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Article
January 1937

CALCIUM METABOLISM IN SCLERODERMA

Author Affiliations

Assistant Professor of Dermatology, University of Illinois College of Medicine; Attending Dermatologist, Cook County Hospital; Instructor in Physiology, University of Illinois College of Medicine CHICAGO

From the Department of Dermatology and the Department of Physiology College of Medicine, University of Illinois.

This work was supported by grants from Mead Johnson & Co., the Wisconsin Alumni Research Foundation and the Dean's Fund.

Arch Derm Syphilol. 1937;35(1):188-201. doi:10.1001/archderm.1937.01470190191015
Abstract

Scleroderma, like many other poorly understood diseases, has been ascribed to numerous causes. According to the peculiar experience or view of the observer, trauma, infection and physical agents have been suggested as etiologic factors in scleroderma. Some investigators have incriminated the nervous system and others the endocrine glands, while still others have expressed the belief that combinations of some or all of these factors are necessary to precipitate the disease. Either such varied theories as to the etiology obscure the true cause of scleroderma or the disease is a symptom complex which can be produced by more than one agent. If many excitants can give rise to scleroderma, it would be useful to find some constant characteristic of this symptom complex. There is increasing evidence that at least one finding is consistently associated with scleroderma, namely, disturbance of calcium metabolism. The association is fairly obvious when scleroderma occurs together

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