BACKGROUND: H. pylori infection is thought to contribute to iron-deficiency anemia, especially during puberty. The ferritin protein Pfr of H. pylori is homologous to eukaryotic and prokaryotic ferritins. The purpose of this study was to analyze the H. pylori pfr status in gastric biopsy specimens according to clinical data, including antral gastritis with or without iron-deficiency anemia. METHODS: A total of 26 H. pylori-positive patients aged from 10-18 years were categorized into subgroups based on the presence or absence of iron-deficiency anemia. All of them had antral gastritis. Sixteen patients were proved to have iron-deficiency anemia by hematological study, two of which had a duodenal ulcer. The other 10 patients showed normal hematological findings. DNA isolation was performed from each of the gastric biopsy specimens. PCR 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 the pfr regions from Korean H. pylori strains and the NCTC 11638 strain, which was obtained from the Genbank. Sequence comparisons were also performed for the pfr regions between the iron-deficiency anemia (+) and (-) groups. RESULTS: Analysis of the complete coding region of the pfr gene revealed three sites of mutation. The Ser39Ala mutation was found in 100% (26/26), Gly111Asn in 26.9% (7/26), and Gly82Ser in 11.5% (3/26). There were no significant differences in the mutations of the pfr regions between the iron deficiency anemia (+) and (-) groups. CONCLUSION: The mutation in the pfr gene did not relate with the clinical phenotype, 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.
BACKGROUND:H. pyloriinfection is thought to contribute to iron-deficiency anemia, especially during puberty. The ferritin protein Pfr of H. pylori is homologous to eukaryotic and prokaryotic ferritins. The purpose of this study was to analyze the H. pylori pfr status in gastric biopsy specimens according to clinical data, including antral gastritis with or without iron-deficiency anemia. METHODS: A total of 26 H. pylori-positive patients aged from 10-18 years were categorized into subgroups based on the presence or absence of iron-deficiency anemia. All of them had antral gastritis. Sixteen patients were proved to have iron-deficiency anemia by hematological study, two of which had a duodenal ulcer. The other 10 patients showed normal hematological findings. DNA isolation was performed from each of the gastric biopsy specimens. PCR 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 the pfr regions from Korean H. pylori strains and the NCTC 11638 strain, which was obtained from the Genbank. Sequence comparisons were also performed for the pfr regions between the iron-deficiency anemia (+) and (-) groups. RESULTS: Analysis of the complete coding region of the pfr gene revealed three sites of mutation. The Ser39Ala mutation was found in 100% (26/26), Gly111Asn in 26.9% (7/26), and Gly82Ser in 11.5% (3/26). There were no significant differences in the mutations of the pfr regions between the iron deficiency anemia (+) and (-) groups. CONCLUSION: The mutation in the pfr gene did not relate with the clinical phenotype, 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. pyloriinfection might lead to iron deficiency anemia.
Authors: Barbara Waidner; Stefan Greiner; Stefan Odenbreit; Holger Kavermann; Jyoti Velayudhan; Frank Stähler; Johannes Guhl; Emmanuel Bissé; Arnoud H M van Vliet; Simon C Andrews; Johannes G Kusters; David J Kelly; Rainer Haas; Manfred Kist; Stefan Bereswill Journal: Infect Immun Date: 2002-07 Impact factor: 3.441