Benidipine-induced lichenoid drug eruption

Lichenoid drug eruption (LDE) is an uncommon adverse cutaneous reaction that mimics idiopathic lichen planus (LP) both clinically and histologically.^1,2 However, several distinguishing features, including the absence of Wickham striae, delayed onset after drug initiation, and histopathological features such as eosinophilic infiltrates, parakeratosis, and basal layer vacuolization, help differentiate LDE from classical LP.^1–3 Antihypertensive drugs are frequently implicated, particularly calcium channel blockers (CCBs) like amlodipine and nifedipine.^4,5 In contrast, benidipine—another dihydropyridine CCB widely used in Asia for its renal and cardio-protective properties—has not previously been reported to cause LDE, to the best of our knowledge.^6,7

A 76-year-old woman who presented with a 3-week history of pruritic, erythematous to violaceous papules and plaques symmetrically distributed on both lower legs and thighs. The lesions developed shortly after starting benidipine 4 mg/day for newly diagnosed hypertension. There was no history of new topical products, infections, or photosensitivity. No oral or scalp lesions were noted. The clinical picture prompted consideration of a lichenoid reaction (Fig. 1). A punch biopsy revealed irregular acanthosis, focal hypergranulosis, basal cell vacuolization, pigment incontinence, apoptotic keratinocytes (Civatte bodies), and a band-like lymphocytic infiltrate in the superficial dermis with sparse eosinophils—findings consistent with a LDE (Fig. 2).

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FIG 1. (a) Widespread erythematous to violaceous papular lesions with well-demarcated borders; (b) Lesions showed excoriation, haemorrhagic crusts predominantly on the lower extremities; (c) Scaling, with lichenified plaques were present on the dorsum of the feet; (d) Lesions on the lower extremities, had a slight extensor predilection

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FIG 2. (a) Band-like inflammation in irregular acanthotic epidermis showing hyperkeratosis (haematoxylin and eosin [H&E], 4 ); (b) Acanthotic epidermis showing hyperkeratosis and hypergranulosis (H&E, 10 ); (c) Isolated dyskeratosis in irregular acanthotic epidermis (H&E, 10 ); (d) Diffuse interface vacuolar degeneration at the dermoepidermal junction with sparse eosinophils (H&E, 20 )

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A differential diagnosis of idiopathic LP, cutaneous lupus erythematosus, fixed drug eruption, and lichenoid graft-versus-host disease was considered. However, the clear temporal association with benidipine, absence of systemic findings, and the histological presence of eosinophils and pigment incontinence favoured LDE. We used the Naranjo adverse drug reaction probability scale, which gave a score of 6, indicating a probable causal relationship.

Benidipine was discontinued, and the patient was started on oral methylprednisolone at 40 mg/day with weekly tapering over 3 weeks. Topical mometasone furoate 0.1% cream and oral levocetirizine 5 mg/day were added. Marked improvement was seen within 10 days, and the eruption fully resolved by 6 weeks. No recurrence was seen at a 3-month follow-up, although mild post-inflammatory hyperpigmentation persisted.

Reports of LDE due to amlodipine, nifedipine, and diltiazem exist in the literature; however, no reports implicating benidipine were found.^4–7 This case, therefore, represents the first documented instance of benidipine-induced LDE. In comparison to prior CCB-induced LDEs, the clinical distribution and histological features were similar. However, unlike some reported instances with mucosal involvement or extensive eruptions, our patient had a localised, rapidly resolving course.^4,5

Benidipine should now be included among CCBs capable of inducing LDE. Early identification and withdrawal of the offending agent remain the cornerstone of management, and systemic corticosteroids may expedite resolution.