Yei Chi-Jung, Chang Jan-Gowth, Shih Mu-Chin, Lin Sheng-Fung, Chang Chao-Sung, Ko Fu-Tsong, Lin Kuang-Yang, Liu Ta-Chih
Blood Bank, and Division of Hematology/Oncology, Department of Internal Medicine, Kaohsiung Medical University Hospital, 100 Shih-Chuan 1st Road, Kaohsiung, Taiwan, China.
World J Gastroenterol. 2005 Aug 21;11(31):4891-4. doi: 10.3748/wjg.v11.i31.4891.
The Lewis b (Le(b)) antigen has been implicated as a possible binding site for attachment of Helicobacter pylori (H pylori) to gastric mucosa. However, studies both supporting and denying this association have been reported in the literature. Differences in secretor (Se) genotype have been suggested as a possible reason for previous discrepancies. Therefore, we investigated the relationship between Le and Se genotypes and H pylori infection rates in people with peptic ulcer or gastric cancer.
Peripheral blood samples were obtained from 347 patients with endoscopic evidence of peptic ulcer disease (235 cases of duodenal ulcer, 62 of gastric ulcer, and 50 of combined duodenal ulcer/ gastric ulcer) and 51 patients with gastric cancer on endoscopy. Peripheral blood specimens from 101 unrelated normal volunteers were used as controls. Lewis phenotype was determined using an antibody method, whereas Le and Se genotypes were determined by DNA amplification and restriction enzyme analysis. Gastric or duodenal biopsies taken from patients with endoscopic evidence of peptic ulcer or gastric cancer were cultured for H pylori. Isolates were identified as H pylori by morphology and production of urease and catalase. The H pylori infection status was also evaluated by rapid urease test (CLO test), and urea breath test ((13)C-UBT). Results of studies were analyzed by chi-square test (taken as significant).
H pylori was isolated from 83.7% (303/347) of patients with peptic ulcer disease. Statistical analysis did not show any significant difference in Lewis phenotype or genotype between patients with and without H pylori infection. No significant association was found between Lewis genotype and peptic ulcer or gastric cancer.
Lewis blood genotype or phenotype may not play a role in the pathogenesis of H pylori infection. However, bacterial strain differences and the presence of more than one attachment mechanism may limit the value of epidemiological studies in elucidating this matter.
Lewis b（Le(b)）抗原被认为可能是幽门螺杆菌（H pylori）附着于胃黏膜的结合位点。然而，文献中既有支持也有否定这种关联的研究报道。分泌型（Se）基因型的差异被认为是先前存在差异的一个可能原因。因此，我们调查了Le和Se基因型与消化性溃疡或胃癌患者幽门螺杆菌感染率之间的关系。
采集了347例有消化性溃疡内镜证据的患者（235例十二指肠溃疡、62例胃溃疡、50例十二指肠溃疡合并胃溃疡）和51例胃癌患者的外周血样本。101名无亲缘关系的正常志愿者的外周血标本用作对照。采用抗体法确定Lewis表型，通过DNA扩增和限制性酶切分析确定Le和Se基因型。对有消化性溃疡或胃癌内镜证据的患者进行胃或十二指肠活检，培养幽门螺杆菌。通过形态学以及脲酶和过氧化氢酶的产生来鉴定分离菌株是否为幽门螺杆菌。还通过快速尿素酶试验（CLO试验）和尿素呼气试验（(13)C-UBT）评估幽门螺杆菌感染状况。研究结果采用卡方检验进行分析（以具有显著性为准）。
从83.7%（303/347）的消化性溃疡患者中分离出幽门螺杆菌。统计学分析未显示幽门螺杆菌感染患者与未感染患者在Lewis表型或基因型上有任何显著差异。未发现Lewis基因型与消化性溃疡或胃癌之间存在显著关联。
Lewis血型基因型或表型可能在幽门螺杆菌感染的发病机制中不起作用。然而，菌株差异以及存在多种附着机制可能会限制流行病学研究在阐明这一问题上的价值。
