Chapter 186 Lichen Planus
Diagnostic Summary
• Lichen planus is an inflammatory, pruritic disease of the skin and mucous membranes described by the “six P’s”: pruritic, polygonal, planar (flat-topped), purple papules, and plaques. Intense pruritus is commonly the primary complaint, although lesions can present without pruritus.
• Skin lesions are flat-topped, violaceous to purple, polygonal or oval, papules 1 to 10 mm wide with sharply defined edges and shiny. Lesions may be grouped, linear (Koebner phenomenon), annular, or disseminated when generalized. White lines (Wickham striae) may be present. A handheld lens and application of a clear oil over a lesion intensifies the visibility of the striae. In dark-skinned patients, postinflammatory hyperpigmentation commonly occurs. Skin lesions may occur anywhere, with a predilection for the trunk and flexor surfaces, particularly the wrists as well as the lumbar region, eyelids, shins, scalp, glans penis, and mouth.
• Oral lesions appear inflamed, with leukohyperkeratosis, manifesting as reticulated white puncta or papules and lines in a lacelike pattern. Plaques may form and can become hyperkeratotic. Erosions with blisters may occur. Usually both buccal mucosae are affected, although the tongue, lips, and gingivae may be as well. Skin lesions occur in 10% to 60% of cases of oral lichen planus. Biopsy should be performed if there is doubt about the diagnosis or if blisters, plaques, or erosions occur in oral lichen planus.
• Other locations include: (1) the genitalia, as papular, annular, or erosive lesions on the penis, scrotum, labia majora, labia minora, and vagina; (2) the scalp, with atrophic skin and scarring alopecia; and (3) the nails, with destruction of the nail fold and bed and with longitudinal splintering.
Variants
• Hypertrophic: Large thick plaques on the feet and shins; more common in African-American males. Hypertrophic lesions may become hyperkeratotic.
• Follicular: Individual keratotic-follicular papules and plaques that lead to cicatricial alopecia. Graham Little syndrome is the complex of spinous follicular lesions, any lichen planus, and cicatricial alopecia.
• Vesicular: Development of vesicular or bullous lesions within or independent of lesions. In the latter, direct immunofluorescence is consistent with bullous pemphigoid, and patients have bullous pemphigoid immunoglobulin (Ig) G autoantibodies.
• Actinicus: Papular lesions in sun-exposed areas, especially the dorsa of the hands and arms.
• Ulcerative: Therapy-resistant ulcers, particularly on the soles, requiring skin grafting.
General Considerations
Etiology is often unknown. Drugs, metals, or infection (hepatitis C virus) resulting in the alteration of cell-mediated immunity may play a role. Human leukocyte antigen–associated genetic susceptibility explains a predisposition in some patients. The immune system plays a role, as evidenced by two findings: First, immunoglobulins (primarily IgM; possibly also IgA and IgG) and complement (C3) are found at the dermal-epidermal junction in 95% of lichen planus lesions. Second, lesions can occur with certain drugs, graft-versus-host disease reactions, dermatomyositis, and as cutaneous manifestations of malignant lymphoma. The primary immune factor involved appears to be cell-mediated processes. In early lesions, activated helper T (TH) cells target basal cells, which may have antigenic alterations. Suppressor T (Ts) cells predominate in older lesions.
Incidence, Onset, and Course
The list of possible causative medications is long. The most common are gold, antimalarial agents, penicillamine, thiazide diuretics, beta blockers, nonsteroidal antiinflammatory drugs, quinidine, and angiotensin converting enzyme inhibitors.1 The interval between administration of the offending agent and the development of lichenoid drug eruptions is usually a few months, ranging from 10 days to several years.1
Therapeutic Considerations
Dental Amalgams
Dental amalgams appear to play a role in the etiology of oral lichen planus. In one study, 161 patients with chronic lichenoid reactions (142) or oral lichen planus (19) underwent replacement of mercury amalgam fillings with alternative substances. Five patients served as controls, receiving no restoration. Evaluation 6 to 12 months after restoration showed that 95% of the patients with chronic lichenoid reactions had marked improvement or complete restoration of normal mucosa. The effect was more apparent for those with gold crowns than those with CM (palladium-based) crowns. In the oral lichen planus group, those areas of lesions in contact with amalgam showed an improvement in 63% of patients, but lesions at other sites were not affected.2 A second study found that if gold crowns are already present, patients should undergo patch testing for gold allergy; removal of the crowns should be considered in those with positive results.3 The former study downplays the significance of patch testing for mercury, as many patch-negative patients still responded to amalgam removal. However, in cases of positive patch-test reactions to mercury compounds, partial or complete replacement of amalgam fillings will lead to a significant improvement in nearly all patients.4,5
Photodynamic Therapy
A retrospective analysis of 50 patients with generalized cutaneous lichen planus treated by broad-band (n = 7) or narrow-band (n = 43) ultraviolet B radiation showed a complete response in 70%; 85% of these respondents were still in remission after a median of 34.7 months.6 Another report is that of a 64-year-old man with lichen planus of the penis that did not respond to steroids; in this case photodynamic therapy was preceded (4 hours prior to treatment) by application of 5-aminolevulinic acid (20%) ointment. The area was irradiated with a Paterson-Whitehurst lamp (Paterson Institute, Christie Hospital, Manchester, United Kingdom) at a center wavelength of 630 nm and a rectangular pass band of 27 nm. The dose was gradually increased to 50 J/cm2 at a fluence rate of 55 mW/cm2 to prevent edema and phimosis. Treatment was repeated after 6 weeks. The lesions resolved completely after another 4 weeks, with no recurrence at 6 months.7 Photodynamic therapy with medium-dose ultraviolet A-1 has successfully treated ulcerative lichen planus of the feet in another case.8
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