Question

Discussion

The answer is D: lichen planus, which was established by skin biopsy. It was not consistent with a drug-induced lichen planus, because there were no eosinophils and no parakeratosis.

An inflammatory dermatosis of unknown etiology, lichen planus classically presents as shiny, violaceous, flat-topped, polygonal papules, 2 mm to 10 mm in diameter. Fine, lacy, white scale (Wickham's striae) adhere to well-developed papules, resembling a reticulate network of lichen. These are easier to appreciate if a drop of microscope lens oil is placed on the papule and a glass slide is pressed gently over the lesion.

Contact dermatitis due to poison ivy can also present as a linear distribution of pruritic lesions. However, instead of flat-topped papules as seen in lichen planus, the lesions of contact dermatitis are often vesicular.

Discoid lupus erythematosus typically presents as atrophic or scarring plaques on the head and neck. They are usually not pruritic.

Guttate psoriasis is characterized by erythematous plaques with thick white scale, unlike lichen planus, which has a fine, lacy scale.

Verruca plana, or flat warts, are flat-topped like the lesions of lichen planus, but are smooth instead of scaly, and are usually skin-colored, pink, or light brown instead of violaceous.

Affecting less than 1 percent of the population worldwide, lichen planus occurs in both sexes, most often between 30 and 60 years of age. The initial lesions are usually located on the flexural surfaces of the wrists, arms, and legs, but the trunk, thighs, and genitalia also may be involved. Evolving over several weeks, lesions may be grouped, annular, or generalized in arrangement. Trauma during the early stages of evolution may induce the isomorphic (Koebner) phenomenon to produce a linear distribution of papules. While some patients remain asymptomatic, the eruption is often pruritic with severity related to the degree of involvement.¹

Involvement of the oral mucosa occurs in 60 percent of patients and may be the only manifestation of the disease. The most common pattern of oral disease reveals a reticular network of white hyperkeratosis on the buccal mucosa. Involvement of the lips, gums, and tongue is not uncommon. While most cases of mucosal lichen planus are nonerosive and asymptomatic, ulcerative and atrophic variants may cause painful erosions and marked distress.

The appearance of the typical lichen planus papule, characterized by the four Ps (purple, pruritic, polygonal, papule), often allows a clinical diagnosis of the lesion.¹ Histopathologic examination of a biopsy specimen can confirm the diagnosis in atypical cases. Other papulosquamous disorders should be considered in the differential diagnosis, including guttate psoriasis, pityriasis rosea, and discoid lupus erythematosus. Annular lesions may mimic those of granuloma annulare or sarcoid; however, the lesions of these granulomatous disorders lack the fine scale of lichen planus papules. The white buccal lesions of oral lichen planus may necessitate biopsy to exclude leukoplakia, candidiasis, and secondary syphilis.²

Lichen planus-like eruptions may occur following exposure to industrial compounds such as color film developer or with use of many commonly prescribed medications, including diuretics, antihypertensives, and hypoglycemic agents. Exposure and medication history should be reviewed as these lesions resolve after discontinuation of the offending agent.¹

Most localized cutaneous eruptions of lichen planus resolve within 12 to 18 months, leaving residual hyperpigmentation that fades with time. Patients with generalized eruptions or mucosal lesions have a more prolonged course. Topical or intralesional steroids suppress inflammation and cause regression of lesions in mild cases, while more severe cases may require systemic corticosteroids, retinoids, or cyclosporine.³ Antihistamines can be useful for pruritus with recurrence in less than 20 percent of patients.²