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Abstract
Cutaneous lupus erythematosus is a chronic inflammatory and autoimmune disease with a broad spectrum of clinical manifestations and avariable course.
Lupus specific skin diseases include the subtypes of CLE such as ACLE, SCLE and CCLE or DLE.
The subdivision of these subtypes with different prognosis and course is supported by genetic, clinical, histopathologic, and immunoserologic findings.
The pathogenesis of CLE is currently under extensive research.
Scientific efforts are beginning to clarify the pathophysiology of the disease, but there are clearly many areas of investigation needed to elucidate the complex mechanisms that culminate in CLE. Genetic association with the disease had been reported. However, the exact genetic abnormalities associated with cutaneous forms of LE remain a challenge. Medications, infections, pregnancy or exposure to cold, trauma, UVR and smoking are frequent triggers of CLE.
Every day billions of cells are eliminated by a very tightly orchestrated process called programmed cell death or apoptosis.
In contrast to cell death by necrosis, apoptosis is characterized by a stereotypical pattern of morphological changes, irrespective of the initiating event. These changes include cellular and nuclear condensation and fragmentation and blebbing of the cell membrane.
In these blebs autoantigens are exposed.
Many genes have been shown to be involved in promotion or inhibition of apoptotic cellular response.