Abstract
Chronic alcohol-use disorder has been imputed as a possible cause of dietary magnesium depletion. The purpose of this study was to assess the prevalence of hypomagnesemia in chronic alcohol-use disorder, and to provide information on intracellular magnesium and on its renal handling. We carried out a structured literature search up to November 2020, which returned 2719 potentially relevant records. After excluding non-significant records, 25 were retained for the final analysis. The meta-analysis disclosed that both total and ionized circulating magnesium are markedly reduced in chronic alcohol-use disorder. The funnel plot and the Egger’s test did not disclose significant publication bias. The I2-test demonstrated significant statistical heterogeneity between studies. We also found that the skeletal muscle magnesium content is reduced and the kidney’s normal response to hypomagnesemia is blunted. In conclusion, magnesium depletion is common in chronic alcohol-use disorder. Furthermore, the kidney plays a crucial role in the development of magnesium depletion.
Highlights
Chronic alcohol-use disorder is a frequent, disabling condition [1], which is often associated with electrolyte derangements such as metabolic acidosis or alkalosis, hypokalemia, hyponatremia, hypocalcemia, and hypophosphatemia [2]
Magnesium plays an essential role in the physiology of the brain, heart, and skeletal muscles; has anti-inflammatory properties; and acts as a calcium-antagonist [3,4]
The results of this meta-analysis and systematic review on magnesium metabolism in chronic alcohol-use disorder may be summarized in three points: (1) both total and ionized circulating magnesium are markedly reduced; (2) skeletal muscle magnesium content is reduced; (3) the normal response to hypomagnesemia of the kidney is blunted
Summary
Chronic alcohol-use disorder is a frequent, disabling condition [1], which is often associated with electrolyte derangements such as metabolic acidosis or alkalosis, hypokalemia, hyponatremia, hypocalcemia, and hypophosphatemia [2]. Magnesium depletion has been reported [2]. Magnesium balance is a function of intake, distribution between the extra- and the intracellular compartments, and excretion. One-third is absorbed in the small bowel. Magnesium is ionized and bound to either small anions or proteins, primarily albumin. Most of the body’s magnesium is inside cells, bound to adenosine triphosphate and other intracellular nucleotides and enzymes, and an integral component of bone mineral. The renal handling of magnesium differs from that of other ions because the major sites of transport are the loop of Henle and the distal convoluted tubule [3,4]
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