Abstract
The term scleroderma includes different systemic and localized conditions responsible for thickening of the skin. Systemic sclerosis is a systemic disorder of connective tissue characterized by fibrosis of the skin (scleroderma) and involvement of internal organs, including the lung, the heart, the kidney and the gastrointestinal tract (Medsger, 1989). According to the ARA Scleroderma Criteria Cooperative Study, systemic sclerosis may be defined by sclerodermatous skin changes of the metacarpophalangeal joints (major criterion) and two or more of the following features: sclerodactyly, digital pitting scars or loss of digital finger pad substances, or bibasilar pulmonary fibrosis (minor criteria) (Masi et al, 1980). Various pathogenic mechanisms have been proposed for scleroderma, including genetic factors, endothelial T lymphocyte-fibroblast interactions, immune dysfunction, dysregulation of collagen synthesis and environmental factors. In recent years, drug-induced systemic sclerosis and sclerodermalike diseases have been reported in association with bleomycin, pentazocine, appetite suppressants, cocaine, I)-penicillamine, L-5-hydroxytryptophan and carbidopa (Table 1).
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