HYPOMAGNESAEMIA: STUDIES OF PARATHYROID HORMONE SECRETION AND FUNCTION

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Abstract
Nine patients with hypomagnesemia were studied. Six had Mg deficiency secondary to malabsorption or diarrhea and 3 had excessive urinary losses of Mg. Hypocalcemia was also present in 8. Parathyroid hormone (PTH) was measured using amino-terminal and carboxy-terminal specific immunoradiometric assays and also, in 1 patient, using a cytochemical bioassay. Amino-terminal PTH (N-PTH) varied directly with the concentration of Mg; carboxy-temrinal PTH (C-PTH) was raised in all patients. When Mg was injected, both N-PTH and C-PTH rose regardless of the initial concentrtion, indicating that hypomagnesemia was limiting PTH secretion. The clearance of endogenous PTH was measured in 1 patient, after injection of Mg. Seven minutes after reaching its peak, C-PTH had fallen to 69% and N-PTH fell to 22% of its maximum values; the initial half life of N-PTH was < 2 min. In the same study biologically active PTH (bio-PTH) disappeared rapidly with a half-time of disappearance of 1.2 min. Responsiveness to PTH was measured by the rise in plasma cAMP following PTH injection. The rise in plasma cAMP was inversely related to the concentrations of Mg and PTH at the time. The concentration of PTH rather than the degree of hypomagnesemia is the most important factor determining the responsiveness of target tissues to PTH in Mg deficiency.