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Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypo‐magnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non‐specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some or all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.

In 1939, Hueber (1) reported clinical improvement in patients with thyrotoxicosis after parenteral administration of magnesium. Wiswell (2) subsequently was unable to demonstrate any change in the peripheral metabolism of thyroid hormone in hyperthyroid patients given magnesium sulfate injections, whereas Neguib (3) reported a decrease in size of both toxic and nontoxic goiters and clinical improvement in three thyrotoxic patients given daily injections of magnesium chloride. Tapley (4) demonstrated that the administration of L-triiodothyronine promptly produced negative magnesium balance in two myxedematous patients and called attention to the similarity between the symptoms of thyrotoxicosis and magnesium deficiency, as well as between myxedema and magnesium excess. That the serum magnesium is elevated in hypothyroidism and decreased in hyperthyroidism has long been known (5-7) but has recently been re-emphasized and associated erythrocyte magnesium alterations reported (8).Dempsey and Astwood (9) demonstrated increased production of thyroid hormone in animals maintained in the cold. Hegsted, Vitale, and McGrath (10) reported that the magnesium requirement to maintain maximal growth rates in animals kept at cold temperatures were four times * Submitted for publication December 6, 1965; accepted February 24, 1966. These studies were carried out in our Clinical Center for Metabolic Studies (U. S. Public Health Service grant AM05578-AMP) and were supported in part by U. S.Public Health Service grant NB 03152.A preliminary report has appeared (Proceedings of the Central Society for Clinical Research 1965, 38, 39 those of animals kept at normal temperatures. Vitale, Hegsted, Nakamura, and Connors (5) later reported that the growth inhibition caused by the addition of thyroxin to the diet of young rats could be partially overcome by extra supplements of magnesium. Magnesium inhibits the action of thyroxin on uncoupling of oxidative phosphorylation in vitro. Conflicting reports exist as to the influence of magnesium deficiency on oxidative phosphorylation (11,12).The present investigation was carried out to assess further the relationship between the functional status of the thyroid gland and magnesium metabolism. Hyperthyroid and hypothyroid patients were studied by determinations of serum and erythrocyte magnesiums, exchangeable magnesiums, and by complete balance studies during therapy with propylthiouracil and triiodothyronine, respectively. MethodsClinical materials. Eight hyperthyroid and eight hypothyroid patients were studied in our clinical center for metabolic studies. Clinical findings were classical, and the diagnoses were confirmed by determinations of protein-bound iodines, 24-hour 'I uptakes, basal metabolic rates, and, in selected hypothyroid patients, repeat 'I uptakes after the intramuscular administration of thyroidstimulating hormone. None of the patients had congestive heart failure or were receiving diuretic agents. Two hyperthyroid patients were taking digitalis for control of arrhythmias...

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