SYSTEMIC AND TOPICAL FACTORS INVOLVED IN THE PRODUCTION OF EXPERIMENTAL CUTANEOUS CALCINOSIS

[摘要] Experiments on rats indicate that, following oral administration of vitamin D2, epilation of a skin region suffices to produce topical cutaneous calcinosis with sclerosis, Intra-or subcutaneous injection of dilute ferric chloride proved even much more effective in this respect. Oral administration of NaH2PO4 or calcium acetate greatly augmented the ability of vitamin D2 to sensitize for the induction of cutaneous calcinosis under these experimental conditions. The same electrolytes also augmented the ability of vitamin D2 overdosage to produce calcium depositions in the cardiovascular system and the kidney. In rats not sensitized by vitamin D2 supplements, similar topical treatment of the skin with FeCl3 induced a histo-chemically demonstrable, rather selective iron deposition in the regional macrophages and collagen fibers. This was not associated with any excessive Ca deposition. Injection of vitamin D2 or DHT into the skin causes no local calcinosis; hence, the effect of these compounds appears to be indirect and not merely dependent upon their concentration in a given tissue area. It remains to be seen whether the experimental cutaneous lesions induced in this manner are fundamentally related to the clinical syndrome of calcifying scleroderma (sclferodermie calcaire); but in any event, they furnish a reliable and simple laboratory model for the study of those factors that influence cutaneous calcification.