Magnesium transport in patients with thyroid disease.

Abstract

The kinetics of radiomagnesium exchange in hyper- and hypothyroid patients was studied by administering high specific activity 28Mg intravenously and utilizing conventional and analog and digital computer techniques of data analysis. In hyperthyroidism, the size of the largest of the 3 exchangeable tissue magnesium fractions derived from the digital computer analysis was increased by 58% compared to control subjects, and in hypothyroidism the size was decreased by 24%. The flux rate of magnesium was increased by 60 to 120 % in all 3 tissue fractions in the hyperthyroid patients compared to the hypothyroid patients. The urinary excretions of 28Mg and 24Mg were 80% greater in the hyperthyroid and 30% smaller in the hypothyroid patients than in the control subjects. In the 4 patients restudied after restoration of euthyroidism, some or all of the abnormalities in magnesium transport returned toward normal. These data indicate that thyroid hormone has a direct stimulatory action on the cellular transport of magnesium. The ability of thyroid hormone, as well as altered extracellular concentrations of magnesium, to influence the cellular transport of magnesium is indicative of a regulated process involving either active transport or facilitated diffusion. A probable but not invariable result of the hormonal stimulation of magnesium transport appears to be a preservation of normal cellular concentrations of magnesium despite a tendency to depletion of extracellular magnesium in hyperthyroidism and to an excess of extracellular magnesium in hypothyroidism.