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.

Neonatal encephalopathy with a pungent body odour.

A neonate had transient unexplained bleeding into the gut, severe encephalopathy, and an abnormal pungent body odour. An inherited metabolic defect was excluded. The malodour was due to methanethiol and hydrogen sulphide, identified in urine. These sulphur compounds may have contributed to encephalopathy. Colonic bacteria were the probable source.

Iron status in athletes. An update.

As more studies are done on the iron status of athletes, the significance of apparent iron deficiency remains controversial. Do observed changes in iron status in athletes indicate an actual iron deficiency or a physiological response to exercise? Iron replacement would clearly be indicated if an iron deficiency was present but would not be necessary or effective if the observed changes were simply a physiological response. There is agreement that serum ferritin and haemoglobin decrease with some exercise conditions and that some indicators of haemolysis, such as serum haptoglobin and bilirubin, change in response to exercise. Expansion of plasma volume and the shift of iron storage from bone marrow to the liver could support the claim that the apparent reduced iron status parameters occurring with exercise are misleading. Countering this concept are studies in athletes which demonstrate dietary iron intake deficiencies and blood loss in the gastrointestinal and urinary tract. Iron deficiency is common in the general population, particularly in women. Therefore, continued monitoring of iron status in athletes appears justified in the face of present knowledge. Replacement therapy, when iron deficiency is apparent, is recommended.

Ranitidine in the newborn.

An infusion of ranitidine 0.2 mg/kg/hour abruptly halted a life threatening gastrointestinal haemorrhage in an anuric infant of 30 weeks' gestation.