simply ignore the problem. That resolve ended when the itchiness increased—leading to his presentation today. He is in decent health but has had a kidney transplant and is taking the standard immunosuppressant (anti-rejection) medications.

EXAMINATION
A faintly pink, scaly rash is located on the patient’s forearm. It is unimpressive in appearance but very bothersome to the patient.

Despite the patient’s history, fungal origin remains a possibility, as does psoriasis. A punch biopsy is performed.

What is the diagnosis?

Normally, dermatophytes (the organisms that cause superficial fungal infections) are incapable of invading deeper tissues, making KOH exam a simple diagnostic method. But with immune suppression, the infection is able to invade deeper structures, making it more difficult to diagnose and treat. In this patient’s case, the use of steroid creams under occlusion (ie, the watch) had suppressed the body’s immune response to the infection.

The terminology used to describe this phenomenon varies according to the severity of infection. Tinea incognito might be used to describe this patient’s case, in which the steroid rendered the condition almost impossible to diagnose visually. With continued use of stronger topical steroids, the degree of inflammation might have been worse, involving deeper, larger nodules instead of faint pink scaling. In such cases, the term Majocchi fungal granuloma is used.

This patient moved his watch to the other arm temporarily and was successfully treated with twice-daily application of topical econazole cream and a two-week course of oral terbinafine (250 mg/d).

TAKE-HOME LEARNING POINTS

• Immunosuppression can make fungal infections more difficult to diagnose and treat.
• Dermatophytes don’t normally invade deeper structures and can usually be detected with a KOH exam of surface skin cells.
• If the patient is immunocompromised, a fungal diagnosis is best confirmed with a punch biopsy, and treatment achieved with a combination of oral and topical antifungal products.
• Mild cases of this kind are termed tinea incognito, while more severe cases are called Majocchi fungal granuloma.

The itchy patch of skin on this 60-year-old man’s forearm, beneath his watch, has troubled him intermittently for a year. It is unresponsive to topical medications, including tolnaftate cream and 1% hydrocortisone cream; the latter seemed to improve the condition initially, but with time, the patch grew larger and itchier.

The patient’s primary care provider believed the rash might be precancerous and prescribed 5-fluorouracil cream, which showed no benefit. The patient was then referred to a dermatologist, who performed a KOH examination. No fungal elements were found.

At that point, the patient decided to simply ignore the problem. That resolve ended when the itchiness increased—leading to his presentation today. He is in decent health but has had a kidney transplant and is taking the standard immunosuppressant (anti-rejection) medications.

EXAMINATION
A faintly pink, scaly rash is located on the patient’s forearm. It is unimpressive in appearance but very bothersome to the patient.

Despite the patient’s history, fungal origin remains a possibility, as does psoriasis. A punch biopsy is performed.

What is the diagnosis?

Normally, dermatophytes (the organisms that cause superficial fungal infections) are incapable of invading deeper tissues, making KOH exam a simple diagnostic method. But with immune suppression, the infection is able to invade deeper structures, making it more difficult to diagnose and treat. In this patient’s case, the use of steroid creams under occlusion (ie, the watch) had suppressed the body’s immune response to the infection.

The terminology used to describe this phenomenon varies according to the severity of infection. Tinea incognito might be used to describe this patient’s case, in which the steroid rendered the condition almost impossible to diagnose visually. With continued use of stronger topical steroids, the degree of inflammation might have been worse, involving deeper, larger nodules instead of faint pink scaling. In such cases, the term Majocchi fungal granuloma is used.

This patient moved his watch to the other arm temporarily and was successfully treated with twice-daily application of topical econazole cream and a two-week course of oral terbinafine (250 mg/d).

TAKE-HOME LEARNING POINTS

• Immunosuppression can make fungal infections more difficult to diagnose and treat.
• Dermatophytes don’t normally invade deeper structures and can usually be detected with a KOH exam of surface skin cells.
• If the patient is immunocompromised, a fungal diagnosis is best confirmed with a punch biopsy, and treatment achieved with a combination of oral and topical antifungal products.
• Mild cases of this kind are termed tinea incognito, while more severe cases are called Majocchi fungal granuloma.

The itchy patch of skin on this 60-year-old man’s forearm, beneath his watch, has troubled him intermittently for a year. It is unresponsive to topical medications, including tolnaftate cream and 1% hydrocortisone cream; the latter seemed to improve the condition initially, but with time, the patch grew larger and itchier.

The patient’s primary care provider believed the rash might be precancerous and prescribed 5-fluorouracil cream, which showed no benefit. The patient was then referred to a dermatologist, who performed a KOH examination. No fungal elements were found.

At that point, the patient decided to simply ignore the problem. That resolve ended when the itchiness increased—leading to his presentation today. He is in decent health but has had a kidney transplant and is taking the standard immunosuppressant (anti-rejection) medications.

EXAMINATION
A faintly pink, scaly rash is located on the patient’s forearm. It is unimpressive in appearance but very bothersome to the patient.

Despite the patient’s history, fungal origin remains a possibility, as does psoriasis. A punch biopsy is performed.

What is the diagnosis?

Normally, dermatophytes (the organisms that cause superficial fungal infections) are incapable of invading deeper tissues, making KOH exam a simple diagnostic method. But with immune suppression, the infection is able to invade deeper structures, making it more difficult to diagnose and treat. In this patient’s case, the use of steroid creams under occlusion (ie, the watch) had suppressed the body’s immune response to the infection.

The terminology used to describe this phenomenon varies according to the severity of infection. Tinea incognito might be used to describe this patient’s case, in which the steroid rendered the condition almost impossible to diagnose visually. With continued use of stronger topical steroids, the degree of inflammation might have been worse, involving deeper, larger nodules instead of faint pink scaling. In such cases, the term Majocchi fungal granuloma is used.

This patient moved his watch to the other arm temporarily and was successfully treated with twice-daily application of topical econazole cream and a two-week course of oral terbinafine (250 mg/d).

TAKE-HOME LEARNING POINTS

• Immunosuppression can make fungal infections more difficult to diagnose and treat.
• Dermatophytes don’t normally invade deeper structures and can usually be detected with a KOH exam of surface skin cells.
• If the patient is immunocompromised, a fungal diagnosis is best confirmed with a punch biopsy, and treatment achieved with a combination of oral and topical antifungal products.
• Mild cases of this kind are termed tinea incognito, while more severe cases are called Majocchi fungal granuloma.

The FP suspected skin cancer, but was not sure if it was a basal cell carcinoma or a squamous cell carcinoma (SCC).

The growth was somewhat pearly with telangiectasias, but there was also a prominent area of keratin on the posterior aspect of the lesion. After injecting local anesthesia with 1% lidocaine and epinephrine, the physician performed a shave biopsy on one edge of the tumor. He was careful to avoid cutting the cartilage and decided that the diagnosis would be obtained without trying to remove the whole tumor. The bleeding did not stop with chemical hemostasis alone, so electrosurgery was used. The biopsy result showed an SCC of the keratoacanthoma type.

The patient was referred for Mohs surgery because it was important to get clear margins, while attempting to preserve the ear anatomy. Also, SCC of the ear has a higher risk for metastasis, so a thorough exam of the head and neck for lymphadenopathy was performed. Fortunately, this SCC was well-differentiated and no metastases were clinically detected.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratocanthoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:977-980.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP suspected skin cancer, but was not sure if it was a basal cell carcinoma or a squamous cell carcinoma (SCC).

The growth was somewhat pearly with telangiectasias, but there was also a prominent area of keratin on the posterior aspect of the lesion. After injecting local anesthesia with 1% lidocaine and epinephrine, the physician performed a shave biopsy on one edge of the tumor. He was careful to avoid cutting the cartilage and decided that the diagnosis would be obtained without trying to remove the whole tumor. The bleeding did not stop with chemical hemostasis alone, so electrosurgery was used. The biopsy result showed an SCC of the keratoacanthoma type.

The patient was referred for Mohs surgery because it was important to get clear margins, while attempting to preserve the ear anatomy. Also, SCC of the ear has a higher risk for metastasis, so a thorough exam of the head and neck for lymphadenopathy was performed. Fortunately, this SCC was well-differentiated and no metastases were clinically detected.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratocanthoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:977-980.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

The FP suspected skin cancer, but was not sure if it was a basal cell carcinoma or a squamous cell carcinoma (SCC).

The growth was somewhat pearly with telangiectasias, but there was also a prominent area of keratin on the posterior aspect of the lesion. After injecting local anesthesia with 1% lidocaine and epinephrine, the physician performed a shave biopsy on one edge of the tumor. He was careful to avoid cutting the cartilage and decided that the diagnosis would be obtained without trying to remove the whole tumor. The bleeding did not stop with chemical hemostasis alone, so electrosurgery was used. The biopsy result showed an SCC of the keratoacanthoma type.

The patient was referred for Mohs surgery because it was important to get clear margins, while attempting to preserve the ear anatomy. Also, SCC of the ear has a higher risk for metastasis, so a thorough exam of the head and neck for lymphadenopathy was performed. Fortunately, this SCC was well-differentiated and no metastases were clinically detected.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratocanthoma. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:977-980.

To learn more about the Color Atlas of Family Medicine, see: www.amazon.com/Color-Family-Medicine-Richard-Usatine/dp/0071769641/.

You can now get the second edition of the Color Atlas of Family Medicine as an app by clicking on this link: usatinemedia.com.

LAKE TAHOE, CALIF. – Evaluation of an infant with a vesiculopustular lesion entails a pragmatic approach, with three assessment steps, according to pediatric dermatologist Lawrence A. Schachner, MD.

At the annual meeting of the Society for Pediatric Dermatology, Dr. Schachner noted that the differential diagnosis of noninfectious, usually benign neonatal vesiculopustular lesions includes acropustulosis of infancy; eosinophilic pustular folliculitis; erythema toxicum neonatorum; miliaria crystallina, rubra, or profunda; transient neonatal pustular melanosis; and neonatal sucking blisters. Noninfectious lesions that can be potentially serious include acrodermatitis enteropathica, bullous pemphigoid, epidermolysis bullosa, epidermolytic hyperkeratosis, incontinentia pigmenti, Langerhans cell histiocytosis, pemphigus vulgaris, pustular psoriasis, and urticarial pigmentosa.

Step 1 for evaluating vesiculopustular lesions involves drawing out the fluid for bacterial cultures and sensitivity, Gram stains, viral culture and/or serology, said Dr. Schachner, who directs the division of pediatric dermatology at the University of Miami.

Step 2 involves snipping off the lesion’s roof for a potassium hydroxide test to send for dermatopathology or frozen pathology.

Step 3 involves scraping the lesion’s base for viral cytology and cell identification. “If we can see a predominant cell type, that’s where the action is,” said Dr. Schachner, professor of pediatrics at the university. If cytology reveals polymorphic neutrophils, differential diagnoses include transient neonatal pustular melanosis, infantile acropustulosis, bullous impetigo, and pustular psoriasis. If cytology reveals eosinophils, differential diagnoses include eosinophilic pustular folliculitis of infancy, erythema toxicum neonatorum, incontinentia pigmenti, bullous pemphigoid, drug reactions, and arthropod bites. The presence of lymphocytes on cytology, meanwhile, may suggest a differential diagnosis miliaria or acrodermatitis enteropathica.

“When in doubt about the diagnosis, biopsy,” Dr. Schachner said. “This, to me, is a pragmatic approach.”

Dr. Schachner disclosed that he is an investigator for Astellas, Ferndale Labs, Novartis, Organogenesis, Stiefel Laboratories, Berg Pharma, Medimetrics, and Lilly. He is a consultant to Beiersdorf, Lexington, TopMD, Cutanea, Hoth Therapeutics, and Mustela.

dbrunk@mdedge.com

LAKE TAHOE, CALIF. – Evaluation of an infant with a vesiculopustular lesion entails a pragmatic approach, with three assessment steps, according to pediatric dermatologist Lawrence A. Schachner, MD.

At the annual meeting of the Society for Pediatric Dermatology, Dr. Schachner noted that the differential diagnosis of noninfectious, usually benign neonatal vesiculopustular lesions includes acropustulosis of infancy; eosinophilic pustular folliculitis; erythema toxicum neonatorum; miliaria crystallina, rubra, or profunda; transient neonatal pustular melanosis; and neonatal sucking blisters. Noninfectious lesions that can be potentially serious include acrodermatitis enteropathica, bullous pemphigoid, epidermolysis bullosa, epidermolytic hyperkeratosis, incontinentia pigmenti, Langerhans cell histiocytosis, pemphigus vulgaris, pustular psoriasis, and urticarial pigmentosa.

Step 1 for evaluating vesiculopustular lesions involves drawing out the fluid for bacterial cultures and sensitivity, Gram stains, viral culture and/or serology, said Dr. Schachner, who directs the division of pediatric dermatology at the University of Miami.

Step 2 involves snipping off the lesion’s roof for a potassium hydroxide test to send for dermatopathology or frozen pathology.

Step 3 involves scraping the lesion’s base for viral cytology and cell identification. “If we can see a predominant cell type, that’s where the action is,” said Dr. Schachner, professor of pediatrics at the university. If cytology reveals polymorphic neutrophils, differential diagnoses include transient neonatal pustular melanosis, infantile acropustulosis, bullous impetigo, and pustular psoriasis. If cytology reveals eosinophils, differential diagnoses include eosinophilic pustular folliculitis of infancy, erythema toxicum neonatorum, incontinentia pigmenti, bullous pemphigoid, drug reactions, and arthropod bites. The presence of lymphocytes on cytology, meanwhile, may suggest a differential diagnosis miliaria or acrodermatitis enteropathica.

“When in doubt about the diagnosis, biopsy,” Dr. Schachner said. “This, to me, is a pragmatic approach.”

Dr. Schachner disclosed that he is an investigator for Astellas, Ferndale Labs, Novartis, Organogenesis, Stiefel Laboratories, Berg Pharma, Medimetrics, and Lilly. He is a consultant to Beiersdorf, Lexington, TopMD, Cutanea, Hoth Therapeutics, and Mustela.

dbrunk@mdedge.com

LAKE TAHOE, CALIF. – Evaluation of an infant with a vesiculopustular lesion entails a pragmatic approach, with three assessment steps, according to pediatric dermatologist Lawrence A. Schachner, MD.

At the annual meeting of the Society for Pediatric Dermatology, Dr. Schachner noted that the differential diagnosis of noninfectious, usually benign neonatal vesiculopustular lesions includes acropustulosis of infancy; eosinophilic pustular folliculitis; erythema toxicum neonatorum; miliaria crystallina, rubra, or profunda; transient neonatal pustular melanosis; and neonatal sucking blisters. Noninfectious lesions that can be potentially serious include acrodermatitis enteropathica, bullous pemphigoid, epidermolysis bullosa, epidermolytic hyperkeratosis, incontinentia pigmenti, Langerhans cell histiocytosis, pemphigus vulgaris, pustular psoriasis, and urticarial pigmentosa.

Step 1 for evaluating vesiculopustular lesions involves drawing out the fluid for bacterial cultures and sensitivity, Gram stains, viral culture and/or serology, said Dr. Schachner, who directs the division of pediatric dermatology at the University of Miami.

Step 2 involves snipping off the lesion’s roof for a potassium hydroxide test to send for dermatopathology or frozen pathology.

Step 3 involves scraping the lesion’s base for viral cytology and cell identification. “If we can see a predominant cell type, that’s where the action is,” said Dr. Schachner, professor of pediatrics at the university. If cytology reveals polymorphic neutrophils, differential diagnoses include transient neonatal pustular melanosis, infantile acropustulosis, bullous impetigo, and pustular psoriasis. If cytology reveals eosinophils, differential diagnoses include eosinophilic pustular folliculitis of infancy, erythema toxicum neonatorum, incontinentia pigmenti, bullous pemphigoid, drug reactions, and arthropod bites. The presence of lymphocytes on cytology, meanwhile, may suggest a differential diagnosis miliaria or acrodermatitis enteropathica.

“When in doubt about the diagnosis, biopsy,” Dr. Schachner said. “This, to me, is a pragmatic approach.”

Dr. Schachner disclosed that he is an investigator for Astellas, Ferndale Labs, Novartis, Organogenesis, Stiefel Laboratories, Berg Pharma, Medimetrics, and Lilly. He is a consultant to Beiersdorf, Lexington, TopMD, Cutanea, Hoth Therapeutics, and Mustela.

dbrunk@mdedge.com