Abstract
Administration of desoxycorticosterone acetate in comparatively high doses causes nephrosclerosis with increased blood pressure and disturbances in electrolyte metabolism, a fact which has been demonstrated in the chick, dog, cat, rat and monkey. Unilateral nephrectomy and a high intake of sodium chloride facilitate the production of these toxic actions of desoxycorticosterone acetate.1In addition to the nephrosclerosis, the most striking features of this overdosage are the formation of Aschoff bodies in the heart and the presence of periarteritis nodosa,2a condition occasionally seen in man following an attack of rheumatic fever. Since in addition choreiform twitches and a few rare cases of arthritis were also encountered in desoxycorticosterone acetate treated animals, it may be said that all the elements of the complex rheumatic syndrome were reproduced in the experimental animal. However, the great frequency of joint manifestations in the spontaneous disease of man and its comparative rarity in
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