UNLABELLED: Magnesium seems to be an important factor both for acid gastric secretion regulation (together with Ca2+) and for Helicobacter pylori survival and virulence. It can therefore be useful to evaluate if Helicobacter pylori (HP) infection is accompanied by variations in the host Mg availability. In this study serum, erythrocytary and gastric tissue Mg concentration was measured in 36 patients affected by chronic antral gastritis. Based on the presence of Helicobacter pylori infection, the patients were subdivided in two groups: group A: Helicobacter pylori negative, n = 23; group B: Helicobacter pylori positive, n = 13. RESULTS: While no differences were found between the two groups for serum Mg (group A 0.81 +/- 0.07 mm/L, group B 0.81 +/- 0.11 mm/L), both erythrocytary Mg (EMg) and gastric tissue Mg were found significantly lower in the HP positive subjects (erythrocytary Mg: 2.14 +/- 0.55 vs. 1.81 +/- 0.34 mm/L; gastric tissue Mg: 729.2 +/- 333.8 vs. 510.6 +/- 178.8 microg/g of dried tissue for group A and B respectively, p < 0.001 for both determinations). Erythrocytary Mg reduction is a clue of the whole body reduction in Mg availability (and consequently in gastric cells as well); the erythrocytary Mg reduction detected in the present paper for Helicobacter pylori positive patients can weaken gastric cells by impairing their metabolism. The hypothesis submitted is to impair Mg utilization in Helicobacter pylori, in order to improve eradication treatment, and in the meantime to preserve Mg homeostasis in infected cells.
UNLABELLED: Magnesium seems to be an important factor both for acid gastric secretion regulation (together with Ca2+) and for Helicobacter pylori survival and virulence. It can therefore be useful to evaluate if Helicobacter pylori (HP) infection is accompanied by variations in the host Mg availability. In this study serum, erythrocytary and gastric tissue Mg concentration was measured in 36 patients affected by chronic antral gastritis. Based on the presence of Helicobacter pylori infection, the patients were subdivided in two groups: group A: Helicobacter pylori negative, n = 23; group B: Helicobacter pylori positive, n = 13. RESULTS: While no differences were found between the two groups for serum Mg (group A 0.81 +/- 0.07 mm/L, group B 0.81 +/- 0.11 mm/L), both erythrocytary Mg (EMg) and gastric tissue Mg were found significantly lower in the HP positive subjects (erythrocytary Mg: 2.14 +/- 0.55 vs. 1.81 +/- 0.34 mm/L; gastric tissue Mg: 729.2 +/- 333.8 vs. 510.6 +/- 178.8 microg/g of dried tissue for group A and B respectively, p < 0.001 for both determinations). Erythrocytary Mg reduction is a clue of the whole body reduction in Mg availability (and consequently in gastric cells as well); the erythrocytary Mg reduction detected in the present paper for Helicobacter pylori positive patients can weaken gastric cells by impairing their metabolism. The hypothesis submitted is to impair Mg utilization in Helicobacter pylori, in order to improve eradication treatment, and in the meantime to preserve Mg homeostasis in infected cells.