Suppression of secondary hyperparathyroidism by propranolol in renal failure patients.

Renal osteodystrophy in part due to secondary hyperparathyroidism, is one of the major unresolved problems affecting patients on chronic hemodialysis. In addition, evidence has shown that parathyroid hormone (PTH) is toxic to other organ systems besides bone. The results of a prospective study on the effect of propranolol in reducing PTH levels in chronic renal failure patients on hemodialysis are reported. Propranolol administration reduced PTH levels by over 50-75%. The levels of calcium, phosphorus, alkaline phosphatase and hematocrit were variable, but patients with severe derangements in these measurements also seemed to benefit from propranolol. It should now be determined by larger and longer studies whether these biochemical improvements can be translated into clinical benefits.

Hyperthyroidism with normal serum total T4, T3, and thyroid binding protein concentration.

A 60-year-old woman, free of other disease, with severe clinical hyperthyroidism had normal total serum T4 with elevated free T4 concentration and T3 resin uptake characteristic of hyperthyroidism, with thyroid binding globulin (TBG) deficiency. However, serum TBG concentration as determined by immunoassay was normal, suggesting that the biochemical defect affecting the T4 binding sites did not affect is antigenicity. Her total and free serum T3 levels were low-normal with a markedly elevated reverse T3 concentration. These findings, in the presence of clinical hyperthyroidism, are consistent with an impairment in peripheral conversion of T4 to T3, apparently, in this case, due only to long-standing severe hyperthyroidism.

Effects of parathyroid hormone infusion and primary hyperparathyroidism on serum prolactin in man.

Serum PRL, parathyroid hormone (PTH), and Ca levels were measured in 14 patients (8 women and 6 men) with primary hyperparathyroidism. Six normal volunteers (3 men and 3 women) received a 1-h control infusion of 5% glucose containing 2% human serum albumin, a 1-h infusion of the same fluid containing 450 U bovine PTH, and a repeated 1-h infusion of glucose and albumin. Serum PRL was measured during these infusion periods and showed a peak within 30 min of the start of bovine PTH infusion; PRL levels declined therafter in spite of continued PTH infusion. Serum PRL levels returned to normal within 1 h of discontinuance of bovine PTH infusion. The serum PRL levels in patients with primary hyperparathyroidism were within the normal range, and there was no correlation between serum PTH and PRL levels. These results suggest that the PRL response to PTH infusion is a pharmacological rather than a physiological or pathophysiological effect of PTH.

Galactorrhea in sarcoidosis: dynamic studies of prolactin, growth and gonadotropic hormone levels.

Five of 300 women with sarcoidosis had galactorrhea. Basal prolactin levels were mildly but significantly elevated when compared to controls and sarcoidosis patients without galactorrhea. Prolactin levels responded to thyrotropin releasing hormone and L-dopa administration, but not chlorpromazine. Luteinizing hormone and follicle-stimulating hormone concentrations responded normally to luteinizing hormone-releasing hormone in all sarcoidosis patients studied, as did growth hormone to insulin hypoglycemia. These results indicate that galactorrhea in sarcoidosis is an uncommon phenomenon, probably due to hypothalamic dysfunction and associated with mildly elevated prolactin levels.

Symptomatic hypocalcemia following combined calcitonin and mithramycin therapy for hypercalcemia due to malignancy.

Three patients with malignant disease received the usual recommended doses of mithramycin and calcitonin, either concurrently or concomitantly, because of severe life-threatening hypercalcemia. All three patients developed severe, symptomatic hypocalcemia. The mechanisms for this phenomenon are discussed. A possible synergism between calcitonin and mithramycin may prove to be hazardous in such patients and this possibility must be kept in mind when these agents are being considered as a combination treatment for hypercalcemia.

A possible role for propranolol in the treatment of renal osteodystrophy.

The effect of propranolol upon parathyroid hormone (P.T.H) concentrations was investigated in patients undergoing chronic haemodialysis. 9 patients receiving propranolol for the treatment of hypertension or angina pectoris were compared with 25 similar patients not taking the drug. P.T.H. and alkaline phosphatase concentrations were lower in patients receiving propranolol and there was less radiological evidence of renal osteodystrophy in these patients. Prospective studies are needed to determine whether propranolol may be helpful as an adjunct to other therapy in reversing or preventing renal osteodystrophy.

Transient suppression of growth hormone secretion after chronic ethanol intake.

Fifty-two percent of patients with chronic heavy intake of ethanol had an abnormally low growth hormone (GH) response to propranolo-glucagon. The effect of ethanol is transient, since the GH response was normal in patients studied 2 wk or more after withdrawal of ethanol. The low GH response was not due to a difference in the levels of glucose or insulin. Ethanol probably suppresses the GH response by acting on the hypothalamus or pituitary gland. Along with previous data suggesting transient ACTH deficiency in chronic alcoholic patients, our findings suggest that these patients may have multiple hypothalamic-pituitary deficiencies.

Pulmonary function studies before and after jejunoileal bypass surgery.

Nine out of twelve obese patients (75%) demonstrated diminished minute ventilation volume (MVV) prior to jejunoileal bypass surgery. Seven out of the nine patients (78%) showed improvement in the MVV as weight reduction ensued following surgery. Other parameters, including arterial blood gases, did not change after weight loss. Weight reduction as a result of jejunoileal bypass surgery brings about an improvement in pulmonary function.

Glucose metabolism and the response to insulin by human adipose tissue in spontaneous and experimental obesity. Effects of dietary composition and adipose cell size.

[1-(14)C]glucose oxidation to CO(2) and conversion into glyceride by adipose tissue from nonobese and obese subjects has been studied in vitro in the presence of varying medium glucose and insulin concentrations as functions of adipose cell size, the composition of the diet, and antecedent weight gain or loss. Increasing medium glucose concentrations enhance the incorporation of glucose carbons by human adipose tissue into CO(2) and glyceride-glycerol. Insulin further stimulates the conversion of glucose carbons into CO(2), but not into glyceride-glycerol. Incorporation of [1-(14)C]glucose into glyceride-fatty acids by these tissues could not be demonstrated under any of the conditions tested. Both adipose cell size and dietary composition influence the in vitro metabolism of glucose in, and the response to insulin by, human adipose tissue. During periods of ingestion of weight-maintenance isocaloric diets of similar carbohydrate, fat, and protein composition, increasing adipose cell size is associated with (a) unchanging rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet.The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible with weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.