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Biomedical subjects

J F Caro

Publications and source records attributed to J F Caro.

13 recordsLinked to original sources
PubMed1979

Prostaglandin E and hypercalcemia in breast carcinoma: only a tumor marker? A need for perspective.

Prostaglandin E concentrations were measured in a patiet with breast carcinoma, hypercalcemia, undetectable parathyroid hormone (PTH) and no evidence of bone metastases. Catheterization of the drainage bed of her tumor documented production of E series prostaglandins. Treatment with the largest recommended doses of indomethacin for 10 days failed to lower her plasma prostaglandin E (PGE) concentrations or to correct the hypercalcemia, but it normalized urinary excretion of PGE. Subsequent chemotherapy reduced prostaglandin concentrations toward normal values concomitant with a reduction of clinically estimated tumor burden. During this period of time, serum calcium concentrations had no consistent relationship to the plasma PGE levels. We suggest that PGE merely reflected the tumor burden of this patient and did not directly contribute to the genesis of her hypercalcemia. The pertinent literature relating PGE and hypercalcemia is reviewed.

Antineoplastic Agents↗
PubMed1978

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.

Adolescent↗
PubMed1978

Mechanisms of hypercalcemia in malignancy.

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.

Bone Neoplasms↗
PubMed1978

"Normal suppression" to dexamethasone in Cushing's disease: an expression of decreased metabolic clearance for dexamethasone.

The adrenal cortical function of a patient with pituitary-dependent Cushing's syndrome exhibited normal responsiveness to conventional doses of dexamethasone (Dex) over several years of evaluation. "Periodic hormonogenesis" did not seem to explain the phenomenon. Plasma concentrations of Dex were measured to ascertain whether an abnormality in Dex metabolism might explain the apparent discrepancy in Dex responsiveness. Plasma levels of Dex after oral administration of the steroid were higher than normal, suggesting that decreased clearance of Dex accounts for the phenomenon of "normal suppression" in this patient with Cushing's syndrome.

Adrenocorticotropic Hormone↗
PubMed1978

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.

Calcitonin↗
PubMedDate not supplied

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.

Adult↗