At first the pathogenesis of sclerodermia is discussed. Disturbed immunological control mechanisms for the activity of fibroblasts with an increased humoral activity are mentioned as causes. Then relevant clinical changes in connection with own investigations are outlined and finally some therapeutic possibilities are mentioned. The pathobiochemical changes of the collagen metabolism of sclerodermia are analysed and own investigations about the laboratory parameters, hydroxyprolin and N-acetyl-neuraminic acid which summarizingly reflect the collagen metabolism in patients with sclerodermia follow. Finally diagnostic possibilities of a renal participation are shown with the help of a quantitative and qualitative protein analysis in the collective urine, in which case a particular point is to be made of the distinction of selectively and unselectively excreted proteins.
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