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FUNCTIONAL HYPOPARATHYROIDISM AND PARATHYROID HORMONE END‐ORGAN RESISTANCE IN HUMAN MAGNESIUM DEFICIENCY
Author(s) -
RUDE ROBERT K.,
OLDHAM SUSAN B.,
SINGER FREDERICK R.
Publication year - 1976
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1976.tb01947.x
Subject(s) - hypocalcaemia , medicine , endocrinology , hypoparathyroidism , parathyroid hormone , magnesium , calcium , magnesium deficiency (plants) , chemistry , organic chemistry
SUMMARY Hypocalcaemia is a well‐recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5.6 mg/dl and mean initial serum magnesium concentration was 0.75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (<150 pg/ml) or normal (<550 pg/ml) in all but two patients. Serial measurments made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24 h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144‐300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30‐60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end‐organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the