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AT-A-GLANCE
Lichen nitidus consists of small, glistening, monomorphic, flesh-colored to pink or reddish-brown papules of unknown etiology.
On histopathology, lichen nitidus has a distinct, circumscribed infiltrate of lymphocytes, histiocytes, and giant cells in papillary dermis directly beneath a thinned epidermis.
With lichen nitidus, there is no association with systemic disease.
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The epidemiology of lichen nitidus is unknown. Lichen nitidus does not show a clear racial or sexual predilection and is more common in children and young adults.1 The true prevalence is unknown; however, an early clinical experience reported from the early 1900s estimated lichen nitidus to be approximately 34 cases per 100,000 African American individuals.2 At the Mayo Clinic, the ratio of biopsies of lichen nitidus to lichen planus is 1.7 per 100. Assuming a prevalence of 1% in lichen planus and that the rates of biopsy of lichen planus and lichen nitidus are similar, this would imply a prevalence of approximately 17 cases per 100,000.
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ETIOLOGY AND PATHOGENESIS
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Once considered a tuberculoid reaction, lichen nitidus is currently regarded as an idiopathic lichenoid tissue reaction with distinctive clinical and histologic features.3 The relationship between lichen nitidus and lichen planus is debated.4 The coexistence of both diseases in some patients, the development of lichen planus after generalized lichen nitidus, and the clinical similarities to small papules of lichen planus support the view that lichen nitidus is a variant of lichen planus.5 However, most clinicians and researchers favor the separation of these two diseases as distinct entities based on both clinical and immunologic differences and distinctive histologic changes.6,7 Table 33-1 summarizes some of these differences and similarities. One common theory is that exogenous antigens and allergens stimulate epidermal and dermal antigen-presenting cells (eg, Langerhans cells) to activate a cell-mediated response, initiate lymphocyte accumulation, and form discrete inflammatory papules. Large numbers of Langerhans cells in the infiltrate supports this theory.4,6 After antigen stimulation occurs, the cytokine milieu produced by the inflammatory infiltrate may lead to T-helper type 2 (Th2) cell polarization, which results in superficial dermal granulomas in the appropriate genetic background.8 Functional impairment in cellular immunity has been reported in lichen nitidus with anergic responses to antigen stimulations and the documentation of photo-induced lichen nitidus in association with HIV.8-10
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