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A deficiency of thyroxine-binding globulin (TBG) has been recognized in euthyroid subjects but has not been reported in conjunction with a depressed thyroidal I131 uptake. We have studied a 35-yr-old Indonesian male physician who lacked TBG but showed the normal localization of thyroxine (T4) binding in the albumin and prealbumin serum protein fractions. No physical abnormalities were present and mild serum hepatitis was the only prior illness of note. The subject had a consistently low protein-bound iodine (PBI), an increased red blood cell (RBC) uptake of triiodothyronine, and a normal basal metabolic rate (BMR) and serum cholesterol. The thyroidal I131 uptake was markedly low but showed a 7-fold increase after thyroidstimulating hormone (TSH); an abnormal release of trapped I131 was not induced by KSCN. The half-life of radioiodinated thyroxine (T4-I131) was shortened and the turnover rate was increased with a proportionally reduced extrathyroidal organic iodine pool. These findings imply a no...

The complex aspects of androgen steroid metabolism make it important to investigate the relationship between the production rate of testosterone from analysis of a urinary metabolite and the production rate of steroid in the plasma. The plasma production rate of testosterone was estimated by the product of metabolic clearance rate (M. C. R.) and mean plasma concentration and this was compared with the urinary production rate by analysis of specific activity of a urinary metabolite, testosterone glucuronoside. The M. C. R. following single injection of tritiated testosterone calculated according to the method of Tait was 980 1/d S.D.±120 in 5 normal males and 760 and 840 1 in 2 females. The product M. C. R. and mean plasma testosterone indicates a plasma or inner pool production rate of 6.9 mg/d in normal male and maximum 0.8 mg/d in adult female. The urinary production rate was determined by injection of tritiated testosterone, enzyme hydrolysis of urine, chromatographic isolation of testosterone and its oxidized derivative, and determination of the cumulative specific activity. The urinary production rate was 6.5 mg S. D. ±1.9 in male and 1.9 mg/d S. D. ± 0.9 mg in normal female. 1 % of injected tracer was excreted as testosterone glucuronoside. The plasma production and urinary production rates in the male were quite similar, however the discrepancy in the female suggests that approximately 1 mg of testosterone precursor is converted to testosterone in a second compartment not in equilibrium with plasma testosterone.

During the first month after removal of a unilateral aldosterone-producing adenoma, sodium conservation is poor and restriction of sodium intake may result in adrenal insufficiency. The excretion of aldosterone is reduced and does not increase in response to stimulation by administration of corticotropin, angiotensin, and by restriction of sodium intake. Chronic hypervolemia in patients with primary aldosteronism can result in selective suppression of the ability of the adrenal gland to secrete normal amounts of aldosterone immediately after removal of an aldosterone-secreting tumor.

Plasma glucose and glucagon responses to standard meals containing carbohydrate, fat, and protein as in normal diets were studied in 12 subjects with insulin-dependent diabetes and 12 normal subjects. Diabetics had two to three times greater glucagon responses than did normal subjects. Fifteen units of insulin injection did not normalize these excessive glucagon responses, although postprandial hyperglycemia was reduced. Infusion of somatostatin at a dosage of 500 mug/hr prevented glucagon responses and diminished postprandial hyperglycemia by 60%. The combination of insulin and somatostatin caused a progressive fall in plasma glucose levels despite meal ingestion. Somatostatin and insulin, administered subcutaneously in the same syringe, also abolished postprandial hyperglycemia. These studies indicate that excessive glucagon secretion participates in the genesis of diabetic postprandial hyperglycemia. Somatostatin, an inhibitor of glucagon secretion, may thus prove useful as an adjunct to insulin in the treatment of diabetes mellitus.

Growth hormone assays were performed before and after androgen administration in a 12-year-old boy with unexplained growth retardation. A subnormal growth hormone secretion in response to a standard hypoglycemic stimulus was demonstrated, and it was corrected by androgen pretreatment. After that, a normal serum growth hormone level and a temporary growth spurt were demonstrated.

The availability of a sensitive assay for human growth hormone has made it possible to directly measure the effects of various agents purported to alter growth patterns. Acromegalic patients present a special problem both in early diagnosis and in therapy. Being able to measure growth hormone in these patients provides an accurate index of activity and a precise measure of therapeutic effectiveness. In an attempt to determine whether a pituitary block of growth hormone secretion is feasible in this condition, a study was made of the effects of estrogen, androgen and glucocorticoid administration on growth hormone response to a standard insulin tolerance test in a patient with active acromegaly. In the dosage schedules used in this study, it was not possible to suppress either basal growth hormone secretion or blunt its responsiveness to the normal physiologic stimulus of hypoglycemia.