 There is suggestive evidence that H. pylori gastritis without peptic ulcer disease is a cause of IDA. There have been individual case reports and case series describing patients with refractory IDA that resolved following successful H. pylori treatment. The effect of H. pylori on iron metabolism will be studied through specific aims: 1. To assess whether H. pylori results in abnormal oral iron absorption 2. To assess if differences in H. pylori strains are associated with iron deficiency due to: a. genetic differences in H. pylori strains or b. differences in the pattern of gastritis which could be due to host, bacterial or environmental factors 3. To assess if H. pylori infection results in storage of iron in the gastric mucosa and an elevated gastric iron concentration. The study will consist of three aspects: 1. Determining whether oral iron absorption is abnormal for H. pylori-positive IDA patients, and comparison of oral iron absorption for H. pylori positive and negative IDA patients. This will also include an experimental component in which oral iron absorption will be repeated after H. pylori treatment for H. pylori-infected IDA subjects and after an equivalent time period for H. pylori negative controls to exclude changes in iron absorption that occur over time. 2. Comparison of H. pylori strain characteristics for IDA patients and non-anemic H. pylori-infected controls. Characterization of H. pylori strains will include: genetic analysis using a whole genome microarray technique that assesses the presence or absence of H. pylori genes, evaluation of expression of genes related to iron metabolism, and comparison of pattern of gastritis pan gastritis vs. antrum-predominant. 3. Determination of whether H. pylori stores a significant quantity of iron in the gastric mucosa in vivo. This will be assessed by measuring the iron concentration in mucosal biopsy specimens and comparing results for H. pylori-infected IDA patients to H. pylori-uninfected IDA controls. 