Choe Y H, Hwang T S, Kim H J, Shin S H, Song S U, Choi M S
Department of Pediatrics, Inha University Hospital, Inchon, Korea.
Helicobacter. 2001 Mar;6(1):55-9. doi: 10.1046/j.1523-5378.2001.00007.x.
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.
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.
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.
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.
幽门螺杆菌感染被认为与缺铁性贫血有关，尤其是在青春期。幽门螺杆菌的铁蛋白Pfr蛋白与真核和原核铁蛋白同源。本研究的目的是根据临床数据，包括有无缺铁性贫血的胃窦炎，分析胃活检标本中幽门螺杆菌的pfr状态。
将26例年龄在10至18岁之间的幽门螺杆菌阳性患者根据有无缺铁性贫血分为亚组。他们均患有胃窦炎。通过血液学研究证实16例患者患有缺铁性贫血，其中2例患有十二指肠溃疡。其他10例患者血液学检查结果正常。从每个胃活检标本中提取DNA。使用两组引物对编码pfr基因进行PCR扩增。通过连接两个PCR产物的序列产生501bp的pfr区域。比较韩国幽门螺杆菌菌株与从Genbank获得的NCTC 11638菌株的pfr区域之间的核苷酸和蛋白质序列。还对缺铁性贫血（+）和（-）组之间的pfr区域进行了序列比较。
对pfr基因完整编码区的分析揭示了三个突变位点。Ser39Ala突变在100%（26/26）中发现，Gly111Asn在26.9%（7/26）中发现，Gly82Ser在11.5%（3/26）中发现。缺铁性贫血（+）和（-）组之间pfr区域的突变没有显著差异。
pfr基因突变与临床表型缺铁性贫血无关。需要在宿主方面或其他复杂因素方面进行进一步研究，以阐明幽门螺杆菌感染可能导致缺铁性贫血的机制。
