Short-Term Effect of High-Dose Pantoprazol on Serum and Urinary Magnesium Levels.

BACKGROUND: Proton pump inhibitor (PPI) induced hypomagnesemia is a completely unexplained issue and cases are still being reported. Long-term use is the main factor, but there are a few articles stating that it may also emerge with short-term use. We aimed to evaluate the changes of serum and urine magnesium levels during shortterm high dose pantoprazol treatment. METHODS: The serum and 24-hour urine magnesium levels of 58 patients were evaluated during the course of 2 days. Of 58 patients, 25 were allowed oral intake on the 3rd day of hospitalization and thus, 24-hour urine for 3 days was collected from 33 patients. RESULTS: There were no significant differences in the mean levels of serum magnesium and the median levels of urine magnesium. When the magnesium levels were evaluated by age over and under 60 years, the baseline serum magnesium level was significantly higher than the 1st level in patients aged ≥ 60 years (p = 0.029). The 3rd day serum magnesium level was significantly higher than the baseline and 1st day levels in those aged < 60 years (p = 0.049). CONCLUSIONS: We showed that plasma levels and urinary excretion of magnesium did not change significantly during high-dose pantoprazol treatment. It can be hypothesized that magnesium levels are not affected by PPIs in short-term usage. Age and other contributing factors may have more impact on PPI induced hypomagnesemia. Patients aged over 60 years might be handled carefully under proton pump inhibitors treatment.

Genetic causes of hypomagnesemia, a clinical overview.

Magnesium is essential to the proper functioning of numerous cellular processes. Magnesium ion (Mg2+) deficits, as reflected in hypomagnesemia, can cause neuromuscular irritability, seizures and cardiac arrhythmias. With normal Mg2+ intake, homeostasis is maintained primarily through the regulated reabsorption of Mg2+ by the thick ascending limb of Henle's loop and distal convoluted tubule of the kidney. Inadequate reabsorption results in renal Mg2+ wasting, as evidenced by an inappropriately high fractional Mg2+ excretion. Familial renal Mg2+ wasting is suggestive of a genetic cause, and subsequent studies in these hypomagnesemic families have revealed over a dozen genes directly or indirectly involved in Mg2+ transport. Those can be classified into four groups: hypercalciuric hypomagnesemias (encompassing mutations in CLDN16, CLDN19, CASR, CLCNKB), Gitelman-like hypomagnesemias (CLCNKB, SLC12A3, BSND, KCNJ10, FYXD2, HNF1B, PCBD1), mitochondrial hypomagnesemias (SARS2, MT-TI, Kearns-Sayre syndrome) and other hypomagnesemias (TRPM6, CNMM2, EGF, EGFR, KCNA1, FAM111A). Although identification of these genes has not yet changed treatment, which remains Mg2+ supplementation, it has contributed enormously to our understanding of Mg2+ transport and renal function. In this review, we discuss general mechanisms and symptoms of genetic causes of hypomagnesemia as well as the specific molecular mechanisms and clinical phenotypes associated with each syndrome.

Hypomagnesemia due to two novel TRPM6 mutations.

BACKGROUND: Although most hypocalcemia with hypomagenesemia in the neonatal period is due to transient neonatal hypoparathyroidism, magnesium channel defects should also be considered. CASE: We report a case of persistent hypomagnesemia in an 8-day-old Hispanic male who presented with generalized seizures. He was initially found to have hypomagnesemia, hypocalcemia, hyperphosphatemia and normal parathyroid hormone. Serum calcium normalized with administration of calcitriol and calcium carbonate. Serum magnesium improved with oral magnesium sulfate. However, 1 week after magnesium was discontinued, serum magnesium declined to 0.5 mg/dL. Magnesium supplementation was immediately restarted, and periodic seizure activity resolved after serum magnesium concentration was maintained above 0.9 mg/dL. The child was eventually weaned off oral calcium and calcitriol with persistent normocalemia. However, supraphysiologic oral magnesium doses were necessary to prevent seizures and maintain serum magnesium at the low limit of normal. METHODS AND RESULTS: As his clinical presentation suggested primary renal magnesium wastage, TRPM6 gene mutations were suspected; subsequent genetic testing revealed the child to be compound heterozygous for TRPM6 mutations. CONCLUSION: Two novel TRPM6 mutations are described with a new geographic and ethnic origin. This case highlights the importance of recognizing disorders of magnesium imbalance and describing new genetic mutations.

Serum calcium and magnesium levels in women presenting with pre-eclampsia and pregnancy-induced hypertension: a case-control study in the Cape Coast metropolis, Ghana.

BACKGROUND: Hypertensive disorders of pregnancy are important causes of morbidity and mortality. The levels of calcium (Ca2+) and magnesium (Mg2+) in pregnancy may implicate their possible role in pregnancy-induced hypertension. This study assessed serum Ca2+ and Mg2+ levels in women with PIH (pregnancy-induced hypertension) and PE (pre-eclampsia), compared to that in normal pregnancy. METHODS: This case-control study was conducted on 380 pregnant women (≥20 weeks gestation) receiving antenatal care at three hospitals in the Cape Coast metropolis, Ghana. This comprised 120 women with PIH, 100 women with PE and 160 healthy, age-matched pregnant women (controls). Demographic, anthropometric, clinical and obstetric data were gathered using an interview-based questionnaire. Venous blood samples were drawn for the estimation of calcium and magnesium. RESULTS: Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were significantly raised in women with PIH (p < 0.0001) and PE (p < 0.0001). Women with hypertensive disorders (PE and PIH) had significantly lower serum calcium and magnesium levels than those in the control group (p < 0.0001 each). Of those with PIH, SBP correlated positively with BMI (r = 0.575, p < 0.01) and Ca2+ correlated positively with Mg2+ (r = 0.494, p < 0.01). This was similar amongst the PE group for SBP and BMI as well as for Ca2+and Mg2+ but was not significant. Multivariate analysis showed that women aged ≥40 years were at a significant risk of developing PIH (OR = 2.14, p = 0.000). CONCLUSION: In this study population, serum calcium and magnesium levels are lower in PIH and PE than in normal pregnancy. Mineral supplementation during the antenatal period may influence significantly, the occurrence of hypertensive disorders in pregnancy.

Does post-cardiac surgery magnesium supplementation improve outcome?

Hypomagnesemia has been linked with increased morbidity and mortality in critically ill patients. Since the condition is common after cardiopulmonary bypass surgery, the objective of this study was to determine whether magnesium supplementation in the immediate postoperative period may improve outcomes of patients undergoing cardiac surgery with cardiopulmonary bypass. This prospective, randomized, double-blind, placebo-controlled study was conducted in a third-level, cardiac surgery intensive care unit (ICU) at a university hospital. Two hundred and sixteen patients undergoing elective cardiac surgery with cardiopulmonary bypass were randomized to receive either an intravenous bolus of 1.5 g of magnesium sulphate followed by an infusion of 12 g of the same salt in 24 h (105 patients), or placebo (111 patients) administered according to the same schedule as the treatment group. No significant differences were found either in the primary end point (hours of intubation) or in the secondary end points (length of inotropic support, new atrial fibrillation, ventricular tachycardia or ventricular fibrillation, length of intensive care unit stay, or ICU or hospital mortality). Hypomagnesemia was present in 12% of patients on admission to the intensive care unit. The magnesium group had a greater need for pacemaker stimulation. In conclusion, under the conditions of the present study, magnesium supplementation after cardiac surgery with cardiopulmonary bypass does not favourably affect clinical outcomes.

Correlations of serum concentrations of 1,25-dihydroxyvitamin D, phosphorus, and parathyroid hormone in tumoral calcinosis.

The inherited metabolic disorder tumoral calcinosis is characterized by elevated serum phosphorus and 1,25-dihydroxyvitamin D [1,25-(OH)2D] levels and paraarticular calcific tumors. The pathogenesis of this disease is obscure, but an elevated renal phosphate reabsorption threshold and increased production of 1,25-(OH)2D are postulated as defects. We studied nine affected patients and found that both serum phosphorus and renal phosphate reabsorption threshold (TmP/GFR) were positively correlated with serum 1,25-(OH)2D levels. Since tumoral calcinosis is a disorder with abnormal renal phosphate transport, we compared the TmP/GFR and serum 1,25-(OH)2D levels to values obtained in patients with two other diseases with renal phosphate transport defects: oncogenic osteomalacia and X-linked hypophosphatemic rickets. We found a significant correlation between TmP/GFR and 1,25-(OH)2D levels in all three diseases, suggesting that in these diseases 1,25-(OH)2D production is regulated in some manner by phosphate transport. Furthermore, previous work indicated that in tumoral calcinosis broad variation exists in serum phosphorus levels. In our patients a negative correlation was found between the serum PTH concentrations and both serum phosphorus levels and TmP/GFR values, respectively. We postulate that although the basic defect in tumoral calcinosis most likely resides in the proximal renal tubular cell, the variation in serum phosphorus levels and possibly disease expression is modulated in part by PTH.

A new variant of Lowe oculocerebrorenal syndrome.

A case is reported of a 5-year-old boy with Lowe syndrome. The patient was unusual in that he had only mild and transient acidosis with no rickets. The corneal opacities in the parents suggest that this disease might be autosomal recessive.