質子泵抑製劑特異性差，似乎都不同程度地抑製腸道的質子-鉀泵，也許還有其它泵，影響鉀和鎂的吸收，長期使用可引起低鉀低鎂。

Curr Drug Saf. 2011 Jul;6(3):204-6.

Hypomagnesaemia/hypokalemia associated with the use of esomeprazole.

Negri AL¹, Valle EE.

Author information

• ¹Instituto de Investigaciones Metabólicas, Universidad del Salvador, School of Medicine, Buenos Aires, Argentina. [e-mail]

Erratum in

• Curr Drug Saf. 2013 Feb;8(1):75.

Abstract

Magnesium homeostasis is essential for many intracellular processes and depends on dynamic interplay of intestinal absorption, exchange with the bone reservoir, and renal excretion. Hypomagnesaemia may arise from various disorders. We review the case of a 59 year-old man whose only complaint was irritability with a routine analysis showing hypomagnesaemia and hypokalemia while using esomeprazole, a proton pump inhibitor (PPI). Fractional magnesium excretion was low, excluding excessive renal loss. Potassium excretion was 80 mEq/24 Hr in the presence of hypokalemia suggesting hypomagnesaemia-induced kaliuresis as its cause. Hypomagnesaemia partially resolved after oral magnesium supplementation. Esomeprazol suppression corrected hypomagnesaemia. A causal relationship with esomeprazol use was supported by the recurrence of hypomagnesaemia after rechallenge. We review the literature on hypomagnesaemia due to the use of proton pump inhibitors. In the past decade our understanding of transcellular magnesium transport was enhanced by the discovery of the magnesium channel, transient receptor potential (TR PM) 6 and 7 and other proteins that play an important role in its transport. In this light we discuss the possible etiology of proton pump inhibitor related hypomagnesaemia/hypokalemia.

PMID:

22122397

[PubMed - indexed for MEDLINE]

 

 

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Pflugers Arch. 2013 Nov;465(11):1613-20. doi: 10.1007/s00424-013-1306-0. Epub 2013 Jun 12.

Omeprazole enhances the colonic expression of the Mg(2+) transporter TRPM6.

Lameris AL¹, Hess MW, van Kruijsbergen I, Hoenderop JG, Bindels RJ.

Author information

• ¹Department of Physiology, Nijmegen Centre for Molecular Life Science, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Abstract

Proton pump inhibitors (PPIs) are potent blockers of gastric acid secretion, used by millions of patients suffering from gastric acid-related complaints. Although PPIs have an excellent safety profile, an increasing number of case reports describe patients with severe hypomagnesemia due to long-term PPI use. As there is no evidence of a renal Mg²? leak, PPI-induced hypomagnesemia is hypothesized to result from intestinal malabsorption of Mg²?. The aim of this study was to investigate the effect of PPIs on Mg ²?homeostasis in an in vivo mouse model. To this end, C57BL/6J mice were treated with omeprazole, under normal and low dietary Mg²? availability. Omeprazole did not induce changes in serum Mg²? levels (1.48 ± 0.05 and 1.54 ± 0.05 mmol/L in omeprazole-treated and control mice, respectively), urinary Mg²? excretion (35 ± 3 μmol/24 h and 30 ± 4 μmol/24 h in omeprazole-treated and control mice, respectively), or fecal Mg²? excretion (84 ± 4 μmol/24 h and 76 ± 4 μmol/24 h in omeprazole-treated and control mice, respectively) under any of the tested experimental conditions. However, omeprazole treatment did increase the mRNA expression level of the transient receptor potential melastatin 6 (TRPM6), the predominant intestinal Mg²? channel, in the colon (167 ± 15 and 100 ± 7 % in omeprazole-treated and control mice, respectively, P < 0.05). In addition, the expression of the colonic H?,K?-ATPase (cHK-α), a homolog of the gastric H?,K?-ATPase that is the primary target of omeprazole, was also significantly increased (354 ± 43 and 100 ± 24 % in omeprazole-treated and control mice, respectively, P < 0.05). The expression levels of other magnesiotropic genes remained unchanged. Based on these findings, we hypothesize that omeprazole inhibits cHK-α activity, resulting in reduced extrusion of protons into the large intestine. Since TRPM6-mediated Mg²?absorption is stimulated by extracellular protons, this would diminish the rate of intestinal Mg²? absorption. The increase of TRPM6 expression in the colon may compensate for the reduced TRPM6 currents, thereby normalizing intestinal Mg²? absorption during omeprazole treatment in C57BL/6J mice, explaining unchanged serum, urine, and fecal Mg²? levels.

PMID:

23756852

[PubMed - indexed for MEDLINE]

 

 

 

 

所有跟帖： 

• 如果這是主要原因，多吃富含鉀和鎂的食物可能有助於減輕質子泵抑製劑的副作用。 -吃與活- ♂ (138 bytes) () 04/08/2016 postreply 11:18:08

• Thank you for advise. -tryyyyyy- ♂ (32 bytes) () 04/08/2016 postreply 12:12:22