Alam K, Schubert T T, Bologna S D, Ma C K
Department of Pathology, Henry Ford Hospital, Detroit, Michigan.
Am J Gastroenterol. 1992 Apr;87(4):424-8.
An increased risk of ulcers and severity of inflammation with increased degree of Helicobacter pylori (HP) infection (biological gradient) would support the hypothesis that HP causes ulcers. A blinded pathologist evaluated antral biopsies obtained at endoscopy in 903 patients. The level of HP infection was assessed on Warthin Starry stain, and the severity of acute and chronic inflammation on hematoxylin and eosin graded from 0 to 3. The presence of duodenal ulcers was associated with increasing HP density (grade 0, 6%; grade 1, 16%; grade 2, 19%; and grade 3, 27%) (p less than 0.0001, Wilcoxon rank sum test). Only a weak association between HP and gastric ulcers was detected (p = 0.06, Wilcoxon rank sum test), and this association diminished after adjusting for other risk factors. An increased acute and chronic inflammatory response correlated with increasing HP concentration (p less than 0.0001, Cochran-Mantel-Haenszel correlation statistic. The presence of this biologic gradient supports the hypothesis that HP is pathogenic in duodenal ulcers and in acute and chronic gastritis.
幽门螺杆菌(HP)感染程度增加时溃疡风险及炎症严重程度也增加(生物学梯度),这将支持HP导致溃疡的假说。一名盲法病理学家对903例患者内镜检查时获取的胃窦活检标本进行评估。通过Warthin Starry染色评估HP感染水平,苏木精和伊红染色评估急性和慢性炎症严重程度,分级为0至3级。十二指肠溃疡的存在与HP密度增加相关(0级,6%;1级,16%;2级,19%;3级,27%)(p<0.0001,Wilcoxon秩和检验)。仅检测到HP与胃溃疡之间存在微弱关联(p = 0.06,Wilcoxon秩和检验),在调整其他风险因素后这种关联减弱。急性和慢性炎症反应增加与HP浓度增加相关(p<0.0001,Cochran-Mantel-Haenszel相关统计量)。这种生物学梯度的存在支持HP在十二指肠溃疡以及急性和慢性胃炎中具有致病性的假说。