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The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.
AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.
The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.
At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.
Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.
Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.
Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.
Richard Vinson, MD, has disclosed no relevant financial relationships.
The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.
AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.
The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.
At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.
Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.
Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.
Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.
Richard Vinson, MD, has disclosed no relevant financial relationships.
The patient is diagnosed with atopic dermatitis (AD) on the basis of clinical findings and historical features, morphology and distribution of skin lesions, and associated clinical signs.
AD continues to be a clinical diagnosis. Pruritus and eczema (acute, subacute, or chronic) are essential features for the diagnosis of AD. The eczema should follow characteristic morphology and age-specific patterns (eg, facial/neck/extensor involvement in children, flexural involvement in any age group, sparing of the groin and axillary regions). A personal or family history of atopy is an important historical feature that supports the diagnosis of AD, as are xerosis and early age of onset.
The majority of patients with AD (60%) develop symptoms during the first year of life and 90% experience an eruption by 5 years of age, but disease onset can occur at any age. Some studies have found an association between late-onset AD and persistence of disease into adulthood.
At present, there are no reliable biomarkers that can differentiate AD from other entities. An elevated total and/or allergen-specific serum IgE level is the most commonly associated laboratory feature, but it is not seen in about 20% of individuals with AD. Additionally, elevated allergen-specific IgE levels are found in 55% of the general population in the United States, making it nonspecific for AD. Moreover, while total IgE level usually varies in accordance with disease severity, it is not a reliable marker of disease severity, and it is possible for individuals with severe disease to have normal levels. Nonatopic conditions (eg, parasitic infection, some cancers, and autoimmune disease) may also lead to elevations in IgE levels.
Consistent prognostic markers are also lacking, although elevated total serum IgE levels and filaggrin gene null mutations do tend to be predictive of a more severe and prolonged disease course.
Topical agents including nonpharmacologic moisturizers and topical corticosteroids are the mainstay of treatment for AD; immunomodulatory agents and targeted biologic therapies are also available. For patients with more severe or recalcitrant disease, systemic therapy or phototherapy may be used, often in conjunction with topical therapies.
Richard Vinson, MD, President, Mountain View Dermatology, El Paso, Texas.
Richard Vinson, MD, has disclosed no relevant financial relationships.
A 15-year-old boy presents with widespread pruritic lesions on his torso. His mother explains that he had been seen by his pediatrician 2 weeks before and was diagnosed with scabies. The patient was treated with a topical scabicidal agent (permethrin 5% lotion) on diagnosis, with a repeat application 7 days later. Despite treatment, no improvement in the patient's symptoms have been noted. Physical examination reveals poorly defined, erythematous, scaly, and crusted patches and plaques. No other family members are experiencing symptoms. There is a positive family history for atopy.
