Can calcium channel blockers cause increased serum levels of parathyroid hormone or calcium?

Fråga: Can calcium channel blockers cause increased serum levels of parathyroid hormone or calcium?

Sammanfattning: Isolated cases of increased concentrations of calcium or parathyroid hormone associated with treatment with calcium channel blockers have been reported in the literature.

Svar: Calcium channel blockers have been reported to cause abnormalities in plasma calcium concentration and parathyroid hormone (PTH) levels. As reviewed in (1), the studies have, however, been conflicting. In some studies, verapamil, nifedipine, and nisoldipine, as well as felodipine, have been reported to increase ionised calcium concentrations, while other studies have not been able to show such an effect (1). Recently, two case reports have described hypercalcaemia during treatment with calcium channel blockers. Samani (2) reported on the worsening of hypercalcemia in a patient with primary hyperparathyroidism who was treated with nifedipine. The calcium concentration fell after treatment with nifedipine was stopped. Subsequently, Sinzinger and co-workers (3) reported on four patients with malignant disease in whom treatment with calcium channel blockers was associated with increased plasma levels of calcium. It was suggested that this might be caused by the stimulatory effect of calcium channel antagonists on the generation of prostacyclin, which, like prostaglandin E2, may increase circulatory calcium by mobilising it in a PTH-like effect from the bones.<br><br>No cases of hypercalcaemia or hyperparathyroidism have been reported to the Swedish Adverse Drug Reactions Advisory Committee.<div id="referenser" style="display:none;">1 Davies, Textbook of adverse drug reactions. 1991; 4th ed: 417 (bifogas)<br>2 Samani NJ: Nifedipine and hypercalcaemia of primary hyperparathyroidism. Lancet 1991; 337: 372 (bifogas)<br>3 Sinzinger H, Rauscha F, Fitscha P, Peskar BA: Calcium antagonists and hypercalcaemia. Lancet 1991; 337: 924 (bifogas)</div>