Increases in serum growth hormone which characterize acute starvation in non-obese individuals were usually absent in anorexia nervosa. Serum LH was decreased with serum FSH apparently normal in the majority. Increased adrenocortical activity as indicated by high basal 11 (OH)-corticosteroids and their incomplete suppression by dexamethasone and hyperresponsiveness to exogenous ACTH was recorded in about one-half of the patients tested. Urinary steroid responses to intravenous metyrapone were normal in all but one patient who had hypothalamic-pituitary hypofunction. Thyroid function was normal but TSH shortage has been reported. Resistance to insulin and a waning of insulin responses to hyperglycemia were noted in these individuals with anorexia nervosa.

Quingestanol acetate (17-α-ethynyl-19-nortestosterone acetate, 3-cyclopentylenol ether), a synthetic progestational steroid, was well tolerated at a dosage of 300 µg/day per os by 17 diabetic women who, with but one exception, were between 50 and 65 years of age and had ceased menstruating. Body weight, systolic and diastolic blood pressure, and the pulse rate were of the same orders of magnitude prior to and during the 12 months of quingestanol treatment. The diabetes mellitus was not affected but oscillometric readings at certain body points decreased during the year of treatment, probably reflecting the natural course of vascular disease in diabetic individuals.Despite changes in certain laboratory indices, i.e. slight increases of variable but usually short duration in serum sodium, chloride, total globulins and their α₂, β- and γ-fractions, SGOT, SGPT, LDH, FSH, chylomicrons, and blood platelets and the decreases in serum potassium, albumin, α₁-globulin, nonesterified fatty acids, β-lipoproteins, and plasma ll(OH)corticosteroids, most of the values remained within the ranges established for normal persons. One year of quingestanol therapy was associated with decreased first-day responses to metyrapone. This suggests, among other possibilities, that quingestanol inhibits the hypothalamic-pituitary controlled output of ACTH.All of the other items monitored during this course of quingestanol therapy remained unchanged.

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Exophthalmos usually did not appear nor did pre-existent exophthalmos progress in thyrotoxic patients treated with desiccated thyroid in full replacement dosages, 2½ to 3 grains per day, simultaneously with thyroid blocking agent therapy, ¹³¹I administration, or thyroidectomy. Indeed, in most patients so treated, exophthalmos present prior to therapy of the hyperthyroidism decreased or disappeared. Our observations are consonant with the hypothesis that full replacement dosages of thyroid hormones started at essentially the same time that treatment of the thyrotoxic state is initiated may provide prophylaxis against the appearance or the progression of the exophthalmos which follows treatment of thyrotoxicosis. We do not intend to suggest, however, that exophthalmos which appears, progresses, or enters a malignant phase after successful treatment of hyperthyroidism at some time in the past is benefited by such treatment.

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