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of sodium and aldosterone possessed by amphenone. Thyroid function also was not affected. SU 4885 is much the less toxic of the two drugs, gastric disturbances being the only consistent symptom. The excessive drowsiness which severely limits the use of amphenone did not occur.Although the action of SU 4885 on other adrenal steroids, notably oestrogens, has not yet been studied, the relatively large doses required to suppress hydrocortisone together with the formation of 1 l-deoxyhydrocortisone and probably deoxycortone do not indicate that this particular drug has immediate clinical application as an adrenal inhibitor. On the other hand, it seems likely that further compounds will be elaborated by means of which selective inhibition of adrenal enzyme systems may be satisfactorily achieved in patients.Summary The effect of a new adrenal inhibitory compound, SU 4885, has been studied in eight patients. Inhibition is directed particularly at adrenal steroid 1 1,3-hydroxylation, so that 11-deoxyhydrocortisone (compound S) and its urinary metabolite tetrahydro-S were found in relatively large quantities in blood and urine. In sufficient dosage, orally or intravenously, SU 4885 appeared capable of reducing the levels of hydrooortisone and its urinary metabolites.The toxicity of SU 4885 was significantly less than that of amphenone B.

Serum zinc, copper, iron, and vitamin A levels were determined in patients with leprosy and healthy controls. Leprosy patients were classified according to the Ridley and Jopling classification and divided into two main groups as follows: tuberculoid, which consisted mainly of borderline tuberculoid patients and lepromatous, which consisted of borderline lepromatous and true lepromatous patients. The lepromatous group was found to have significantly lower serum levels of zinc and iron and elevated levels of copper. Vitamin A levels were also significantly lower in the lepromatous groups than in the tuberculoid group. Furthermore, the true lepromatous vitamin A determinations were significantly lower than those of the borderline lepromatous patients. The mechanism of these alterations in trace elements is probably due to a redistribution of these metals from the blood to various tissues; brought about by the release of leucocyte endogenous mediators by continuing phagocytosis of tissue macrophages in the lepromatous group of patients.

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