A possible relation of the Helicobacter pylori pfr gene to iron deficiencyanemia?

Background. H. pylori infection is thought to contribute to iron-deficiency anemia, especially during puberty. The ferritin protein Pfr of H. pylori i s homologous to eukaryotic and prokaryotic ferritins. The purpose of this s tudy was to analyze the N, pylori pfr status in gastric biopsy specimens ac cording to clinical data, including antral gastritis with or without iron-d eficiency anemia. Methods. A total of 26 H, pylori-positive patients aged from 10-18 years we re categorized into subgroups based on the presence or absence of iron-defi ciency anemia. All of them had antral gastritis. Sixteen patients were prov ed to have iron-deficiency anemia by hematological study, two of which had a duodenal ulcer. The other 10 patients showed normal hematological finding s. DNA isolation was performed from each of the gastric biopsy specimens. P CR amplification of the pfr gene coding was done using two sets of primers. The pfr region, 501 bp, was generated by linking the sequences of the two PCR products. The nucleotide and protein sequences were compared between th e pfr regions from Korean H. pylori strains and the NCTC 11638 strain, whic h was obtained from the Genbank. Sequence comparisons were also performed f or the pfr regions between the iron-deficiency anemia (+) and (-) groups. Results. Analysis of the complete coding region of the pfr gene revealed th ree sites of mutation. The Ser39Ala mutation was found in 100% (26/26), Gly 111Asn in 26.9% (7/26), and Gly82Ser in 11.5% (3/26). There were no signifi cant differences in the mutations of the pfr regions between the iron defic iency anemia (+) and (-) groups. Conclusion. The mutation in the pfr gene did not relate with the clinical p henotype, iron deficiency anemia. Further studies are needed on the aspects of host side or other complex factors to elucidate the mechanisms by which the H. pylori infection might lead to iron deficiency anemia.