DIF does not replace routine histologic staining as the method of choice for establishing a diagnosis.
DLE 120 TURNING SKIN
DIF of lesional skin can be useful in establishing a diagnosis of cutaneous LE in cases where routine histopathology is equivocal. Dermal mucinosis along with thickened basement membrane is usually noted.Įxamination of the skin for deposits of immunoreactants is called direct immunofluorescence (DIF). In discoid lupus lesions, periadnexal inflammation, follicular plugging, and hyperkeratosis are primarily seen in addition to the interface dermatitis.
In cutaneous LE, basal cell damage (also referred to as vacuolar degeneration, hydropic change, or interface dermatitis) and lymphohistiocytic inflammatory infiltrates are commonly seen. Overlap can be seen in the histologic findings among the various clinical phenotypes, particularly ACLE, SCLE, and discoid lesions. The findings of histopathologic examination in cutaneous lupus vary based on the subtype. Keratinocytes may also participate in lupus skin damage by increasing the apoptotic rate and the production of proinflammatory cytokines such as IFN-alpha and IL-6 for SLE and IFN-lambda for DLE. Another explanation might be that smoking provokes DNA damage, resulting in the formation of DNA adducts and the production of ds-DNA antibodies. hypothesized that smoking might play a pathogenic role in cutaneous lupus erythematosus variants (DLE, tumid lupus) by inducing apoptosis, stimulating T-cell proliferation, and increasing photosensitivity. found that smoking is highly associated with discoid lupus erythematosus. Genes previously associated with SLE are TYK2, IRF5, and CTLA4 and confer an increased risk of developing DLE.Īn analysis of 405 patients by Bockle et al. The interaction between these multiple factors triggers an inflammatory cascade of cytokine, chemokine, and inflammatory cell responses. Some contributing environmental factors include ultraviolet radiation (UVR), medications, cigarette smoking, and possibly, viruses. The pathogenesis of cutaneous lupus erythematosus is multifactorial, with an interplay between genetic and environmental factors. Other less common forms of chronic cutaneous lupus erythematosus include hypertrophic lupus erythematosus, tumid lupus erythematosus, lupus erythematosus panniculitis (LEP or lupus profundus), chilblain LE, oral DLE, as well as DLE lesions on the palms and/or soles.
DLE can also occur as a manifestation of SLE in approximately 20% of patients.
Most patients with DLE do not have significant systemic disease. These patients may or may not report photosensitivity, but lesions are frequently photo distributed and tend to have secondary atrophy or scarring.
The most common subset of chronic cutaneous lupus erythematosus is DLE. Within the category of specific cutaneous lesions, he subdivided these into acute cutaneous lupus erythematosus, subacute cutaneous lupus erythematosus, and chronic cutaneous erythematosus. Gilliam segregated skin lesions into those that are specific and those that are not specifically based upon whether an interface dermatitis was seen on histopathologic examination. James Gilliam described the most commonly used classification of cutaneous lesions in lupus erythematosus. The most common types are acute cutaneous lupus (ACLE), subacute cutaneous lupus (SCLE), and discoid lupus (DLE). There are several types of cutaneous lupus. Lupus erythematosus is a multisystem disorder that predominantly affects the skin.
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