Hipomagnesemia asociada a tratamiento con omeprazol y test genético negativo para mutación en TRPM6

Fernández–Fernández, Francisco José; Sesma, Pascual; Caínzos-Romero, Tamara; Ferreira, L F

doi:10.1016/j.medcli.2010.07.015

Cited by 7 publications

(2 citation statements)

References 9 publications

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“…They were 45 reports detailing individual cases [ 2 , 19 – 62 ], 14 case-control, cross-sectional studies [ 5 – 18 ] and one report based on the United States Food and Drug Administration data [ 63 ]. The case of a Spanish patient reported twice in the literature was considered only once [ 33 , 34 ].…”

Section: Resultsmentioning

confidence: 99%

Hypomagnesemia Induced by Long-Term Treatment with Proton-Pump Inhibitors

Janett

Camozzi

Peeters

et al. 2015

Gastroenterology Research and Practice

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In 2006, hypomagnesemia was first described as a complication of proton-pump inhibitors. To address this issue, we systematically reviewed the literature. Hypomagnesemia, mostly associated with hypocalcemic hypoparathyroidism and hypokalemia, was reported in 64 individuals on long-term proton-pump inhibitors. Hypomagnesemia recurred following replacement of one proton-pump inhibitor with another but not with a histamine type-2 receptor antagonist. The association between proton-pump inhibitors and magnesium metabolism was addressed in 14 case-control, cross-sectional studies. An association was found in 11 of them: 6 reports found that the use of proton-pump inhibitors is associated per se with a tendency towards hypomagnesemia, 2 found that this tendency is more pronounced in patients concurrently treated with diuretics, carboplatin, or cisplatin, and 2 found a relevant tendency to hypomagnesemia in patients with poor renal function. Finally, findings likely reflecting decreased intestinal magnesium uptake were observed on treatment with proton-pump inhibitors. Three studies did not disclose any relationship between magnesium metabolism and treatment with histamine type-2 receptor antagonists. In conclusion, proton-pump inhibitors may cause hypomagnesemia. In these cases, switching to a histamine type-2 receptor antagonist is advised.

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Section: Resultsmentioning

confidence: 99%

Hypomagnesemia Induced by Long-Term Treatment with Proton-Pump Inhibitors

Janett

Camozzi

Peeters

et al. 2015

Gastroenterology Research and Practice

View full text Add to dashboard Cite

show abstract

“…There have been few genetic studies, but in one patient no mutation was found in TRPM6the gene encoding the active magnesium transporter in the renal tubule and intestine. 6 The two cases described demonstrate the key aspects of PPI-induced severe hypomagnesaemia. Both patients had been on PPI treatment for >1 year and had been highly adherent to treatment.…”

Section: Severe Proton Pump Inhibitor-induced Hypomagnesaemia In a Momentioning

confidence: 85%

Severe proton pump inhibitor‐induced hypomagnesaemia in a mother and daughter

Eberhard

Macdonald

Cundy

2017

Internal Medicine Journal

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Omeprazole enhances the colonic expression of the Mg2+ transporter TRPM6

Lameris

Hess

Kruijsbergen

et al. 2013

Pflugers Arch - Eur J Physiol

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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.

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Hipomagnesemia asociada a tratamiento con omeprazol y test genético negativo para mutación en TRPM6

Cited by 7 publications

References 9 publications

Hypomagnesemia Induced by Long-Term Treatment with Proton-Pump Inhibitors

Hypomagnesemia Induced by Long-Term Treatment with Proton-Pump Inhibitors

Severe proton pump inhibitor‐induced hypomagnesaemia in a mother and daughter

Omeprazole enhances the colonic expression of the Mg2+ transporter TRPM6

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