Vulvar lichen planus -

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Vulvar lichen planus Gunther , MD UpToDate performs a continuous review of over 375 journals and other resources. Updates are added as important new information is published. The literature review for version 15.3 is current through September 2007; this topic was last changed on January 22, 2007. The next version of UpToDate (16.1) will be released in March 2008. INTRODUCTION —

Lichen planus (LP) refers to an inflammatory dermatologic condition that affects the skin, nails, and mucous membranes, including the mouth, esophagus, conjunctivae, bladder, nose, larynx, stomach, and anus [1]. On the skin, it is most commonly expressed as an eruption of shiny, flat, polygonal, violaceous papules with white striae (Wickham's striae); white reticulate lesions occur on mucosal surfaces. LP may be isolated to the vulva or may be part of a generalized skin eruption. ETIOLOGY — The etiology of LP is not known. An autoimmune mechanism involving activated T cells directed against basal keratinocytes has been proposed [2]. One study of serological typing for

HLA class II antigens in 72 patients reported that DR1 was present in 80 percent of patients with generalized LP, 54 percent with localized LP, 56 percent with drug-induced LP, and 31 percent with mucosal LP, compared to 25 percent of normal controls [3]. The drug-induced form of this disorder usually develops insidiously and can affect any area of the body surface. Oral lesions occur in 30 to 70 percent of cases; the mucosa may be painful and ulcerated [4]. Beta blockers, methyldopa, penicillamine, quinidine, nonsteroidal antiinflammatory drugs (NSAIDs), angiotensin converting enzyme (ACE) inhibitors, sulfonylurea agents, carbamazepine, gold, lithium, and quinidine have all been associated with LP [5]. LP can also be seen in patients with a variety of liver diseases, particularly advanced liver disease associated with hepatitis C virus (HCV); anti-HCV antibodies are present in 10 to 40 percent of these patients but a cause-and-effect relation is uncertain [6]. There are reports of the development or exacerbation of lichen planus during interferon treatment for chronic HCV; the lesions improved when interferon was stopped [7]. LP usually occurs at nonvulvar sites in patients with liver disease. EPIDEMIOLOGY AND PREVALENCE —

Vulvar LP is considered uncommon, occurring in fewer than 10 percent of women with LP seen over a three year period in a dermatology practice [8]. Lichen planus, however, can be difficult to diagnose. Signs and symptoms can be intermittent; it is frequently confused with candidiasis, or even vulvodynia. Vulvar involvement is present in one-half of women with LP elsewhere on the body [9]. The peak incidence of disease is from 30 to 60 years of age [5].