Correct Answer: D. Atopic dermatitis
Atopic dermatitis (AD) is the most probable diagnosis given the clinical triad of age, pruritus, and positive family history of atopy. The patient is a 15-year-old with itchy lesions and a family history of asthma—both cardinal features of AD. Atopic dermatitis is a chronic inflammatory skin condition characterized by intense pruritus, xerosis, and impaired skin barrier function due to filaggrin mutations and altered immune response (Th2-mediated). The "atopic march" describes the progression from AD to allergic rhinitis, asthma, and food allergies; a positive family history of asthma strongly suggests the patient carries the atopic phenotype. In Indian clinical practice, AD is increasingly recognized in adolescents and young adults, particularly in urban populations with higher hygiene standards (hygiene hypothesis). The diagnosis is clinical, based on Hanifin and Rajka criteria (≥3 of 4 major criteria: pruritus, early onset, chronic course, personal/family history of atopy). Lesions typically appear on flexural surfaces (antecubital/popliteal fossae, neck, face) and are intensely pruritic, often with lichenification from chronic scratching. Management follows the Indian Academy of Dermatology guidelines: emollients as first-line, topical corticosteroids for acute flares, and calcineurin inhibitors for steroid-sparing therapy.
Why the other options are wrong
A. Erysipelas — Erysipelas is an acute bacterial infection (Group A Streptococcus) presenting with sharply demarcated, raised, warm, erythematous plaques and systemic symptoms (fever, chills). It lacks the chronic pruritic nature and family history of atopy seen here. Erysipelas is acute-onset, not chronic, and would show systemic toxicity—absent in this case. B. Seborrhoeic dermatitis — Seborrhoeic dermatitis presents with greasy, scaly lesions on sebum-rich areas (scalp, face, chest, intertriginous zones) and is NOT intensely pruritic. It lacks the strong family history of atopy and typically affects older individuals or those with Parkinson's disease/HIV. The age and pruritus profile do not fit. C. Allergic contact dermatitis — Allergic contact dermatitis requires prior sensitization to a specific allergen and presents with acute vesicles/plaques in a localized distribution matching the allergen exposure pattern. It lacks the chronic course, family history of atopy, and systemic predisposition seen in AD. ACD is triggered by external contact; AD is intrinsic.
High-Yield Facts
- Atopic dermatitis is a Th2-mediated chronic inflammatory disorder with filaggrin gene mutations causing impaired skin barrier and increased transepidermal water loss (TEWL).
- Atopic triad/march: AD → allergic rhinitis → asthma; positive family history of any atopic disease is a major diagnostic criterion.
- Flexural distribution in adolescents/adults (antecubital fossae, popliteal fossae, neck, face); infants show extensor surfaces.
- Hanifin & Rajka criteria: ≥3 of 4 major criteria (pruritus, early onset, chronic relapsing course, personal/family history of atopy) confirm diagnosis.
- First-line management: emollients (frequent application), topical corticosteroids (Class III–IV for body, Class I–II for face), calcineurin inhibitors (tacrolimus/pimecrolimus) for steroid-sparing therapy.
- Lichenification and excoriation from chronic scratching are hallmark signs; 'itch that scratches' is the defining feature.
Mnemonics
ATOPIC MARCH AD → Allergic Rhinitis → asThma → food allergy (Oral allergy). Remember: atopic diseases progress in sequence; presence of one increases risk of others. HANIFIN & RAJKA (3 of 4 needed) Pruritus + Early onset + Chronic relapsing + (personal OR family history of atopy). Use this to confirm AD diagnosis clinically.
NBE Trap
NBE may pair "itchy lesions + family history of asthma" with contact dermatitis to trap students who confuse extrinsic (contact) triggers with intrinsic atopic predisposition. The family history is the key discriminator—ACD does not run in families; AD does.
Clinical Pearl
In Indian urban practice, AD is increasingly seen in adolescents with a "clean" lifestyle (hygiene hypothesis); the combination of intense pruritus, family atopy, and flexural lesions is pathognomonic. Always ask about sleep disturbance from scratching—it's a quality-of-life marker and guides treatment intensity.
_Reference: Robbins & Cotran Pathologic Basis of Disease, Ch. 25 (Skin); Harrison's Principles of Internal Medicine, Ch. 325 (Eczema); Indian Academy of Dermatology Guidelines on Atopic Dermatitis Management_