HELICOBACTER-PYLORI AND ATROPHIC GASTRITIS - IMPORTANCE OF THE CAGA STATUS
HELICOBACTER-PYLORI AND ATROPHIC GASTRITIS - IMPORTANCE OF THE CAGA STATUS
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DOI：
10.1093/jnci/87.23.1777
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发表时间：
1995-12-06
期刊：
影响因子：
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通讯作者：
BLASER, MJ
中科院分区：
文献类型：
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作者：
KUIPERS, EJ;PEREZPEREZ, GI;BLASER, MJ
背景资料：幽门螺杆菌（Helicobacter pylori，Hp）感染是萎缩性胃炎和胃癌发生的主要危险因素，Hp菌株在cagA的存在方面存在差异（细胞毒素相关基因A），编码高分子量免疫显性抗原的基因，具有cagA的幽门螺杆菌菌株与急性胃炎症的增强诱导相关。目的：方法：采用胃镜检查和活检的方法，对58例H. pylori感染者的胃炎自然史进行研究。在平均11.5年的随访期前后获得活检标本（范围，10-13岁），每个个体的cagA状态在随访时使用酶联免疫吸附测定法确定，所述酶联免疫吸附测定法设计用于检测针对CagA蛋白的血清免疫球蛋白G的存在，双侧Fisher精确检验，McNemar检验，Student t检验，采用Wilcoxon秩和检验进行统计学分析。58例受试者中有24例（41%）血清中有CagA抗体（即，他们是cagA阳性的），34名受试者是cagA阴性的。在初次访视时，在8名（33%）cagA阳性受试者和6名（18%）cagA阴性受试者中观察到中度至重度萎缩性胃炎。此时，cagA阳性状态与胃萎缩无明显相关性（P = 0.22; Fisher精确检验;比值比[OR] 2.33; 95%置信区间[CI] = 0.58-9.65），随访期间，44例最初萎缩阴性受试者中有16例（36%）发展为萎缩性胃炎（16名cagA阳性受试者中有8名[50%] vs 28名cagA阴性受试者中有8名[29%]; P = 0.20，Fisher精确检验;相对风险[RR] = 1.75; 95% CI = 0.82-3.76），在这16例受试者中的6例中（5例cagA阳性对1例cagA阴性），萎缩性胃炎伴有肠上皮化生的发展（即，存在的特化细胞类型的变化）（P = 0.02; Fisher精确检验; RR = 9.06; 95%CI = 1.16-71.0），一名最初萎缩阴性、cagA阳性的受试者发生了早期胃癌，14名最初诊断为萎缩性胃炎的受试者中有4名（29%）在随访期间显示萎缩消退（1例cagA阳性，3例cagA阴性），因此，在随访结束时，24例cagA阳性受试者中有15例（62%）患有萎缩性胃炎，而34例cagA阴性受试者中有11例（32%）患有萎缩性胃炎结论：cagA阳性的H，pylori菌株感染与萎缩性胃炎和肠上皮化生的发生有关。
Background: Infection with Helicobacter pylori is a major risk factor for the development of atrophic gastritis and gastric cancer, H, pylori strains can differ with respect to the presence of cagA (cytotoxin-associated gene A), a gene encoding a high-molecular-weight immunodominant antigen, H, pylori strains possessing cagA have been associated with enhanced induction of acute gastric inflammation, Purpose: We investigated the relationship between cagA status and the development of atrophic gastritis in a cohort of subjects infected with H, pylori, Methods: Gastrointestinal endoscopy with biopsy sampling was used to study the natural history of gastritis in 58 subjects infected with H. pylori, Biopsy specimens were obtained before and after a mean follow-up period of 11.5 years (range, 10-13 years), The cagA status of each individual was determined at the follow-up visit with the use of an enzyme-linked immunosorbent assay designed to detect the presence of serum immunoglobulin G directed against the CagA protein, Two-sided Fisher's exact tests, McNemar's tests, Student's t tests, and Wilcoxon sum rank tests were used to analyze the data, Results: Twenty-four (41%) of the 58 evaluated subjects had serum antibodies against CagA (i,e,, they were cagA positive), and 34 subjects were cagA negative, At the initial visit, moderate to severe atrophic gastritis was observed in eight (33%) of the cagA-positive subjects and in six (18%) of the cagA-negative subjects, At that time, positive cagA status and gastric atrophy were not significantly related (P = .22; Fisher's exact test; odds ratio [OR] 2.33; 95% confidence interval [CI] = 0.58-9.65), During follow-up, 16 (36%) of the 44 initially atrophy-negative subjects developed atrophic gastritis (eight [50%] of 16 cagA-positive subjects versus eight [29%] of 28 cagA-negative subjects; P = .20, Fisher's exact test; relative risk [RR] = 1.75; 95% CI = 0.82-3.76), In six of these 16 subjects (five cagA positive versus one cagA negative), atrophic gastritis was accompanied by the development of intestinal metaplasia (i,e,, a change in the type of specialized cells present) (P = .02; Fisher's exact test; RR = 9.06; 95% CI = 1.16-71.0), One of the initially atrophy-negative, cagA-positive subjects developed early gastric cancer, Four (29%) of the 14 subjects initially diagnosed with atrophic gastritis showed regression of atrophy during follow-up (one cagA positive and three cagA negative), Therefore, at the end of follow-up, 15 (62%) of the 24 cagA-positive subjects had atrophic gastritis compared with 11 (32%) of the 34 cagA-negative subjects (P = .02; Fisher's exact test; OR = 3.48; 95% CI = 1.02-12.18), Conclusion: Infection with cagA-positive H, pylori strains is associated with an increased risk for the eventual development of atrophic gastritis and intestinal metaplasia.