Dermatology

Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

Alopecia areata is associated with greater frequency of mental health disorders, according to a new analysis of U.S. hospitalizations.

Specifically, the analysis found, alopecia areata patients are at risk for any mental health disorder, anxiety disorders, attention-deficit/hyperactivity disorder, dementia, mood disorders, personality disorders, and suicide or intentionally self-inflicted injury. The report was published in the Journal of the American Academy of Dermatology.

The researchers worked with 87,053,155 adult and child records from the 2002-2012 National Inpatient Sample, which represents 20% of U.S. hospitalizations. They identified inpatients with alopecia areata based on the ICD-9-CM code and compared them to all patients without the condition.

Overall, 5,605 patients had alopecia areata, which was the secondary diagnosis more than 99% of the time. Compared with inpatients without alopecia areata, those with the disorder were more likely to be younger (42.2 vs. 47.9 years; P less than .0001), female (61.7% vs. 58.6%; P = .0297), and uninsured (8.1% vs. 5.5%; P less than .0001). In addition, inpatients with alopecia areata had a greater frequency of mental health disorders (32.8% vs. 20.0%; P less than .0001) and were more likely to have a primary mental health diagnosis (5.5% vs. 2.2%; P less than .0001), reported Vivek Singam of Northwestern University, Chicago, and his associates.

Among 15 mental health or classes of disorders examined, alopecia areata patients were at greater risk in 13 of them. The only exceptions were delirium/dementia/amnestic/cognitive disorders and disorders diagnosed in infancy, childhood, or adolescence.

Alopecia areata patients with a mental health disorder had a mean hospital stay of 6.0 days (95% confidence interval, 5.4.-6.6) and hospitalization cost of $11,907 (95% CI, $10,312-$13,503).

Previous studies had shown similar relationships. However, previous studies showed lower risk of alopecia areata and schizophrenia and no increased risk of ADHD, compared with the current study’s findings. The authors could offer no explanation for those differences.

The strengths of the current analysis include its use of a large-scale, nationally representative cohort and its large sample size, as well its inclusion of a broad range of mental health disorders. Because of its cross-sectional design, the study could not establish the temporal relationship between alopecia areata and mental health disorders.

It is unclear whether psychosocial stress might cause or exacerbate alopecia areata, or whether alopecia areata can lead to or worsen mental health disorders.

The researchers called for additional studies to understand this relationship and potential mechanisms.

The Agency for Healthcare Research and Quality and the Dermatology Foundation funded the study. The researchers declared having no conflicts of interest.

SOURCE: Singam V et al. J Am Acad Dermatol. 2018 Aug 6. doi: 10.1016/j.jaad.2018.07.044.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

The treatment choice is oral terbinafine for tinea capitis with kerion, a scalp dermatophyte infection with a concurrent inflammatory process. Tinea capitis is a very common infection with the peak occurrence at age 3-7 years. Tinea capitis is caused by a variety of dermatophyte species, most commonly by Trichophyton tonsurans or Microsporum canis. T. tonsurans is an endothrix infection, invading the hair shaft and superficial hair while M. canis is an ectothrix infection. T. tonsurans has a person to person transmission; in contrast, M. canis is a zoonotic infection most commonly acquired from infected pets.¹ The epidemiology of tinea capitis is affected by multiple factors, including immigration patterns. For example, in Montreal, a study showed a sixfold increase of African dermatophyte species, M. audouinii and T. soudanense.² Similarly, global variation has increased prevalence of T. violaceum, more commonly found in Europe and Africa, which has been seen in immigrant populations in the United States.¹ Kerion is thought to be a hypersensitivity reaction to dermatophytes. Often, misdiagnosis of kerion can result in unnecessary antibiotic prescription and delays in initiation of antifungal therapy.^3,4

Tinea capitis can present with focal, “patchy,” well-demarcated hair loss and overlying scale, broken-off hairs at the scalp, and often with pustules. It may be associated with occipital or posterior cervical lymphadenopathy. Tinea can be complicated by kerion development, which presents as a painful boggy scalp mass with or without purulent drainage. Kerions can have associated fever. It is important to differentiate tinea capitis with kerion from processes requiring a different treatment course.^3,5 Bacterial folliculitis may have erythema and pustules but only rarely causes hair loss. Similarly, alopecia areata can present with focal alopecia but lacks the scalp inflammation and pustules. Scalp psoriasis is quite scaly, but is more thickened, and usually does not have pustules, nor would purulent drainage be evident. There is a broader differential for other inflammatory focal alopecias including discoid lupus, lichen planopilaris, and dissecting cellulitis of the scalp, which can have similar pus-filled lumps, and cause permanent hair loss, but may be differentiated by associated conditions such as acne conglobata, hidradenitis suppurativa, and pilonidal sinus.

While some clinicians advocate clinical diagnosis of tinea capitis, we advocate confirmation of infection by fungal culture, which can identify the causative organism and influence therapy selection.¹ The presence of a fungal infection can be confirmed on potassium hydroxide wet mount prep if hyphae and small spores are seen.^6,7 Wood lamp examination will fluoresce if there are ectothrix species, however a negative fluorescence does not differentiate between an endothrix species or lack of infection.

It is important that tinea capitis with kerion is treated with systemic antifungal treatments to allow resolution of the infection, recovery of hair growth, and to prevent or minimize scarring. Systemic antifungal options include terbinafine, griseofulvin, and azoles. Terbinafine is becoming the treatment of choice given shorter duration of treatment with similar efficacy.¹T. tonsurans also is thought to respond better to terbinafine than to griseofulvin.⁸ Griseofulvin is the historical treatment of choice because of its history of clinical safety and no need for laboratory testing. It is important to note that higher doses of griseofulvin (20-25 mg/kg) are recommended, as older lower dose regimens have high rates of failure. Griseofulvin may be more effective for treatment of Microsporum spp than is terbinafine.⁸ Fluconazole is the only oral antifungal agent that is approved for patients younger than 2 years of age, however it has lower cure rates, compared with terbinafine and griseofulvin.¹ Tinea capitis with kerion does not generally require antibiotics unless there is superimposed bacterial infection. Kerion also do not require incision or drainage, which may increase scarring and complicate the clinical course.

Management of tinea capitis should include evaluation of any other household members for coinfection. Depending on the dermatophyte involved there can be risk of person-to-person transmission.⁵ Families should be educated about fomite transmission via shared combs or hats. Additionally, if a zoophilic dermatophyte is suspected, pets also should be appropriately examined and treated. Topical antifungals are insufficient to eradicate tinea capitis but can be used as adjunctive therapy. Kerion can be treated with oral prednisone in addition to oral antifungals if the lesions are very painful, however there is limited data on this treatment option.⁹

Ms. Kaushik is a research fellow and Dr. Eichenfield is professor of dermatology and pediatrics in the division of pediatric and adolescent dermatology at Rady Children’s Hospital and the University of California, both in San Diego. They have no conflicts of interest or relevant financial disclosures.

References

1. “Red Book: Report of the Committee on Infectious Diseases,” 31st Edition, (Elk Grove Village, Ill.: American Academy of Pediatrics, 2018, p. 1264).

2. Pediatr Dermatol. 2018 May;35(3):323-8

3. Arch Dis Child. 2016 May;101(5):503.

4. IDCases. 2018 Jun 28;14:e00418.

5. Int J Dermatol. 2018 Jan;57(1):3-9.

6. Pediatr Rev. 2007 May;28(5):164-74.

7. Clin Cosmet Investig Dermatol. 2010;3:89-98.

8. Cochrane Database Syst Rev. 2016 May 12;(5):CD004685.

9. Med Mycol. 1999 Apr;37(2):97-9.

At birth, this child had a lesion on his shoulder that now—a year later—has doubled in size. His parents report no systemic symptoms or medication use for their son. They say that the child exhibits no distress; he does not attempt to scratch at the affected patch of skin. However, they observe that if the lesion is touched, it swells and then (within minutes) returns to normal.

There is no family history of similar problems. However, both the patient and his mother are highly atopic.

EXAMINATION
The lesion—a low, orange, oval plaque—measures about 3.5 x 2 cm. Barely palpable, it urticates when stroked with a fingernail edge but does not appear to cause any discomfort.

No other lesions of note are found. The child appears quite healthy and is in no distress.

What is the diagnosis?

When stroked, mast cell lesions degranulate portions of the cell, releasing histamine precursors and leukotrienes (eg, IL 1 and IL 31). In most cases, stroking merely leads to short-lived urtication. But if the problem is more widespread (eg, urticaria pigmentosa) and the lesions are sufficiently traumatized, the release of these substances can lead to problems such as hypotension, malaise, fever, and abdominal pain.

Fortunately, this is rare, as is systemic mastocytosis—a condition in which mast cells infiltrate internal organs and bone marrow, interrupting normal function and, in the extreme, leading to mast cell leukemia. Our patient is not at risk for these complications; his lesion should resolve completely by age 3.

The differential for this patient’s lesion includes congenital nevus, lichen aureus, and café au lait spot.

TAKE-HOME LEARNING POINTS

• Cutaneous mastocytosis manifests as a reddish orange maculopapular patch, which urticates upon forceful stroking.
• Stroking the lesion degranulates the mast cells comprising it, leading to the release of histamine precursors.
• Mast cells can infiltrate internal organs and bone marrow, leading, in the extreme, to mast cell leukemia.
• Urticaria pigmentosa is a variation of mastocytosis in which hundreds of such lesions develop all over the body.

At birth, this child had a lesion on his shoulder that now—a year later—has doubled in size. His parents report no systemic symptoms or medication use for their son. They say that the child exhibits no distress; he does not attempt to scratch at the affected patch of skin. However, they observe that if the lesion is touched, it swells and then (within minutes) returns to normal.

There is no family history of similar problems. However, both the patient and his mother are highly atopic.

EXAMINATION
The lesion—a low, orange, oval plaque—measures about 3.5 x 2 cm. Barely palpable, it urticates when stroked with a fingernail edge but does not appear to cause any discomfort.

No other lesions of note are found. The child appears quite healthy and is in no distress.

What is the diagnosis?

When stroked, mast cell lesions degranulate portions of the cell, releasing histamine precursors and leukotrienes (eg, IL 1 and IL 31). In most cases, stroking merely leads to short-lived urtication. But if the problem is more widespread (eg, urticaria pigmentosa) and the lesions are sufficiently traumatized, the release of these substances can lead to problems such as hypotension, malaise, fever, and abdominal pain.

Fortunately, this is rare, as is systemic mastocytosis—a condition in which mast cells infiltrate internal organs and bone marrow, interrupting normal function and, in the extreme, leading to mast cell leukemia. Our patient is not at risk for these complications; his lesion should resolve completely by age 3.

The differential for this patient’s lesion includes congenital nevus, lichen aureus, and café au lait spot.

TAKE-HOME LEARNING POINTS

• Cutaneous mastocytosis manifests as a reddish orange maculopapular patch, which urticates upon forceful stroking.
• Stroking the lesion degranulates the mast cells comprising it, leading to the release of histamine precursors.
• Mast cells can infiltrate internal organs and bone marrow, leading, in the extreme, to mast cell leukemia.
• Urticaria pigmentosa is a variation of mastocytosis in which hundreds of such lesions develop all over the body.

At birth, this child had a lesion on his shoulder that now—a year later—has doubled in size. His parents report no systemic symptoms or medication use for their son. They say that the child exhibits no distress; he does not attempt to scratch at the affected patch of skin. However, they observe that if the lesion is touched, it swells and then (within minutes) returns to normal.

There is no family history of similar problems. However, both the patient and his mother are highly atopic.

EXAMINATION
The lesion—a low, orange, oval plaque—measures about 3.5 x 2 cm. Barely palpable, it urticates when stroked with a fingernail edge but does not appear to cause any discomfort.

No other lesions of note are found. The child appears quite healthy and is in no distress.

What is the diagnosis?

When stroked, mast cell lesions degranulate portions of the cell, releasing histamine precursors and leukotrienes (eg, IL 1 and IL 31). In most cases, stroking merely leads to short-lived urtication. But if the problem is more widespread (eg, urticaria pigmentosa) and the lesions are sufficiently traumatized, the release of these substances can lead to problems such as hypotension, malaise, fever, and abdominal pain.

Fortunately, this is rare, as is systemic mastocytosis—a condition in which mast cells infiltrate internal organs and bone marrow, interrupting normal function and, in the extreme, leading to mast cell leukemia. Our patient is not at risk for these complications; his lesion should resolve completely by age 3.

The differential for this patient’s lesion includes congenital nevus, lichen aureus, and café au lait spot.

TAKE-HOME LEARNING POINTS

• Cutaneous mastocytosis manifests as a reddish orange maculopapular patch, which urticates upon forceful stroking.
• Stroking the lesion degranulates the mast cells comprising it, leading to the release of histamine precursors.
• Mast cells can infiltrate internal organs and bone marrow, leading, in the extreme, to mast cell leukemia.
• Urticaria pigmentosa is a variation of mastocytosis in which hundreds of such lesions develop all over the body.

Among psoriasis patients, treatment with infliximab was associated with an increased risk of serious infections that led to hospitalization, the use of intravenous antimicrobial therapy, or death, according to a prospective cohort study of cases in the United Kingdom and the Republic of Ireland.

The new data suggest a risk associated with infliximab treatment that previous clinical trials and observational studies were insufficiently powered to detect, according to the investigators, led by Zenas Yiu, of the University of Manchester (England). They found no associations between infection risk and treatment with etanercept, adalimumab, or ustekinumab, and they noted that there are no such data yet on more recently approved biologic therapies for psoriasis, such as secukinumab or ixekizumab.

The British Association of Dermatologists (BAD) recommends infliximab, a tumor necrosis factor (TNF)–blocker, only for severe cases of psoriasis (Psoriasis Area and Severity Index greater than or equal to 20 and a Dermatology Life Quality Index greater than 18), or when other biologics fail or cannot be used.

To address the insufficient power of earlier studies, the researchers used data from the BAD Biologic Interventions Register (BADBIR), a large, prospective psoriasis registry in the United Kingdom and Ireland established in 2007. The analysis included 3,421 subjects in the nonbiologic systemic therapy cohort, and 422 subjects in the all-lines infliximab cohort. The median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.*

Treatment with infliximab was associated with a statistically significant increased risk of serious infection (defined as an infection associated with prolonged hospitalization or use of IV antimicrobial therapy; or an infection that resulted in death), with an adjusted hazard ratio of 1.95 (95% confidence interval, 1.01-3.75), compared with nonbiologic systemic treatments. The risk was higher in the first 6 months (adjusted HR, 3.49; 95% CI, 1.14-10.70), and from 6 months to 1 year (aHR, 2.99; 95% CI, 1.10-8.14,) but did not reach statistical significance at 1 year to 2 years (aHR, 2.03; 95% CI, 0.61-6.79).

There was also an increased risk of serious infection with infliximab compared with methotrexate (aHR, 2.96; 95% CI, 1.58-5.57).

“Given our findings of a higher risk of serious infection associated with infliximab, we provide real-world evidence to reinforce the position of infliximab in the psoriasis treatment hierarchy,” the authors wrote, adding that “patients with severe psoriasis who fulfill the criteria for the prescription of infliximab should be counseled” about the risk of serious infection.

Dr. Yiu disclosed having received nonfinancial support form Novartis, two authors had no disclosures, and the remainder had various disclosures related to pharmaceutical companies. BADBIR is funded by BAD, which receives funding from Pfizer, Janssen Cilag, AbbVie, Novartis, Samsung Bioepis and Eli Lilly for providing pharmacovigilance services.

SOURCE: Yiu ZZN et al. Br J Dermatol. 2018 Aug 2. doi: 10.1111/bjd.17036.

*This article was updated to correctly indicate that the median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.

Among psoriasis patients, treatment with infliximab was associated with an increased risk of serious infections that led to hospitalization, the use of intravenous antimicrobial therapy, or death, according to a prospective cohort study of cases in the United Kingdom and the Republic of Ireland.

The new data suggest a risk associated with infliximab treatment that previous clinical trials and observational studies were insufficiently powered to detect, according to the investigators, led by Zenas Yiu, of the University of Manchester (England). They found no associations between infection risk and treatment with etanercept, adalimumab, or ustekinumab, and they noted that there are no such data yet on more recently approved biologic therapies for psoriasis, such as secukinumab or ixekizumab.

The British Association of Dermatologists (BAD) recommends infliximab, a tumor necrosis factor (TNF)–blocker, only for severe cases of psoriasis (Psoriasis Area and Severity Index greater than or equal to 20 and a Dermatology Life Quality Index greater than 18), or when other biologics fail or cannot be used.

To address the insufficient power of earlier studies, the researchers used data from the BAD Biologic Interventions Register (BADBIR), a large, prospective psoriasis registry in the United Kingdom and Ireland established in 2007. The analysis included 3,421 subjects in the nonbiologic systemic therapy cohort, and 422 subjects in the all-lines infliximab cohort. The median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.*

Treatment with infliximab was associated with a statistically significant increased risk of serious infection (defined as an infection associated with prolonged hospitalization or use of IV antimicrobial therapy; or an infection that resulted in death), with an adjusted hazard ratio of 1.95 (95% confidence interval, 1.01-3.75), compared with nonbiologic systemic treatments. The risk was higher in the first 6 months (adjusted HR, 3.49; 95% CI, 1.14-10.70), and from 6 months to 1 year (aHR, 2.99; 95% CI, 1.10-8.14,) but did not reach statistical significance at 1 year to 2 years (aHR, 2.03; 95% CI, 0.61-6.79).

There was also an increased risk of serious infection with infliximab compared with methotrexate (aHR, 2.96; 95% CI, 1.58-5.57).

“Given our findings of a higher risk of serious infection associated with infliximab, we provide real-world evidence to reinforce the position of infliximab in the psoriasis treatment hierarchy,” the authors wrote, adding that “patients with severe psoriasis who fulfill the criteria for the prescription of infliximab should be counseled” about the risk of serious infection.

Dr. Yiu disclosed having received nonfinancial support form Novartis, two authors had no disclosures, and the remainder had various disclosures related to pharmaceutical companies. BADBIR is funded by BAD, which receives funding from Pfizer, Janssen Cilag, AbbVie, Novartis, Samsung Bioepis and Eli Lilly for providing pharmacovigilance services.

SOURCE: Yiu ZZN et al. Br J Dermatol. 2018 Aug 2. doi: 10.1111/bjd.17036.

*This article was updated to correctly indicate that the median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.

Among psoriasis patients, treatment with infliximab was associated with an increased risk of serious infections that led to hospitalization, the use of intravenous antimicrobial therapy, or death, according to a prospective cohort study of cases in the United Kingdom and the Republic of Ireland.

The new data suggest a risk associated with infliximab treatment that previous clinical trials and observational studies were insufficiently powered to detect, according to the investigators, led by Zenas Yiu, of the University of Manchester (England). They found no associations between infection risk and treatment with etanercept, adalimumab, or ustekinumab, and they noted that there are no such data yet on more recently approved biologic therapies for psoriasis, such as secukinumab or ixekizumab.

The British Association of Dermatologists (BAD) recommends infliximab, a tumor necrosis factor (TNF)–blocker, only for severe cases of psoriasis (Psoriasis Area and Severity Index greater than or equal to 20 and a Dermatology Life Quality Index greater than 18), or when other biologics fail or cannot be used.

To address the insufficient power of earlier studies, the researchers used data from the BAD Biologic Interventions Register (BADBIR), a large, prospective psoriasis registry in the United Kingdom and Ireland established in 2007. The analysis included 3,421 subjects in the nonbiologic systemic therapy cohort, and 422 subjects in the all-lines infliximab cohort. The median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.*

Treatment with infliximab was associated with a statistically significant increased risk of serious infection (defined as an infection associated with prolonged hospitalization or use of IV antimicrobial therapy; or an infection that resulted in death), with an adjusted hazard ratio of 1.95 (95% confidence interval, 1.01-3.75), compared with nonbiologic systemic treatments. The risk was higher in the first 6 months (adjusted HR, 3.49; 95% CI, 1.14-10.70), and from 6 months to 1 year (aHR, 2.99; 95% CI, 1.10-8.14,) but did not reach statistical significance at 1 year to 2 years (aHR, 2.03; 95% CI, 0.61-6.79).

There was also an increased risk of serious infection with infliximab compared with methotrexate (aHR, 2.96; 95% CI, 1.58-5.57).

“Given our findings of a higher risk of serious infection associated with infliximab, we provide real-world evidence to reinforce the position of infliximab in the psoriasis treatment hierarchy,” the authors wrote, adding that “patients with severe psoriasis who fulfill the criteria for the prescription of infliximab should be counseled” about the risk of serious infection.

Dr. Yiu disclosed having received nonfinancial support form Novartis, two authors had no disclosures, and the remainder had various disclosures related to pharmaceutical companies. BADBIR is funded by BAD, which receives funding from Pfizer, Janssen Cilag, AbbVie, Novartis, Samsung Bioepis and Eli Lilly for providing pharmacovigilance services.

SOURCE: Yiu ZZN et al. Br J Dermatol. 2018 Aug 2. doi: 10.1111/bjd.17036.

*This article was updated to correctly indicate that the median follow-up period was 1.49 person-years (interquartile range, 2.50 person-years) for the all-lines (not just first-line) infliximab group, and 1.51 person-years (1.84 person-years) for the nonbiologics group.

The FP noted that the lesion had a central keratin core (resembling a volcano) surrounded by a somewhat pearly raised border. He suspected that this was a squamous cell carcinoma (SCC) of the keratoacanthoma type and recommended a biopsy.

A shave biopsy was performed, and the result confirmed the diagnosis of SCC of the keratoacanthoma type. (See the Watch & Learn video on “Shave biopsy.”) The pathologist added that the lesion was well-differentiated (which was to be expected with a keratoacanthoma). While some keratoacanthomas actually resolve spontaneously, the standard of care is to treat them with either excision, electrodesiccation and curettage, or cryotherapy. On the follow-up visit, these options were presented to the patient and he decided to have cryotherapy. He accepted the risk of hypopigmentation in the treated area, but said that he preferred to avoid surgery.

The area was anesthetized with an injection of 1% lidocaine and epinephrine, and cryotherapy was performed with a 5 mm margin. The area was frozen with liquid nitrogen spray for 30 seconds and allowed to thaw. A second freeze for 30 seconds was then applied. Sun protection and sun avoidance were encouraged. At a 1-year follow-up, there was no recurrence and there was hypopigmentation at the treatment site.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratoacanthoma. 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 noted that the lesion had a central keratin core (resembling a volcano) surrounded by a somewhat pearly raised border. He suspected that this was a squamous cell carcinoma (SCC) of the keratoacanthoma type and recommended a biopsy.

A shave biopsy was performed, and the result confirmed the diagnosis of SCC of the keratoacanthoma type. (See the Watch & Learn video on “Shave biopsy.”) The pathologist added that the lesion was well-differentiated (which was to be expected with a keratoacanthoma). While some keratoacanthomas actually resolve spontaneously, the standard of care is to treat them with either excision, electrodesiccation and curettage, or cryotherapy. On the follow-up visit, these options were presented to the patient and he decided to have cryotherapy. He accepted the risk of hypopigmentation in the treated area, but said that he preferred to avoid surgery.

The area was anesthetized with an injection of 1% lidocaine and epinephrine, and cryotherapy was performed with a 5 mm margin. The area was frozen with liquid nitrogen spray for 30 seconds and allowed to thaw. A second freeze for 30 seconds was then applied. Sun protection and sun avoidance were encouraged. At a 1-year follow-up, there was no recurrence and there was hypopigmentation at the treatment site.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratoacanthoma. 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 noted that the lesion had a central keratin core (resembling a volcano) surrounded by a somewhat pearly raised border. He suspected that this was a squamous cell carcinoma (SCC) of the keratoacanthoma type and recommended a biopsy.

A shave biopsy was performed, and the result confirmed the diagnosis of SCC of the keratoacanthoma type. (See the Watch & Learn video on “Shave biopsy.”) The pathologist added that the lesion was well-differentiated (which was to be expected with a keratoacanthoma). While some keratoacanthomas actually resolve spontaneously, the standard of care is to treat them with either excision, electrodesiccation and curettage, or cryotherapy. On the follow-up visit, these options were presented to the patient and he decided to have cryotherapy. He accepted the risk of hypopigmentation in the treated area, but said that he preferred to avoid surgery.

The area was anesthetized with an injection of 1% lidocaine and epinephrine, and cryotherapy was performed with a 5 mm margin. The area was frozen with liquid nitrogen spray for 30 seconds and allowed to thaw. A second freeze for 30 seconds was then applied. Sun protection and sun avoidance were encouraged. At a 1-year follow-up, there was no recurrence and there was hypopigmentation at the treatment site.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Guzman A, Usatine R. Keratoacanthoma. 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.

WASHINGTON – Currently available options for treating itch in patients with atopic dermatitis continue to be somewhat limited, but range from several topical agents to oral medications, including antihistamines and an oral antiemetic approved for preventing chemotherapy-related nausea and vomiting, Peter Lio, MD, said at a symposium presented by the Coalition United for Better Eczema Care (CUBE-C).

There are four basic areas of treatment, which Dr. Lio, a dermatologist at Northwestern University, Chicago, referred to as the “itch therapeutic ladder.” In a video interview at the meeting, he reviewed the treatments, starting with topical therapies, which include camphor and menthol, strontium-containing topicals, as well as “dilute bleach-type products” that seem to have some anti-inflammatory and anti-itch effects.

The next levels: oral medications – antihistamines, followed by “more intense” options that may carry more risks, such as the antidepressant mirtazapine, and aprepitant, a neurokinin-1 receptor antagonist approved for the prevention of chemotherapy-induced and postoperative nausea and vomiting. Gabapentin and naltrexone can also be helpful for certain populations; all are used off-label, he pointed out.

Dr. Lio, formally trained in acupuncture, often uses alternative therapies as the fourth rung of the ladder. These include using a specific acupressure point, which he said “seems to give a little bit of relief.”

In the interview, he also discussed considerations in children with atopic dermatitis and exciting treatments in development, such as biologics that target “one of the master itch cytokines,” interleukin-31.

“Itch is such an important part of this disease because we know not only is it one of the key pieces that pushes the disease forward and keeps these cycles going, but also contributes a huge amount to the morbidity,” he said.

CUBE-C, established by the National Eczema Association (NEA), is a “network of cross-specialty leaders, patients and caregivers, constructing an educational curriculum based on standards of effective treatment and disease management,” according to the NEA.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Lio reported serving as a speaker, consultant, and/or advisor for companies developing and marketing atopic dermatitis therapies and products.

[email protected]

WASHINGTON – Currently available options for treating itch in patients with atopic dermatitis continue to be somewhat limited, but range from several topical agents to oral medications, including antihistamines and an oral antiemetic approved for preventing chemotherapy-related nausea and vomiting, Peter Lio, MD, said at a symposium presented by the Coalition United for Better Eczema Care (CUBE-C).

There are four basic areas of treatment, which Dr. Lio, a dermatologist at Northwestern University, Chicago, referred to as the “itch therapeutic ladder.” In a video interview at the meeting, he reviewed the treatments, starting with topical therapies, which include camphor and menthol, strontium-containing topicals, as well as “dilute bleach-type products” that seem to have some anti-inflammatory and anti-itch effects.

The next levels: oral medications – antihistamines, followed by “more intense” options that may carry more risks, such as the antidepressant mirtazapine, and aprepitant, a neurokinin-1 receptor antagonist approved for the prevention of chemotherapy-induced and postoperative nausea and vomiting. Gabapentin and naltrexone can also be helpful for certain populations; all are used off-label, he pointed out.

Dr. Lio, formally trained in acupuncture, often uses alternative therapies as the fourth rung of the ladder. These include using a specific acupressure point, which he said “seems to give a little bit of relief.”

In the interview, he also discussed considerations in children with atopic dermatitis and exciting treatments in development, such as biologics that target “one of the master itch cytokines,” interleukin-31.

“Itch is such an important part of this disease because we know not only is it one of the key pieces that pushes the disease forward and keeps these cycles going, but also contributes a huge amount to the morbidity,” he said.

CUBE-C, established by the National Eczema Association (NEA), is a “network of cross-specialty leaders, patients and caregivers, constructing an educational curriculum based on standards of effective treatment and disease management,” according to the NEA.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Lio reported serving as a speaker, consultant, and/or advisor for companies developing and marketing atopic dermatitis therapies and products.

[email protected]

WASHINGTON – Currently available options for treating itch in patients with atopic dermatitis continue to be somewhat limited, but range from several topical agents to oral medications, including antihistamines and an oral antiemetic approved for preventing chemotherapy-related nausea and vomiting, Peter Lio, MD, said at a symposium presented by the Coalition United for Better Eczema Care (CUBE-C).

There are four basic areas of treatment, which Dr. Lio, a dermatologist at Northwestern University, Chicago, referred to as the “itch therapeutic ladder.” In a video interview at the meeting, he reviewed the treatments, starting with topical therapies, which include camphor and menthol, strontium-containing topicals, as well as “dilute bleach-type products” that seem to have some anti-inflammatory and anti-itch effects.

The next levels: oral medications – antihistamines, followed by “more intense” options that may carry more risks, such as the antidepressant mirtazapine, and aprepitant, a neurokinin-1 receptor antagonist approved for the prevention of chemotherapy-induced and postoperative nausea and vomiting. Gabapentin and naltrexone can also be helpful for certain populations; all are used off-label, he pointed out.

Dr. Lio, formally trained in acupuncture, often uses alternative therapies as the fourth rung of the ladder. These include using a specific acupressure point, which he said “seems to give a little bit of relief.”

In the interview, he also discussed considerations in children with atopic dermatitis and exciting treatments in development, such as biologics that target “one of the master itch cytokines,” interleukin-31.

“Itch is such an important part of this disease because we know not only is it one of the key pieces that pushes the disease forward and keeps these cycles going, but also contributes a huge amount to the morbidity,” he said.

CUBE-C, established by the National Eczema Association (NEA), is a “network of cross-specialty leaders, patients and caregivers, constructing an educational curriculum based on standards of effective treatment and disease management,” according to the NEA.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Lio reported serving as a speaker, consultant, and/or advisor for companies developing and marketing atopic dermatitis therapies and products.

[email protected]

The FP also was concerned about a possible skin cancer, especially for the larger of the 2 lesions. The FP recommended 2 shave biopsies, which the patient agreed to. (See the Watch & Learn video on “Shave biopsy.”) The patient was directed to apply petrolatum once or twice daily to the biopsy sites and to cover them with dressings for the next 1 to 2 weeks. On the 2-week follow-up, the physician diagnosed the larger lesion as squamous cell carcinoma in situ (Bowen disease) and the top lesion as actinic keratosis.

The physician explained that the actinic keratosis did not need further treatment; however, the options for treating Bowen disease included cryosurgery, electrodesiccation and curettage, or elliptical excision. The patient chose an elliptical excision, which was performed without complications at the following visit.

The margins were clear and the surgery site healed without any problems. The patient said that he planned to wear long sleeves more often and use sunscreen when his arms were exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Wah Y. Actinic keratosis and Bowen disease. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:969-976.

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 also was concerned about a possible skin cancer, especially for the larger of the 2 lesions. The FP recommended 2 shave biopsies, which the patient agreed to. (See the Watch & Learn video on “Shave biopsy.”) The patient was directed to apply petrolatum once or twice daily to the biopsy sites and to cover them with dressings for the next 1 to 2 weeks. On the 2-week follow-up, the physician diagnosed the larger lesion as squamous cell carcinoma in situ (Bowen disease) and the top lesion as actinic keratosis.

The physician explained that the actinic keratosis did not need further treatment; however, the options for treating Bowen disease included cryosurgery, electrodesiccation and curettage, or elliptical excision. The patient chose an elliptical excision, which was performed without complications at the following visit.

The margins were clear and the surgery site healed without any problems. The patient said that he planned to wear long sleeves more often and use sunscreen when his arms were exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Wah Y. Actinic keratosis and Bowen disease. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:969-976.

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 also was concerned about a possible skin cancer, especially for the larger of the 2 lesions. The FP recommended 2 shave biopsies, which the patient agreed to. (See the Watch & Learn video on “Shave biopsy.”) The patient was directed to apply petrolatum once or twice daily to the biopsy sites and to cover them with dressings for the next 1 to 2 weeks. On the 2-week follow-up, the physician diagnosed the larger lesion as squamous cell carcinoma in situ (Bowen disease) and the top lesion as actinic keratosis.

The physician explained that the actinic keratosis did not need further treatment; however, the options for treating Bowen disease included cryosurgery, electrodesiccation and curettage, or elliptical excision. The patient chose an elliptical excision, which was performed without complications at the following visit.

The margins were clear and the surgery site healed without any problems. The patient said that he planned to wear long sleeves more often and use sunscreen when his arms were exposed to the sun.

‌

Photos and text for Photo Rounds Friday courtesy of Richard P. Usatine, MD. This case was adapted from: Usatine R, Wah Y. Actinic keratosis and Bowen disease. In: Usatine R, Smith M, Mayeaux EJ, et al. Color Atlas of Family Medicine. 2nd ed. New York, NY: McGraw-Hill; 2013:969-976.

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.

WASHINGTON – The National Eczema Association (NEA) has established the Coalition United for Better Eczema Care (CUBE-C) to provide practitioners with a resource for “trustworthy, up-to-date, state of the art” information on atopic dermatitis, with the goal of improving health outcomes, according to Julie Block, president and chief executive officer of the NEA.

In an interview at a symposium presented by CUBE-C, Ms. Block provided more information on CUBE-C, including how and why it started and what it can offer to dermatologists, as well as primary care physicians, who care for patients with atopic dermatitis. She said that the NEA convened dermatologists, allergists, immunologists, psychologists, nurse practitioners, physician assistants, and patients “to design a curriculum that provided an entire picture of the patient experience, so that we could go out and educate not only on the basics of eczema and atopic dermatitis for a variety of practitioners ... but also for the specialists who are now going to be engaging in new innovations and new therapies for their patients.”

She was joined by Adam Friedman, MD, professor of dermatology and residency program director at George Washington University, Washington, where the symposium, a resident’s boot camp, was held. The boot camp was somewhat unique in that it was geared more towards trainees; typically, the CUBE-C program is a CME program for practitioners, but this reflects the flexibility of the program, which can be tailored to the audience, Dr. Friedman pointed out. “The hope is that programs like these pop up all over the place ... anywhere you have a critical mass of individuals who want to learn about this,” where planners can choose from a menu of topics provided by CUBE-C – which include therapeutics, infections, pathogenesis, and access to care – and “easily formulate a conference like we held here today for the right audience.”

Topics covered at the George Washington University symposium included the impact of climate on the prevalence of childhood eczema, the diagnosis and differential diagnosis in children, infections in atopic dermatitis patients, and itch treatment.

More information on CUBE-C is available on the NEA website.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Friedman reported serving as a speaker for Regeneron, Pfizer, and other companies. He also consults and serves on the advisory board for Pfizer and multiple other companies developing and marketing atopic dermatitis therapies and products.
 

[email protected]

WASHINGTON – The National Eczema Association (NEA) has established the Coalition United for Better Eczema Care (CUBE-C) to provide practitioners with a resource for “trustworthy, up-to-date, state of the art” information on atopic dermatitis, with the goal of improving health outcomes, according to Julie Block, president and chief executive officer of the NEA.

In an interview at a symposium presented by CUBE-C, Ms. Block provided more information on CUBE-C, including how and why it started and what it can offer to dermatologists, as well as primary care physicians, who care for patients with atopic dermatitis. She said that the NEA convened dermatologists, allergists, immunologists, psychologists, nurse practitioners, physician assistants, and patients “to design a curriculum that provided an entire picture of the patient experience, so that we could go out and educate not only on the basics of eczema and atopic dermatitis for a variety of practitioners ... but also for the specialists who are now going to be engaging in new innovations and new therapies for their patients.”

She was joined by Adam Friedman, MD, professor of dermatology and residency program director at George Washington University, Washington, where the symposium, a resident’s boot camp, was held. The boot camp was somewhat unique in that it was geared more towards trainees; typically, the CUBE-C program is a CME program for practitioners, but this reflects the flexibility of the program, which can be tailored to the audience, Dr. Friedman pointed out. “The hope is that programs like these pop up all over the place ... anywhere you have a critical mass of individuals who want to learn about this,” where planners can choose from a menu of topics provided by CUBE-C – which include therapeutics, infections, pathogenesis, and access to care – and “easily formulate a conference like we held here today for the right audience.”

Topics covered at the George Washington University symposium included the impact of climate on the prevalence of childhood eczema, the diagnosis and differential diagnosis in children, infections in atopic dermatitis patients, and itch treatment.

More information on CUBE-C is available on the NEA website.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Friedman reported serving as a speaker for Regeneron, Pfizer, and other companies. He also consults and serves on the advisory board for Pfizer and multiple other companies developing and marketing atopic dermatitis therapies and products.
 

[email protected]

WASHINGTON – The National Eczema Association (NEA) has established the Coalition United for Better Eczema Care (CUBE-C) to provide practitioners with a resource for “trustworthy, up-to-date, state of the art” information on atopic dermatitis, with the goal of improving health outcomes, according to Julie Block, president and chief executive officer of the NEA.

In an interview at a symposium presented by CUBE-C, Ms. Block provided more information on CUBE-C, including how and why it started and what it can offer to dermatologists, as well as primary care physicians, who care for patients with atopic dermatitis. She said that the NEA convened dermatologists, allergists, immunologists, psychologists, nurse practitioners, physician assistants, and patients “to design a curriculum that provided an entire picture of the patient experience, so that we could go out and educate not only on the basics of eczema and atopic dermatitis for a variety of practitioners ... but also for the specialists who are now going to be engaging in new innovations and new therapies for their patients.”

She was joined by Adam Friedman, MD, professor of dermatology and residency program director at George Washington University, Washington, where the symposium, a resident’s boot camp, was held. The boot camp was somewhat unique in that it was geared more towards trainees; typically, the CUBE-C program is a CME program for practitioners, but this reflects the flexibility of the program, which can be tailored to the audience, Dr. Friedman pointed out. “The hope is that programs like these pop up all over the place ... anywhere you have a critical mass of individuals who want to learn about this,” where planners can choose from a menu of topics provided by CUBE-C – which include therapeutics, infections, pathogenesis, and access to care – and “easily formulate a conference like we held here today for the right audience.”

Topics covered at the George Washington University symposium included the impact of climate on the prevalence of childhood eczema, the diagnosis and differential diagnosis in children, infections in atopic dermatitis patients, and itch treatment.

More information on CUBE-C is available on the NEA website.

The symposium was supported by an educational grant from Sanofi Genzyme, Regeneron Pharmaceuticals, and Pfizer. Dr. Friedman reported serving as a speaker for Regeneron, Pfizer, and other companies. He also consults and serves on the advisory board for Pfizer and multiple other companies developing and marketing atopic dermatitis therapies and products.
 

[email protected]

LAKE TAHOE, CALIF. – Children experience a wide range of cutaneous manifestations of immunosuppression, including atopic dermatitis (AD), skin cancer, and side effects of vemurafenib treatment.

In a presentation on the cutaneous sequelae of different immunosuppressive regimens at the annual meeting of the Society for Pediatric Dermatology, Carrie C. Coughlin, MD, opened with a discussion of AD triggered by the tumor necrosis factor (TNF) blocker infliximab, especially in the setting of therapy for Crohn’s disease. “In this patient population you often think of psoriasis as a consequence of infliximab and other TNF therapies,” said Dr. Coughlin, a pediatric dermatologist at Washington University, St. Louis. “But you can also get true atopic dermatitis with infliximab as well. Who’s more at risk for this? Patients with Crohn’s disease seem to be. Most of the literature is in adults, but there are a few series of children. In a series of children looking at cutaneous sequelae of infliximab therapy, about 20% of cutaneous eruptions were atopic dermatitis. I think it’s a great opportunity for us in dermatology to do a more research in this area.”

Some researchers have proposed that atopic disease could be a marker of over-suppression of TNF-alpha in young Crohn’s disease patients on infliximab (Inflamm Bowel Dis. 2014; 20[8]:1309-15). “One question you could ask is, could these patients actually tolerate a dose reduction?” Dr. Coughlin said. She promoted the role of dermatologists in working at managing side effects to keep patients on medications helping their GI disease, but acknowledged this is not always possible.

Doug Brunk/MDedge News

[email protected]

LAKE TAHOE, CALIF. – Children experience a wide range of cutaneous manifestations of immunosuppression, including atopic dermatitis (AD), skin cancer, and side effects of vemurafenib treatment.

In a presentation on the cutaneous sequelae of different immunosuppressive regimens at the annual meeting of the Society for Pediatric Dermatology, Carrie C. Coughlin, MD, opened with a discussion of AD triggered by the tumor necrosis factor (TNF) blocker infliximab, especially in the setting of therapy for Crohn’s disease. “In this patient population you often think of psoriasis as a consequence of infliximab and other TNF therapies,” said Dr. Coughlin, a pediatric dermatologist at Washington University, St. Louis. “But you can also get true atopic dermatitis with infliximab as well. Who’s more at risk for this? Patients with Crohn’s disease seem to be. Most of the literature is in adults, but there are a few series of children. In a series of children looking at cutaneous sequelae of infliximab therapy, about 20% of cutaneous eruptions were atopic dermatitis. I think it’s a great opportunity for us in dermatology to do a more research in this area.”

Some researchers have proposed that atopic disease could be a marker of over-suppression of TNF-alpha in young Crohn’s disease patients on infliximab (Inflamm Bowel Dis. 2014; 20[8]:1309-15). “One question you could ask is, could these patients actually tolerate a dose reduction?” Dr. Coughlin said. She promoted the role of dermatologists in working at managing side effects to keep patients on medications helping their GI disease, but acknowledged this is not always possible.

Doug Brunk/MDedge News

[email protected]

LAKE TAHOE, CALIF. – Children experience a wide range of cutaneous manifestations of immunosuppression, including atopic dermatitis (AD), skin cancer, and side effects of vemurafenib treatment.

In a presentation on the cutaneous sequelae of different immunosuppressive regimens at the annual meeting of the Society for Pediatric Dermatology, Carrie C. Coughlin, MD, opened with a discussion of AD triggered by the tumor necrosis factor (TNF) blocker infliximab, especially in the setting of therapy for Crohn’s disease. “In this patient population you often think of psoriasis as a consequence of infliximab and other TNF therapies,” said Dr. Coughlin, a pediatric dermatologist at Washington University, St. Louis. “But you can also get true atopic dermatitis with infliximab as well. Who’s more at risk for this? Patients with Crohn’s disease seem to be. Most of the literature is in adults, but there are a few series of children. In a series of children looking at cutaneous sequelae of infliximab therapy, about 20% of cutaneous eruptions were atopic dermatitis. I think it’s a great opportunity for us in dermatology to do a more research in this area.”

Some researchers have proposed that atopic disease could be a marker of over-suppression of TNF-alpha in young Crohn’s disease patients on infliximab (Inflamm Bowel Dis. 2014; 20[8]:1309-15). “One question you could ask is, could these patients actually tolerate a dose reduction?” Dr. Coughlin said. She promoted the role of dermatologists in working at managing side effects to keep patients on medications helping their GI disease, but acknowledged this is not always possible.

Doug Brunk/MDedge News

[email protected]

When a child presents with hair loss, don’t rule out issues related to genetics and structural abnormalities of the hair itself, according to Maria Hordinsky, MD, of the University of Minnesota, Minneapolis.

The ectodermal dysplasias are a heterogeneous group of disorders in which a main feature is the absent, incomplete, or delayed development of one or more of the appendages derived from ectoderm, such as the hair follicle, Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Patients with pure hair and nail ectodermal dysplasia generally present with absent or sparse eyebrows and eyelashes, as well as follicular papules on the scalp and fragile, irregular hair, Dr. Hordinsky said. The condition is caused by a mutation in a gene associated with the production of keratin. In another rare form of hereditary hair loss – hypotrichosis simplex – patients are born with normal hair but lose it gradually from the scalp during the middle of the first decade of life.

The inability to grow long hair characterizes short anagen syndrome, a congenital disorder not to be confused with loose anagen syndrome, Dr. Hordinsky said. Patients with short anagen syndrome experience an idiopathic short anagen phase and as a result, an increased number of hairs in the telogen phase. Children with short anagen syndrome have unusually short hair in early childhood. “Parents typically complain that their children exhibit short hair even though they have never had a haircut,” she explained.

Trichothiodystrophy, a rare autosomal recessive disease, is distinguished by hair that is brittle and sulfur deficient, Dr. Hordinsky said. She cited a review of 112 patients with trichothiodystrophy in which additional distinguishing features included developmental delay/intellectual impairment (86%), short stature (73%), and ichthyosis (65%).

Some cases of hair loss in children have a structural basis, Dr. Hordinsky noted. Structural hair abnormalities include fractures of the hair shaft, extraneous matter on the hair shaft, and hair shaft irregularities such as coiling or twisting, she said.

In trichoptilosis, extensive cuticle loss results in fraying and splitting of the hair shaft, while in patients with trichoclasis, a fractured hair is splinted by a partially intact cuticle.

In trichorrhexis nodosa, the most common type of structural hair abnormality, “intact nodes [of hair] resemble two paintbrushes thrust together,” Dr. Hordinsky explained. Trichorrhexis nodosa may be congenital or acquired, and occurs in children with mental retardation and argininosuccinic aciduria, she said.

A hair shaft abnormality is the culprit behind uncombable hair syndrome, which can be inherited or can occur sporadically, Dr. Hordinsky said. The key feature of the condition is unruly hair caused by a distinctive hair shaft defect, “possibly related to an abnormality in the inner root sheath.” Abnormal hairs usually become apparent at about 3-4 years of age, but eyebrows and eyelashes appear normal. Many patients have a silvery blonde tint to their hair because of how the abnormal hairs reflect light, she said.

Dr. Hordinsky is a consultant for P&G, Concert, Cassiopea, and BioAZ; and receives grant/research support from Aclaris, Allergan, and the National Alopecia Areata Foundation. SDEF and this news organization are owned by Frontline Medical Communications.

When a child presents with hair loss, don’t rule out issues related to genetics and structural abnormalities of the hair itself, according to Maria Hordinsky, MD, of the University of Minnesota, Minneapolis.

The ectodermal dysplasias are a heterogeneous group of disorders in which a main feature is the absent, incomplete, or delayed development of one or more of the appendages derived from ectoderm, such as the hair follicle, Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Patients with pure hair and nail ectodermal dysplasia generally present with absent or sparse eyebrows and eyelashes, as well as follicular papules on the scalp and fragile, irregular hair, Dr. Hordinsky said. The condition is caused by a mutation in a gene associated with the production of keratin. In another rare form of hereditary hair loss – hypotrichosis simplex – patients are born with normal hair but lose it gradually from the scalp during the middle of the first decade of life.

The inability to grow long hair characterizes short anagen syndrome, a congenital disorder not to be confused with loose anagen syndrome, Dr. Hordinsky said. Patients with short anagen syndrome experience an idiopathic short anagen phase and as a result, an increased number of hairs in the telogen phase. Children with short anagen syndrome have unusually short hair in early childhood. “Parents typically complain that their children exhibit short hair even though they have never had a haircut,” she explained.

Trichothiodystrophy, a rare autosomal recessive disease, is distinguished by hair that is brittle and sulfur deficient, Dr. Hordinsky said. She cited a review of 112 patients with trichothiodystrophy in which additional distinguishing features included developmental delay/intellectual impairment (86%), short stature (73%), and ichthyosis (65%).

Some cases of hair loss in children have a structural basis, Dr. Hordinsky noted. Structural hair abnormalities include fractures of the hair shaft, extraneous matter on the hair shaft, and hair shaft irregularities such as coiling or twisting, she said.

In trichoptilosis, extensive cuticle loss results in fraying and splitting of the hair shaft, while in patients with trichoclasis, a fractured hair is splinted by a partially intact cuticle.

In trichorrhexis nodosa, the most common type of structural hair abnormality, “intact nodes [of hair] resemble two paintbrushes thrust together,” Dr. Hordinsky explained. Trichorrhexis nodosa may be congenital or acquired, and occurs in children with mental retardation and argininosuccinic aciduria, she said.

A hair shaft abnormality is the culprit behind uncombable hair syndrome, which can be inherited or can occur sporadically, Dr. Hordinsky said. The key feature of the condition is unruly hair caused by a distinctive hair shaft defect, “possibly related to an abnormality in the inner root sheath.” Abnormal hairs usually become apparent at about 3-4 years of age, but eyebrows and eyelashes appear normal. Many patients have a silvery blonde tint to their hair because of how the abnormal hairs reflect light, she said.

Dr. Hordinsky is a consultant for P&G, Concert, Cassiopea, and BioAZ; and receives grant/research support from Aclaris, Allergan, and the National Alopecia Areata Foundation. SDEF and this news organization are owned by Frontline Medical Communications.

When a child presents with hair loss, don’t rule out issues related to genetics and structural abnormalities of the hair itself, according to Maria Hordinsky, MD, of the University of Minnesota, Minneapolis.

The ectodermal dysplasias are a heterogeneous group of disorders in which a main feature is the absent, incomplete, or delayed development of one or more of the appendages derived from ectoderm, such as the hair follicle, Dr. Hordinsky said in a presentation at Skin Disease Education Foundation’s Women’s & Pediatric Dermatology Seminar.

Patients with pure hair and nail ectodermal dysplasia generally present with absent or sparse eyebrows and eyelashes, as well as follicular papules on the scalp and fragile, irregular hair, Dr. Hordinsky said. The condition is caused by a mutation in a gene associated with the production of keratin. In another rare form of hereditary hair loss – hypotrichosis simplex – patients are born with normal hair but lose it gradually from the scalp during the middle of the first decade of life.

The inability to grow long hair characterizes short anagen syndrome, a congenital disorder not to be confused with loose anagen syndrome, Dr. Hordinsky said. Patients with short anagen syndrome experience an idiopathic short anagen phase and as a result, an increased number of hairs in the telogen phase. Children with short anagen syndrome have unusually short hair in early childhood. “Parents typically complain that their children exhibit short hair even though they have never had a haircut,” she explained.

Trichothiodystrophy, a rare autosomal recessive disease, is distinguished by hair that is brittle and sulfur deficient, Dr. Hordinsky said. She cited a review of 112 patients with trichothiodystrophy in which additional distinguishing features included developmental delay/intellectual impairment (86%), short stature (73%), and ichthyosis (65%).

Some cases of hair loss in children have a structural basis, Dr. Hordinsky noted. Structural hair abnormalities include fractures of the hair shaft, extraneous matter on the hair shaft, and hair shaft irregularities such as coiling or twisting, she said.

In trichoptilosis, extensive cuticle loss results in fraying and splitting of the hair shaft, while in patients with trichoclasis, a fractured hair is splinted by a partially intact cuticle.

In trichorrhexis nodosa, the most common type of structural hair abnormality, “intact nodes [of hair] resemble two paintbrushes thrust together,” Dr. Hordinsky explained. Trichorrhexis nodosa may be congenital or acquired, and occurs in children with mental retardation and argininosuccinic aciduria, she said.

A hair shaft abnormality is the culprit behind uncombable hair syndrome, which can be inherited or can occur sporadically, Dr. Hordinsky said. The key feature of the condition is unruly hair caused by a distinctive hair shaft defect, “possibly related to an abnormality in the inner root sheath.” Abnormal hairs usually become apparent at about 3-4 years of age, but eyebrows and eyelashes appear normal. Many patients have a silvery blonde tint to their hair because of how the abnormal hairs reflect light, she said.

Dr. Hordinsky is a consultant for P&G, Concert, Cassiopea, and BioAZ; and receives grant/research support from Aclaris, Allergan, and the National Alopecia Areata Foundation. SDEF and this news organization are owned by Frontline Medical Communications.