Alterations of long-chain free fatty acid and magnesium concentrations in acute myocardial infarction.

Sixteen patients with acute myocardial infarction were subjects of a study of the changes in plasma magnesium and long-chain free fatty acid (FFA) levels. In each patient, there was a sharp fall of magnesium levels and a sharp rise of FFA levels shortly after onset of pain. Magnesium and FFA values returned to normal within three days. An absolute fall in total magnesium level and a probable fall in magnesium ion concentration could be important factors in arrhythmias during the first two days. The simultaneous rise in FFA and fall in magnesium levels in a variety of pathologic and physiologic conditions affords an explanation for divergent changes in FFA and magnesium concentrations in acute myocardial infarction. The FFA rise appears to be the fall in magnesium levels, which has been previously unexplained.

Cardioskeletal mitochondrial myopathy associated with chronic magnesium deficiency.

A 3-year-old boy presenting with convulsions and carpopedal spasm had hypomagnesemia and hypermagnesuria due to congenital magnesium-losing nephropathy. Despite chronic oral and intermittent intravenous magnesium supplementation, he remained chronically hypomagnesemic. At age 4, he developed a progressive proximal myopathy and dilated hypertrophic cardiomyopathy that ultimately contributed to his death at age 14 years. Skeletal and cardiac muscle specimens showed a mitochondrial myopathy with increased numbers of enlarged, structurally abnormal mitochondria. Muscle magnesium content was markedly decreased. Chronic oral and intermittent intravenous magnesium supplementation may be inadequate to prevent the progressive cardioskeletal myopathy associated with the chronic magnesium deficiency of congenital magnesium-losing nephropathy.

Relationship of free fatty acids and magnesium in ethanol withdrawal in dogs.

A group of dogs was conditioned to drink 4-6 g ethanol/kg/day for long periods. Ethanol ingestion was interrupted at monthly intervals in order to study some metabolic changes of the withdrawal period. Plasma long chain free fatty acids (FFA) increased by a maximum mean of 1.4 meq/liter (threefold), and magnesium (Mg) decreased by a maximum mean of 0.4 meq/liter (75% of control during the first 24 hr of simple ethanol withdrawal. Because magnesium salts of FFA are very insoluble, these divergent changes of Mg and FFA suggest that lipolysis may be responsible for the hypomagnesemia that occurs in ethanol withdrawal. In order to control lipolysis, glucose-insulin, glucose alone, and fructose alone were given intravenously for a 4-hr period beginning 14 hr after withdrawal. FFA fell by a maximum of 65% or 0.44 meq/liter and Mg fell by a maximum of 0.31 meq/liter during the glucose-insulin infusions. Nicotinic acid (10-20 mg/kg) in saline produced an identical drop in FFA and a slight rise in Mg. After stopping the nicotinic acid infusion, a sharp rebound rise in FFA and a sharp fall in Mg occurred similar to the simple withdrawal experiments. The sharp divergent changes in FFA and Mg after cessation of nicotinic acid infusion support the prime role of FFA-effecting movements of Mg and the thesis that FFA bind Mg. Control of lipolysis is theoretically sound in therapy of the ethanol withdrawal syndrome.

Hirsutism. Pathophysiology, clinical evaluation, treatment.

Hirsutism is generally an androgen-mediated disorder. Tremendous progress has been made in elucidating the numerous clinical disorders that can cause it. Systematic evaluation of hirsute women must be directed at determining the cause of hyperandrogenemia, which in turn allows specific and effective therapy to be initiated.

Magnesium deficiency.

Over the past 40 years, human magnesium deficiency has become recognized as a world-wide clinical problem. In 1926, Leroy (1), demonstrated the absolute need of magnesium for growth and life in mice, and the need for magnesium in plants was demonstrated in 1860. Although clinical deficiency was first reported in 1934, it was not until the 1950s that interest in clinical magnesium deficiency developed rapidly. Before the 1950s, textbooks of medicine, pediatrics and biochemistry did not mention magnesium disturbances. In this paper I shall emphasize the recognition and treatment of magnesium deficiency by giving details of the setting, i.e. illnesses, the multifaceted manifestations, the laboratory findings and safe protocols for treatment.