Helicobacter pylori infection, iron absorption, and gastric acid secretion in Bangladeshi children

Abstract

Nonheme-iron absorption requires an acidic milieu. Reduced gastric acid output as a consequence of Helicobacter pylori infection could be an important limiting factor for iron absorption. We measured gastric acid output and iron absorption from a non-water-soluble iron compound (ferrous fumarate) and a water-soluble iron compound (ferrous sulfate) in children with and without H. pylori infection. Gastric acid output was quantified before (basal acid output, or BAO) and after pentagastrin stimulation (stimulated acid output, or SAO) in 2-5-y-old children with iron deficiency anemia who were (n = 13) or were not (n = 12) infected with H. pylori. Iron absorption was measured by using a double-stable-isotope technique. H. pylori-infected children were studied before and after eradication therapy. BAO and SAO were significantly lower in the H. pylori-infected children (0.2 +/- 0.2 and 1.6 +/- 0.9 mmol/h, respectively) than in the uninfected children (0.9 +/- 0.7 and 3.1 +/- 0.9 mmol/h, respectively; P = 0.01 and P < 0.005). BAO and SAO improved to 0.8 +/- 1.3 and 3.3 +/- 2.4 mmol/h, respectively, after therapy. Iron absorption from ferrous sulfate was significantly greater than that from ferrous fumarate both before (geometric : 19.7% compared with 5.3%; P < 0.0001) and after (22.5% compared with 6.4%; P < 0.0001) treatment in H. pylori-infected children. Corresponding values for uninfected children were 15.6% and 5.4%, respectively (P < 0.001; n = 12). Iron absorption from ferrous fumarate was significantly lower than that from ferrous sulfate in both H. pylori-infected and uninfected Bangladeshi children. Treatment of H. pylori infection improved gastric acid output but did not significantly influence iron absorption. The efficacy of ferrous fumarate in iron fortification programs to prevent iron deficiency in young children should be evaluated.