Schultze V, Hackelsberger A, Günther T, Miehlke S, Roessner A, Malfertheiner P
Dept. of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany.
Scand J Gastroenterol. 1998 Feb;33(2):137-42. doi: 10.1080/00365529850166851.
We investigated the risk relationship between histotopographic patterns of Helicobacter pylori gastritis and peptic ulcer site.
Three hundred and eighty-three infected patients were classified as having duodenal ulcer (n = 79), prepyloric ulcer (n = 39), gastric (angular) ulcer (n = 28), and no ulcer (n = 237). Antral and corpus biopsy specimens were taken. Sydney system-based scores for bacterial density and activity and degree of gastritis were added to antral and corpus sum scores (SS) (range, 0-9). These were used to categorize the phenotype of gastritis. In addition, the presence or absence of mucosal atrophy was taken into account. The relative risk for ulcer association with these conditions was calculated.
High-grade antral (SS > 5) associated with mild to moderate corpus (SS > 5) gastritis increased duodenal (RR = 4.9; confidence interval (CI), 2.8-8.5) and prepyloric ulcer risk (RR = 2.99; CI, 1.4-6.2). High-grade gastritis in the antrum (SS > 5) and corpus (SS > 5) increased gastric ulcer risk (RR = 3.7; CI, 1.6-8.3). Antral atrophy and/or intestinal metaplasia is associated with an increased gastric ulcer risk (RR = 3.3; CI, 1.4-7.8).
The pattern of H. pylori gastritis may define a risk for peptic ulcer at various sites, but additional factors, not reflected in histology, also contribute to this risk.
我们研究了幽门螺杆菌胃炎的组织形态学模式与消化性溃疡部位之间的风险关系。
383例感染患者被分为十二指肠溃疡组(n = 79)、幽门前溃疡组(n = 39)、胃(角部)溃疡组(n = 28)和无溃疡组(n = 237)。采集胃窦和胃体活检标本。基于悉尼系统的细菌密度、活性及胃炎程度评分被加入胃窦和胃体总分(SS)(范围为0 - 9)。这些用于对胃炎表型进行分类。此外,还考虑了黏膜萎缩的有无。计算这些情况与溃疡关联的相对风险。
胃窦高级别(SS > 5)合并轻度至中度胃体(SS > 5)胃炎增加十二指肠溃疡风险(RR = 4.9;置信区间(CI),2.8 - 8.5)和幽门前溃疡风险(RR = 2.99;CI,1.4 - 6.2)。胃窦(SS > 5)和胃体(SS > 5)的高级别胃炎增加胃溃疡风险(RR = 3.7;CI,1.6 - 8.3)。胃窦萎缩和/或肠化生与胃溃疡风险增加相关(RR = 3.3;CI,1.4 - 7.8)。
幽门螺杆菌胃炎模式可能确定不同部位消化性溃疡的风险,但组织学未反映的其他因素也促成了这种风险。