Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a female patient with primary hyperparathyroidism and disturbances of cardiovascular function clinical, biochemical and electrocardiographic as well as bone scintigraphic parameters were analyzed before and during therapy with verapamil (Falicard) for 7 month. Verapamil therapy resulted in decrease of the frequency of the supraventricular tachycardia, and, in higher doses (4 X 120 mg), also reduction of blood pressure, however, with dose limiting bradycardia and prolongation of PQ-time. Both the normalization of serum phosphate level, diminution of hypercalcemia of the ionized calcium and the decrease of hypercalciuria and increase of scintigraphic index as an expression of the decrease of high activity of bone metabolism suggest alterations of the calcium homeostasis. Under oral calcium load the constantly increased PTH values markedly could be suppressed indicating an alteration of intracellular parathyroid calcium set point. Discussion is performed with respect to possible protective metabolic and cardiovascular effects of calcium antagonists in this endocrine functional disorder.
 ...
PMID:[Verapamil in primary hyperparathyroidism]. 276 97

The present investigation was carried out in order to study the acute effects of hypercalcemia on the carbohydrate metabolism in healthy subjects and in patients with non insulin-dependent diabetes mellitus (NIDDM). The combined effect of hypercalcemia and a calcium-antagonistic agent (verapamil) was also studied in healthy subjects, in patients with chronic hypercalcemia, e.g. primary hyperparathyroidism (PHPT). Calcium, infused intravenously to fasting diabetic patients, induced a significant decline in the blood glucose concentration. This was not the case in healthy individuals. When glucose was administered orally during exogenous hypercalcemia, glucose tolerance decreased significantly in the diabetic as well as in the healthy individuals. Verapamil, however, abolished this hypercalcemia effect, and even improved the tolerance for oral glucose when administered intravenously together with calcium in the patients with NIDDM. No such effect of verapamil was seen in the healthy subjects or in the patients with PHPT. Insulin activity was left unaffected by hypercalcemia and/or verapamil in all experimental situations. These findings thus imply that hypercalcemia decreases the tolerance for oral glucose in normoglycemic subjects, and further deteriorates the glucose tolerance in patients with an already impaired carbohydrate metabolism. Verapamil, on the other hand, appears to counteract this effect of hypercalcemia in diabetic patients. Since insulin remains unaffected by calcium and verapamil in the above mentioned situations, it is reasonable to assume that the calcium- and verapamil-induced effects on the glucose tolerance are due to glucose-regulatory factors other than insulin.
 ...
PMID:Hypercalcemic and calcium-antagonistic effects on insulin release and oral glucose tolerance in man. 704 21

Patients with primary hyperparathyroidism have higher serum melatonin concentrations during active disease than after surgical cure. Whether this is caused by hypercalcaemia per se, increased parathyroid hormone secretion or other mechanisms is unknown. We decided to elucidate whether exogenous hypercalcaemia influences melatonin secretion. For this purpose, eight healthy volunteers were infused with calcium and saline on separate days and in random order (experiment A). Hypercalcaemia inhibited nocturnal melatonin secretion by 20% but left urinary melatonin excretion unaffected. If exogenous hypercalcaemia inhibits melatonin secretion, it is reasonable to assume that calcium channel blockers such as verapamil might have the opposite effect. This was investigated in experiment B, in which eight healthy subjects were treated on separate occasions with oral verapamil and placebo. Verapamil did not affect nocturnal melatonin secretion but increased melatonin excretion by 145%. As 6-sulphatoxy-melatonin is the main melatonin metabolite excreted by the kidneys, it was considered important to find out whether verapamil would also influence the excretion of 6-sulphatoxy-melatonin. This was investigated in experiment C, in which eight healthy volunteers were treated, on separate occasions, with oral verapamil and placebo. In this experiment also, verapamil increased urinary melatonin excretion significantly (by 67%), but left excretion of 6-sulphatoxy-melatonin unaffected. These findings imply that verapamil influences the renal and/or hepatic handling of melatonin.
 ...
PMID:Does hypercalcaemia or calcium antagonism affect human melatonin secretion or renal excretion? 917 43