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B Coevoet

Publications and source records attributed to B Coevoet.

At least 55 records · Page 3Linked to original sources
PubMed1979

Acute effects of propranolol and metoprolol on plasma concentrations of parathyroid hormone and calcitonin in uraemic patients.

Nine uraemic patients not yet on dialysis received IV 1 microgram/kg/min of propranolol for 85 min after a priming dose of 1 mg. Fifteen days later six of them received IV 1.2 microgram/kg/min of metoprolol after a priming dose of 1.2 mg. Plasma concentrations of PTH and calcitonin decreased significantly with propranolol but not with metoprolol. No change was observed with either drug as regards plasma concentration of total and ionised Ca and PO4. Heart rate was decreased similarly with both drugs. We conclude that (i) propranolol acutely suppresses PTH and Calcitonin secretion in uraemic patients. This warrants further studies to assess its long term effects on the secretion of these hormones and on renal osteodystrophy; (ii) the contrast between the significant effect of propranolol and the lack of effect with metoprolol supports the concept that PTH and CT secretion are moderated through specific beta 2 receptors.

Adult↗
PubMed1978

Portal hypertension in systemic mastocytosis.

We report the case of a 66-year-old male patient with portal hypertension related to systemic mastocytosis. The liver was enlarged; microscopic examination showed portal mast cell infiltration and fibrosis. Portal hypertension was evidenced by splenomegaly, esophageal varices, and increased wedged-free hepatic venous pressure gradient. Arteriography showed that portal vein was patent. Portal hypertension could be the consequence of intrahepatic block due to mast cell infiltration and/or fibrosis of the liver.

Aged↗
PubMedDate not supplied

[Primary hyperparathyroidism. Current aspects of its diagnosis apropos of a case with digestive and neuropsychiatric manifestations].

On the basis of a dramatic hypercalcemia revealed by digestive and neuropsychic symptoms and related to a primary hyperparathyroidism, the authors recall all the clinical circumstances which should lead to determination of plasma calcium as well as the clinical and biological particularities which, in front of a hypercalcemia, suggest a primary hyperparathyroidism. The stress the usefulness and the limits of the dosage of plasma immunoreactive parathyroid hormone as well as the difficulties to differentiale primary from paraneoplasic hyperparathyroidism. The recent pathophysiological concepts of malignant hypercalcemia reviewed.

Aged↗