A 12-year-old boy is brought to the office due to a rash on the posterior neck. The patient has had this rash intermittently over the past several years. During the last 2 months, the rash has become increasingly pruritic with the cooler weather, and the patient is constantly scratching his neck. The patient has no other medical conditions and takes no medications. Vital signs are normal. The posterior neck is shown in the image below:
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Which of the following is the most likely cause of this patient's rash?
This patient with a pruritic, lichenified plaque on the posterior neck most likely has chronic atopic dermatitis (eczema), a common inflammatory condition that begins in infancy or early childhood and often flares with low humidity (eg, winter months) or excessive heat. The pathogenesis of atopic dermatitis is multifactorial and includes immune dysfunction (eg, a Th2-skewed response) and genetically mediated epidermal barrier dysfunction.
Of the epidermal components, filaggrin is thought to play a key role in maintaining skin barrier function. Loss-of-function mutations result in decreased natural moisturizing factors, impaired keratin filament aggregation, and decreased tight junction expression. These changes result in loss of epidermal water content, increased permeability to environmental allergens/irritants, and skin inflammation.
Clinical findings in acute atopic dermatitis include intensely pruritic, dry, erythematous papules and/or vesicles; histologic findings include spongiosis (ie, epidermal intercellular edema), as well as T-cell, eosinophil, and mast cell infiltration. In contrast, chronic lesions present with lichenified plaques due to repetitive scratching, corresponding to regions of hyperkeratosis (epidermal thickening) with elongated rete ridges.
(Choice A) Cutaneous infection with the mite Sarcoptes scabiei causes scabies, which manifests as intensely pruritic, excoriated papules (not lichenified plaques) in the finger webs, wrists, axillae, and genitalia. When left untreated, the rash spreads and does not follow an intermittent course, as in this patient.
(Choice B) Trichophyton rubrum causes tinea corporis, which presents as pruritic, scaly, annular patches, not lichenified plaques. Untreated infection usually results in expansion or spread of the rash.
(Choice D) Insulin-mediated keratinocyte and dermal fibroblast proliferation occurs in acanthosis nigricans, a rash commonly involving the posterior neck that is typically seen in insulin-resistant states (eg, obesity, type 2 diabetes mellitus). In contrast to the marked pruritus seen in this case, acanthosis nigricans is asymptomatic.
(Choice E) Mutation of the p53 tumor suppressor gene in keratinocytes (eg, from chronic sun exposure) can lead to development of actinic keratosis, the proliferation of atypical keratinocytes within the epidermis. Although this condition causes hyperkeratotic papules or plaques on sun-exposed areas, lesions are typically small (<1 cm) and occur mostly in older adults.
Educational objective:
Atopic dermatitis is characterized by epidermal barrier dysfunction due to loss-of-function mutations in filaggrin, a key epidermal component. Increased transepidermal water loss, skin permeability, and inflammation result in erythematous dry skin and pruritus, with chronic disease presenting as lichenification from repeated scratching.