Dermatology · Eczema
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Atopic dermatitis is characterized by a defective skin barrier, most often attributed to filaggrin (FLG) loss-of-function mutations (present in only about 20-30% of patients), leading to increased transepidermal water loss.
The classic clinical presentation involves intensely pruritic, erythematous, scaly patches located in the flexural surfaces in children and adults.
Infants typically present with erythematous, weeping, or crusted lesions on the extensor surfaces, face, and scalp.
Atopic dermatitis is a key component of the atopic triad, which also includes allergic rhinitis and asthma.
The first-line treatment for acute flares is topical corticosteroids, while long-term maintenance focuses on emollients and skin hydration.
Patients with atopic dermatitis are at an increased risk for eczema herpeticum, a severe superimposed herpes simplex virus infection.
Secondary bacterial infections, most commonly with Staphylococcus aureus, are a frequent complication due to impaired skin integrity and pruritus-induced excoriations.
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A 6-month-old male is brought to the clinic by his mother due to a persistent rash. The mother notes that the infant is extremely fussy and constantly rubs his face against the crib sheets. Physical examination reveals erythematous, weeping, and crusted plaques on the cheeks and extensor surfaces of the extremities. The infant has no history of fever or systemic symptoms. The family history is significant for asthma in the father and allergic rhinitis in the mother.
What is the most likely diagnosis?
Atopic dermatitis
The patient presents with the classic distribution and morphology of atopic dermatitis in an infant, supported by the presence of the atopic triad in the family history.
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Etiology / Epidemiology
Associated with the atopic triad: asthma, allergic rhinitis, and dermatitis. Often presents in infancy.
Clinical Manifestations
Intense pruritus with flexural lichenification in adults; extensor surfaces in infants.
Diagnosis
A clinical diagnosis based on the Hanifin and Rajka criteria; no specific lab test required.
Treatment
Topical corticosteroids are first-line; avoid systemic steroids due to rebound flares.
Prognosis
Most cases resolve by adolescence; secondary bacterial infection (e.g., Staph aureus) is the primary complication.
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Epidemiology & Etiology
Commonly known as eczema, it affects up to 20% of children. It is strongly linked to a family history of atopy. Onset typically occurs before age 5, with many patients experiencing spontaneous resolution.
Pertinent Anatomy
The skin barrier is compromised, specifically in the stratum corneum. This leads to increased transepidermal water loss and susceptibility to environmental irritants.
Pathophysiology
Loss-of-function mutations in the filaggrin gene disrupt the skin barrier. This allows allergen penetration, triggering a Th2-driven inflammatory response (IL-4/IL-13/IL-31), with mixed Type I (IgE) and delayed Type IV hypersensitivity features. Chronic inflammation leads to the characteristic lichenification of the skin.
Clinical Manifestations
Patients present with the itch-scratch cycle, leading to excoriations. Infants typically show involvement of the face and extensor surfaces, while adults exhibit flexural involvement (antecubital/popliteal fossae). Eczema herpeticum is a severe, life-threatening viral superinfection requiring immediate antiviral therapy.
Diagnosis
Diagnosis is clinical using the Hanifin and Rajka criteria, requiring 3 major and 3 minor features. Skin biopsy is rarely indicated unless the diagnosis is unclear or malignancy is suspected. Serum IgE levels are often elevated but are not diagnostic.
Treatment
First-line therapy is topical corticosteroids and aggressive emollients. For sensitive areas like the face, use topical calcineurin inhibitors (e.g., tacrolimus). Newer steroid-sparing topicals with strong 2025 AAD recommendations include roflumilast 0.15% cream (PDE4 inhibitor, mild-to-moderate disease), tapinarof cream (aryl hydrocarbon receptor agonist), and ruxolitinib cream (topical JAK inhibitor). Avoid systemic corticosteroids due to the risk of severe rebound flares. Phototherapy and systemic agents are reserved for refractory moderate-to-severe disease; dupilumab (anti-IL-4Ralpha) is the preferred first-line biologic, with tralokinumab/lebrikizumab (anti-IL-13) and nemolizumab (anti-IL-31 receptor alpha) also carrying strong recommendations in the 2025 AAD focused update. Oral JAK inhibitors (upadacitinib, abrocitinib) are reserved for disease refractory to or unsuitable for biologics and carry a boxed warning for serious infection, malignancy, major adverse cardiovascular events, thrombosis, and death.
Prognosis
Most children outgrow the condition by puberty. Secondary bacterial infection (typically Staphylococcus aureus) is the most common complication. Patients are at lifelong risk for contact dermatitis.
Differential Diagnosis
Seborrheic dermatitis: greasy, yellow scales on the scalp/face
Psoriasis: well-demarcated plaques with silvery scale on extensor surfaces
Tinea corporis: annular lesions with central clearing and positive KOH prep
Scabies: intense nocturnal pruritus with burrows in web spaces
Contact dermatitis: localized reaction to a specific allergen or irritant