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DESPITE numerous investigations, psoriasis still remains not only an etiologic puzzle but a therapeutic problem. The many failures to correct associated metabolic disturbances, revealed by biochemical observations, is a clear indication that the disease is not caused primarily by hemic changes, but is rather a result of hitherto unrecognized factors. Its frequent occurrence in Central and South China also eliminates the so often mentioned dietetic, racial and climatic preferences of the disease. Among the many hypotheses which have been proposed to clarify the causation of psoriasis, hypofunction of the adrenal glands has been favored by many investigators (Grüneberg,1Riehl2and Kissmeyer, Chrom and Jacobson3). This assumption is based not only on the favorable response to adrenal cortical therapy but also on the observation that psoriasis is accompanied with a vitamin C depletion (Reiss4and Mage5) and responds favorably to its administration. Hypercholesteremia, generally associated with
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Frederick Reiss (1949) studied this question.
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