Lichenoid drug eruptions are distinctive eruptions characterized by violaceous, scaling papules and plaques that are typically symmetrical and widespread. Pruritus is a common feature. The classic sites of involvement in lichen planus, such as the wrists, may be spared. Other clinical features that may suggest that a drug is causative include the presence of larger plaques, secondary eczematization, significant post-inflammatory hyperpigmentation, and lack of Wickham striae. Lichenoid drug eruption may progress to exfoliative erythroderma. Photolichenoid eruptions favor photoexposed areas. Oral involvement from a drug is uncommon and may occur with skin involvement or may be isolated.

Multiple medications have been implicated in lichenoid drug eruptions. Classic cutaneous lichenoid drug eruptions may be caused by angiotensin-converting enzyme (ACE) inhibitors, antimalarials, beta blockers, gold, lithium, mercury amalgam, methyldopa, penicillamine, quinidine, sulfonylureas, thiazide diuretics, tumor necrosis factor (TNF)-α inhibitors, and tyrosine kinase inhibitors. Cutaneous and oral lichenoid reactions may be caused by ACE inhibitors, allopurinol, anticonvulsants, antiretrovirals, gold, ketoconazole, and NSAIDs. Photodistributed lichenoid drug eruptions may be caused by carbamazepine, chlorpromazine, diltiazem, ethambutol, quinidine, quinine, tetracyclines, and thiazide diuretics.

Typically, the eruption occurs 2-3 months after initiation of the culprit medication, although onset may be as short as a few weeks or as long as several years. Resolution may take months or up to a year after its discontinuation; however, there are reports of resolution while an individual remains on the medication. Oral lichenoid drug eruptions occur predominantly in adults, although pediatric cases have been reported.

Related topics: lichen planus, oral lichen planus, lichen planopilaris