[Physiopathologic bases of the treatment of systemic scleroderma].
Numerous drugs have been suggested for the treatment of systemic scleroderma. They may be studied and classified according to their site of action on the chain of events that leads from vascular abnormalities to sclerosis of the skin. Thus, proline analogues, colchicine, lathyrogenic agents, D-penicillamine, coagulation factor XIII and oestrogens are thought to act on collagens and their metabolism. Ketanserin has been suggested by the discovery of tryptophan abnormalities. Corticosteroids exert an inhibitory effect on fibroblasts. The use of calcium antagonists, angiotensin-converting enzyme inhibitors, prostacyclin and anti-platelets rests on the presence of vascular abnormalities. The purpose of treatments with immunosuppressive drugs or plasma exchanges is to act on possible lymphocytic and/or macropageal factors.
D001792:Blood Platelets / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D003238:Connective Tissue / Q000378:metabolism; D004727:Endothelium / Q000378:metabolism; D005347:Fibroblasts / Q000378:metabolism; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism; D046911:Macromolecular Substances; D008264:Macrophages / Q000378:metabolism; D012595:Scleroderma, Systemic / Q000188:drug therapy / Q000503:physiopathology*; D014364:Tryptophan / Q000378:metabolism
D046911:Macromolecular Substances; D014364:Tryptophan; D003094:Collagen
Bases physiopathologiques des traitements de la sclérodermie systémique.