Dermatology MCQ - Inflammatory Dermatoses - Lichenoid exanthema
A 58-year-old man undergoing treatment for hypertension and atrial fibrillation develops a widespread, symmetrical eruption 2 weeks after starting a new medication. The rash consists of numerous erythematous to violaceous, scaly papules, many of which coalesce into plaques. Some areas show a fine, reticular, white scale. Lichenoid exanthema
INFLAMMATORY DERMATOSES
10/18/20252 min read
A 58-year-old man undergoing treatment for hypertension and atrial fibrillation develops a widespread, symmetrical eruption 2 weeks after starting a new medication. The rash consists of numerous erythematous to violaceous, scaly papules, many of which coalesce into plaques. Some areas show a fine, reticular, white scale. The eruption is most prominent on the trunk and proximal extremities, sparing the mucosal surfaces. Which of the following is the most characteristic histopathological finding supporting this diagnosis?
A. Necrotic keratinocytes at multiple levels of the epidermis
B. Subepidermal blister with eosinophils
C. Psoriasiform hyperplasia with neutrophils in the stratum corneum
D. Vacuolar degeneration of the basal layer with a band-like lymphocytic infiltrate
E. Non-caseating granulomas in the dermis
Correct Answer: D. Vacuolar degeneration of the basal layer with a band-like lymphocytic infiltrate
Explanation:
The clinical presentation describes a lichenoid exanthema, most commonly a lichenoid drug eruption. This is characterized by widespread, often symmetrical, violaceous, scaly papules and plaques that can resemble lichen planus but is typically caused by a medication. Key clues include the timing relative to a new drug, the widespread (exanthematous) nature, and the description of violaceous, scaly papules. The "fine, reticular, white scale" is a clue to the "lichenoid" interface dermatitis process.
Why the other options are incorrect:
A. Necrotic keratinocytes at multiple levels of the epidermis: This describes the histopathology of erythema multiforme and its spectrum, which is characterized by targetoid lesions and is often triggered by infections (like HSV) or drugs.
B. Subepidermal blister with eosinophils: This is the classic finding in bullous pemphigoid and other autoimmune blistering diseases, not a non-bullous lichenoid eruption.
C. Psoriasiform hyperplasia with neutrophils in the stratum corneum: This is the hallmark of psoriasis. While some drug eruptions can be psoriasiform, the description of violaceous papules and a lichenoid scale points away from psoriasis.
E. Non-caseating granulomas in the dermis: This is the characteristic finding in sarcoidosis and granulomatous diseases, not in lichenoid drug eruptions.
Key Points for Exams
Pathophysiology: A lichenoid tissue reaction is an interface dermatitis where T lymphocytes attack the basal layer of the epidermis, leading to keratinocyte apoptosis (Civatte bodies).
Common Drug Triggers: Key drug classes to know for exams include:
Antihypertensives (e.g., ACE inhibitors, beta-blockers, thiazide diuretics)
Antimalarials (e.g., hydroxychloroquine, quinine)
Anti-inflammatories (e.g., NSAIDs)
Gold salts
Tumor Necrosis Factor-alpha (TNF-α) inhibitors
Prognosis: Excellent upon identification and withdrawal of the offending agent. The eruption typically resolves over several weeks to months. Post-inflammatory hyperpigmentation is very common and can be prolonged.
Management:
Identify and discontinue the causative drug. This is the most critical step.
Symptomatic relief: Topical corticosteroids are first-line to reduce inflammation and pruritus.
Severe cases: For widespread, severe, or symptomatic cases, a short course of systemic corticosteroids may be considered.
Address hyperpigmentation: Patients should be counseled that the hyperpigmentation will fade with time; sun protection is crucial.
© 2025. All rights reserved.