Drug-Induced Lichen Planus

• Several conditions mimic or resemble lichen planus, each with unique characteristics.

Drug-Induced Lichen Planus

• These eruptions are similar or identical to lichen planus, triggered by chemicals through ingestion, contact, or inhalation.
• Manifests as localized or generalized eczematous papules and plaques, with varying desquamation degrees.
• Hyperpigmentation and alopecia may occur; Wickham striae are rare.
• Trunk and extremities are commonly affected symmetrically; flexural involvement is less common.
• Mucous membrane involvement is rare, linked to specific drugs/chemicals.
• A photodistributed pattern can occur with specific drugs/chemicals.
• Immune checkpoint inhibitors like ipilimumab, pembrolizumab, and nivolumab have a high rate of lichenoid eruptions, affecting 17% of patients.
• The latency period ranges from months to over a year, depending on dosage, host response, and other factors.
• Resolution usually occurs in 3-4 months, but gold-induced cases may take years.
• Severity and extent of the disease affect clearance rate; intermittent recurrence is possible.
• Genetic susceptibility is likely important, especially in recurrent cases or with immune-modulating drugs.
• Lichenoid contact dermatitis may result from contact with color film developers, dental amalgams, and aminoglycosides.
• Oral lichenoid eruptions are commonly linked to dental restoration metals like mercury, silver, and gold.

Lichen Planus–Lupus Erythematosus Overlap

• A rare variant combining features of both lichen planus and lupus erythematosus.
• Lesions are red-violet, atrophic patches and plaques with hypopigmentation, telangiectasia, and minimal scale.
• Dorsal extremities, especially hands and nails, are commonly affected; anonychia may develop.
• Classic features of lichen planus and lupus erythematosus are usually absent.
• Some patients may develop systemic lupus erythematosus.
• Lab studies may show weakly positive antinuclear antibody.
• Histology and immunofluorescence show overlapping features of both diseases.
• The disease course is often prolonged and resistant to treatment.

Lichen Planus Pemphigoides

• Combines features of lichen planus and bullous pemphigoid.
• Believed to result from keratinocyte degeneration, exposing autoantigens and leading to antibody formation.
• Alternatively, it may just be lichen planus and bullous pemphigoid coexisting.
• Lichen planus pemphigoides is most common in younger individuals in the four to fifth decades of life.
• Blisters may appear on lichenoid lesions and normal-appearing skin.
• Prognosis is generally good with conventional therapy.
• The Medical College of Wisconsin domain 4 (MCW-4) of bullous pemphigoid antigen 180 (BPAG180) appears to be unique.
• Bullous lichen planus is a key differential diagnosis and can be differentiated on serologies and immunofluorescence.
• Drug-induced cases have been reported.

Keratosis Lichenoides Chronica (Nekam Disease)

• A rare dermatosis with distinct clinical and histologic features.
• Characterized by lichenoid, keratotic papules and plaques in a seborrheic distribution with a linear or reticulate pattern.
• Palms and soles may also be involved.
• Individual lesions tend to be folliculo- and infundibulocentric.
• The eruption is often asymptomatic and difficult to treat.
• Histologically, shows a brisk LTR and parakeratosis with neutrophils in the crust.
• Diagnosis should be made cautiously due to similar reaction patterns in other diseases like lichen planus and lupus erythematosus.

Lichenoid Graft Versus Host Disease (GVHD)

• Chronic GVHD occurs after transplant (typically after 100 days) and can manifest as a dermatitic, sclerodermoid, or lichenoid eruption.
• GVHD is caused by donor cells attacking fast-dividing tissues like the liver, GI tract, and skin.
• Acute GVHD is driven by Th2 cytokine signaling, while chronic GVHD is driven by Th1/Th17 signaling.
• Clinically, characterized by classic lichenoid papules with follicular involvement of the head and neck, as well as oral involvement.
• Onycholysis and cicatricial alopecia may be prominent.
• Histopathology is often indistinguishable from lichen planus, but satellite cell necrosis, plasma cells, and eosinophils may provide subtle clues for diagnosis.

Lichenoid Keratosis

• Typically presents as a single, nonpruritic, brown to red, scaling flat-topped plaque on sun-exposed skin.
• Clinically distinguishable from lichen planus.
• Histologically similar to lichen planus, but may have parakeratosis or remnants of lentigo, seborrheic keratosis, or actinic keratosis.

Lichenoid Dermatitis

• Describes a reaction pattern with nonclassic lichenoid features and spongiosis.
• Further clinical, serologic, and histopathological analysis is needed for alternative diagnoses.
• The differential diagnosis includes dermatitis, drug eruption, lupus erythematosus, lichen planus, and cutaneous T-cell lymphoma.
• The differential diagnosis can be expanded by additional features, specifically granuloma formation.

Drug-induced lichen planus mimics lichen planus, caused by chemical exposure through ingestion, contact, or inhalation. It appears as eczematous papules and plaques. The trunk and extremities are commonly affected, and resolution usually occurs in a few months.