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INTRODUCTION

Lichen planus (LP) is a common inflammatory disease involving the skin and mucous membranes. Many clinical variants exist that include atrophic, ulcerative, bullous, annular, linear, inverse, hypertrophic, lichen planopilaris, actinic LP and LP pigmentosus.

EPIDEMIOLOGY

Incidence: About 0.5%

Age: 30 to 60 years

Race: All races are affected equally in most variants

Sex: Higher incidence in females

Precipitating Factors: Most commonly idiopathic medications may induce a LP-like eruption

PATHOGENESIS

Primarily, a T-helper cell-mediated reaction

PHYSICAL EXAMINATION

Most commonly, primary lesions consist of multiple violaceous, polygonal, flat-topped, grouped papules, and plaques that are usually pruritic. Their surface is shiny or transparent and may exhibit small gray-white punctae or reticular fine white lines known as Wickham’s striae. The lesions favor the oropharynx, flexural wrists, dorsal hands, medial thighs, shins, trunk, and genitalia. Postinflammatory hyperpigmentation is common. Actinic LP and LP pigmentosus can present with melasma-like hyperpigmented patches on the forehead and the face (Figs. 54.154.3).

Figure 54.1

Actinic LP on the forehead, temples, and lateral cheek, mimicking melasma

Figure 54.2

Generalized lichen planus in a patient with skin type 1V–V involving the trunk and buttocks with postinflammatory hyperpigmentation

Figure 54.3

Hypertrophic lichen planus on the legs of 4 years duration resistant to topical and intralesional steroid therapy. The patient improved markedly after 1 month treatment with acetretin

DIFFERENTIAL DIAGNOSIS

Psoriasis, lichen simplex, lichenoid graft-versus-host disease, chronic cutaneous lupus erythematosus, lichenoid drug eruption, melasma.

LABORATORY DATA

Given the association with hepatitis B and C, hepatitis serologies can be investigated.

Dermatopathology

Pathology reveals lichenoid interface dermatitis, hyperkeratosis, hypergranulosis, saw-tooth acanthosis, associated with colloid or civatte bodies.

COURSE

Spontaneous remission of cutaneous LP occurs within 1 year of onset in the majority of patients. Oral LP persists for many years. Squamous cell carcinoma may arise from these lesions, predominantly from the oral variant (Fig. 54.4).

Figure 54.4

(A) Oral lichen planus at baseline. (B) Two month follow-up after 18 treatments with excimer laser administered weekly (Courtesy of Charles Taylor, MD)

MANAGEMENT

Topical Treatment

  • Corticosteroids, topical, intralesional

  • Immunomodulators, such as tacrolimus

  • Cyclosporine retention mouthwash for oral LP

Systemic Treatment

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