A controlled study of the effects of thyrotoxicosis and propranolol treatment on mineral metabolism and parathyroid hormone immunoreactivity

L. E. Mallette, Sheldon Rubenfeld, V. Silverman

Research output: Contribution to journalArticle

9 Scopus citations

Abstract

We studied mineral metabolism in 15 thyrotoxic patients and 15 controls matched for sex, age, and weight. Thyrotoxic subjects showed significantly higher serum calcium, phosphate, alkaline phosphatase, and globulin and lower serum creatinine, magnesium, and albumin. Parathyroid hormone immunoreactivity (iPTH) was measured with three different antisera. Thyrotoxic patients showed markedly reduced iPTH values in the most sensitive assay, a midregion-specific assay based on homologous antiserum BG-6. Antiserum 211 32 gave slightly reduced iPTH values, but antiserum NG-1 gave values that were increased by 65%. The limited sensitivity of these later two antisera, like that of others used earlier for such studies, may have blunted the apparent fall in iPTH (antiserum 211 32) or predisposed the assay to a systematic artifact (antiserum NG-1). These results show that for use in the evaluation of hypercalcemia in thyrotoxic patients, a PTH assay must first be characterized as to the expected result in uncomplicated thyrotoxicosis. Twelve of the thyrotoxic subjects entered a random order cross-over study in which propranolol and placebo were given in double-masked fashion for 6 consecutive days each. Overall, the drug did not alter calcium, phosphate, or magnesium metabolism. It lowered serum calcium only in two overtly hypercalcemic subjects, whose urinary calcium excretion did not decline. These results confirm that propranolol may reduce elevated serum calcium levels in thyrotoxicosis and suggest that in this setting the drug may have a direct or indirect effect on renal calcium metabolism.

Original languageEnglish (US)
Pages (from-to)999-1006
Number of pages8
JournalMetabolism
Volume34
Issue number11
DOIs
StatePublished - Nov 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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