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Magnesium and cardiac arrhythmias: nutrient or drug?

The antiarrhythmic potency of Mg has been described repeatedly since 1935, both as a factor in human disease and in animal experiments. Nevertheless, this therapeutic efficacy is rarely mentioned in textbooks. Both the pharmacological effect of Mg and the correction of Mg deficiency have been used in treatment of digitalis toxicity, variant angina, Torsades de Pointes, as well as in arrhythmia of unknown origin. Mg-deficiency can be caused by malabsorption or by excessive urinary loss. Both situations can occur on a congenital basis. The most frequent cause is probably alcoholism. Iatrogenic f

PTH and vitamin D responses during treatment of hypomagnesaemic hypoparathyroidism.

The response of calcium regulating hormones in a patient with hypomagnesaemic hypoparathyroidism was assessed during magnesium infusion. Magnesium repletion was accompanied by prompt restoration of PTH secretion which subsequently stimulated 1,25-diOHD3 production, thus correcting hypocalcaemia. Further, failure of the patient to respond to previous 1 alpha-OHD3 therapy suggests that severe magnesium depletion may also result in a state of acquired resistance to the active metabolites of vitamin D.

Hypomagnesemia, a risk factor in diabetic retinopathy.

The serum magnesium concentration was measured in 71 insulin-treated diabetic outpatients who had had the disease for 10 to 20 years. The patients were divided into two subgroups according to the severity of their retinopathy. As a whole the patients exhibited a definite hypomagnesemia (P less than 0.001) that was most pronounced in the subgroup having the severest degree of retinopathy (P less than 0.01). The subgroups were comparable regarding known risk factors implicated in diabetic retinopathy. Thus, hypomagnesemia appears to be an additional risk factor in the development and progress of

Hypomagnesemia due to renal disease of unknown etiology.

A young man, investigated because of tetanic convulsions and arthritic pains, was shown to have hypomagnesemia, hypermagnesuria, hypokalemia, hypercalciuria, progressive nephrocalcinosis and chondrocalcinosis. In this syndrome, renal function was normal except for the abnormal excretion of electrolytes. Renal sodium conservation was normal. Light and electron microscopic studies of renal biopsy specimens showed the presence of several abnormal tubules. Immunofluorescent staining showed deposits of immunoglobulins in the glomeruli and tubules. Magnesium therapy was started under balance study c

Bone magnesium pools in uremia.

Bone magnesium pools were studied in vitro in bone specimens obtained from control subjects, from patients with chronic renal failure before and after renal transplantation, and in a patient with chronic hypomagnesemia. 30% of bone magnesium is in a surface limited pool present either within the hydration shell or else on the crystal surface. The larger fraction of bone magnesium was shown not to be associated with bone matrix but rather to be an integral part of the bone crystal. With incineration this pool was mobilized at the same temperature that sudden enlargement of bone crystal size occ

Plasma magnesium concentration in primary hyperparathyroidism.

The plasma magnesium concentration has been determined in 73 patients with primary hyperparathyroidism. In most patients it lay within the normal range (1.7-2.3 mg./100 ml.), but in five it was less than 1.6 mg./100 ml. These patients had relatively high urinary magnesium outputs, and one of them, studied in greater detail, failed to retain parenterally administered magnesium. Hence hypomagnesaemia in hyperparathyroidism may be associated with a defect in renal magnesium conservation, which may be reversible.

Синдром мозга из Протон-Помп Инхибитор, вызванный гипомагнетомией: два презентабельных, но повторных случая.

ВВЕДЕНИЕ: Синдромы головного мозга являются редкими, но потенциально серьезными презентациями в отделении экстренной помощи, требующими своевременного диагностики и вмешательства. Дифференциальный диагноз широк, охватывает инсульт, множественный склероз, токсичные реакции и метаболические дисбалансы, такие как гипомагнетемия. Ингибиторы протонных насосов (ИПЦ) все чаще признаются в качестве причины сильной гипомагнетемии, которая может привести к обратимому синдрому головного мозга. Мы представляем два случая обратимого синдрома головного мозга, вызванного гипомагнетемией. Первое дело касается

Совпадение в аннотации оригинала
INTRODUCTION: Cerebellar syndromes are rare yet potentially serious presentations in the emergency department, requiring timely diagnosis an … . DISCUSSION: Hypomagnesemia is an often overlooked but important cause of cerebellar dysfunction. Magnesium deficiency leads to neuronal hyperexcitability, particularly affecting the cerebellum. In both cases, PPI use was the primary cause of hypomagnesemia, with magnesium supplementation reversing most symptoms. Cerebellar symptoms from hypomagnesemia may fluctuate …