Reversible hypertension caused by calcium overloading in a patient with postoperative hypoparathyroidism.

Abstract

A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a twomonth hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] AII. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] AII. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance.These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.Reversible hypertension has been reported to occur during a hypercalcemic period in many patients with or without hyperparathyroidism (Cope, 1960;Moore and Smith, 1963;Major et al., 1966;Weidmann et al., 1972;Brinton et al., 1975;Overbeck et al., 1975;Blum et al., 1977;Marone et al., 1980;Waeber et al., 1982). In these patients, the hypertension has been explained by a direct vasoconstrictor effect of calcium on peripheral blood vessels (Moore and Smith, 1963;Weidmann et al., 1972;Overbeck et al., 1975;Blum et al., 1977;Marone et al., 1980) or a change in the reninangiotensin system (Brinton et al., 1975;Waeber et al., 1982).Recently, we had a patient with postoperative hypoparathyroidism whose blood pressure and plasma renin activity (PRA) rose during The present report deals with this case and the investigation into the pathogenesis of this reversible hypertension. MethodsPRA was determined by the method of Skinner (1967), and plasma aldosterone and plasma cortisol were measured by RIA. The details of these methods are described elsewhere (Takeda et al., 1976). Serum parathyroid hormone levels were measured by RIA with carboxy-and amino-terminal specific antibodies (SRL, Tokyo). Serum calcitonin was determined by RIA (SRL, Tokyo). Urinary aldosterone was determined by RIA as the acid-labile conjugate of aldosterone (Malvano et al., 1976

Australian Endocrine Surgeons Guidelines Aes06/01. Postoperative Parathyroid Hormone Measurement and Early Discharge After Total Thyroidectomy: Analysis of Australian Data and Management Recommendations

“…Clinicians must be alert to the possibility of patients presenting with symptomatic hypercalcaemia (cCa 2+ > 3.0 mmol/L) after being placed on calcium and vitamin D supplementation despite an undetectable PTH level 4 h postoperatively. Any patient with calcium supplementation (especially if combined with vitamin D therapy) is at risk of developing symptomatic hypercalcaemia in the postoperative period and requires weekly monitoring until supplements are ceased 19,20 …”