[Acute hypercalcemia and hypomagnesemia in a case of primary hyperparathyroidism].
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Biomedical subjects
Publications and source records attributed to J Corvilain.
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The present study concerns eighteen chronic alcoholics with minimal liver damage. A significant reduction in total serum T4 with an accompanying drop in circulating TBG was observed in these otherwise euthyroid patients. During alcohol withdrawal, we observed a rapid increase in T4 and TBG into the normal range. We suggest that the fall in the level of circulating thyroxine-binding globulin is related to a defect in its synthesis or secretion by the liver due to ethanol consumption. Caution is recommended in the interpretation of thyroid function tests in chronic alcoholics.
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Plasma immunoreactive parathyroid hormone level, urinary excretion of adenosine cyclic 3',5'-monophosphate (cyclic AMP) and the sensitivity of the renal tubule to calcium infusion and to parathyroid extract were investigated in a patient with nonfamilial hypophosphatemic osteomalacia. Plasma immunoreactive parathyroid hormone concentration was normal and basal urinary excretion of cyclic AMP was increased. Renal cortical adenylate cyclase, as measured by urinary cyclic AMP excretion, was certainly as sensitive to exogenous parathyroid extract as in normal subjects. After a previous calcium infusion, a greater parathyroid-hormone-sensitive component of phosphorus transport in the kidney was present than in two control subjects. Our results indicate that in nonfamilial hypophosphatemic osteomalacia the renal tubule could be hyperresponsive to parathyroid hormone.
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Mineral metabolism is frequently disturbed in hyperthyroidism. In a group of seventy-two patients with hyperthyroidism, we observed an increase in serum diffusible calcium in 50% of the cases, elevated inorganic phosphorus in 30% and elevated alkaline phosphatase in 44% of the cases. Correlations existed between the values of diffusible calcium, inorganic phosphorus, alkaline phosphatase and certain indices of thyroid function (T4, FT41, T3, FT3I), of which that with T3 was the best (P less than 0.001). Our results suggest that the magnitude of the disturbances of mineral metabolism depends on the severity of the hyperthyroidism and that it is the T3 level that constitutes the best index of that severity.
Plasma levels of immunoreactive calcitonin (iCT) and parathyroid hormone (iPTH) have been measured sequentially in 6 patients following successful renal transplantation (RT) and in 3 patients during the recovery phase of acute renal failure (ARF). iCT and iPTH returned to normal values within a few days when glomerular filtration improved; both hormones rose in cases of acute graft rejection. Unlike iPTH iCT did not follow closely the variations of creatinine, iCT even rising before creatinine in one graft rejection. These observations could possibly be explained by a dissociation between the renal metabolism of iCT and the glomerular filtration.
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1. The parathyroid hormone-like biological activity of concentrated urine was measured by the increase of plasma calcium concentration after intravenous injection of the sample into chickens. 2. Urine was tested in hypoparathyroid patients, normal volunteer subjects, primary hyperparathyroid patients before and after surgery and patients with secondary hyperparathyroidism. 3. In primary and secondary hyperparathyroidism the biological activity was significantly higher than in urine from normal subjects, which was in turn significantly higher than the activity in the urine of hypoparathyroid patients. This bioactivity diminished after surgical removal of a hyperparathyroid adenoma. 4. Decreased activity after trypsinization indicated the peptidic nature of the hypercalcaemic substance.
Urinary cyclic AMP was studied in 22 female and in 6 male hyperthyroid normocalcemic patients and in 3 hyperthyroid hypercalcemic men. Cyclic AMP/creatinine ratios were elevated both in female (4.12 +/- 0.26 mumoles/gm creatinine) and male (3.92 +/- 0.41 mumoles/gm creatinine) hyperthyroid normocalcemic patients as compared with normal female and male controls (2.85 +/- 0.20 and 2.54 +/- 0.14 mumoles/gm creatinine, respectively). However, there was no difference in the 24-hour urinary cyclic AMP excretion of both hyperthyroid and normal subjects. The hyperthyroid hypercalcemic men excreted less (2.47 +/- 0.19) mumoles/24 hr) cyclic AMP/24 hr than the normal male controls. In the thirteen female patients, studied when euthyroid, the cyclic AMP/creatinine ratio was normalised.
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