Seroprevalence of Helicobacter pylori in patients with colorectal polyps and colorectal carcinoma

被引:16
作者
Siddheshwar, RK
Muhammad, KB
Gray, JC
Kelly, SB
机构
[1] N Tyneside Gen Hosp, Reg Sch Med, Dept Surg, N Shields NE29 8NH, Tyne & Wear, England
[2] Univ Teesside, Ctr Hlth & Med Res, Dept Stat, Middlesbrough, England
关键词
D O I
暂无
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
OBJECTIVES: The role of Helicobacter pylori in the pathogenesis of colorectal polyps and colorectal carcinoma is unknown. H. pylori infection causes fasting and meal stimulated hypergastrinemia. Gastrin increases colorectal mucosal proliferation and promotes tumor growth. We performed a prospective study to determine the seroprevalence of H. pylori in patients with colorectal polyps and colorectal carcinoma and in controls. METHODS: Blood samples were collected from 189 patients with colorectal carcinoma, 57 patients with colorectal polyps, and 179 controls. H. pylori serology was determined by an ELISA assay. RESULTS: Logistic regression showed no difference in seroprevalence of H. pylori between patients with colorectal cancer and controls (odds ratio, 1.1; 95% confidence interval, 0.7 to 1.8) or between patients with colorectal polyps and controls (odds ratio 1.3; 95% confidence interval, 0.7 to 2.5). Age and sex were not found to be associated with H. pylori infection. Patients in social classes IV and V were 2.3 times more likely to have H. pylori infection than those in social classes I, II, and III (95% confidence interval, 1.3 to 4.2). CONCLUSIONS: This study shows that there is no increase in the seroprevalence of H. pylori in patients with colorectal polyps or colorectal carcinoma compared with controls. These results do not support the hypothesis that there is a relationship between H. pylori infection and the development of colorectal neoplasia. (Am J Gastroenterol 2001;96: 84-88. (C) 2001 by Am. Coll. of Gastroenterology).
引用
收藏
页码:84 / 88
页数:5
相关论文
共 56 条
[1]  
[Anonymous], 2010, PORT CLASS OCC
[2]   Colorectal adenomateous polyps and Helicobacter pylori infection [J].
Aydin, A ;
Karasu, Z ;
Zeytinoglu, A ;
Kumanlioglu, K ;
Özacar, T .
AMERICAN JOURNAL OF GASTROENTEROLOGY, 1999, 94 (04) :1121-1122
[3]  
Basynat PS, 1999, GUT, V45, pA73
[4]   Helicobacter pylori and the risk of colonic adenomas [J].
Breuer-Katschinski, B ;
Nemes, K ;
Marr, A ;
Rump, B ;
Leiendecker, B ;
Breuer, N ;
Goebell, H .
DIGESTION, 1999, 60 (03) :210-215
[5]  
CHARNLEY RM, 1992, ANN ROY COLL SURG, V74, P138
[6]   EXPRESSION, PROCESSING, AND SECRETION OF GASTRIN IN PATIENTS WITH COLORECTAL-CARCINOMA [J].
CICCOTOSTO, GD ;
MCLEISH, A ;
HARDY, KJ ;
SHULKES, A .
GASTROENTEROLOGY, 1995, 109 (04) :1142-1153
[7]   IS HELICOBACTER-PYLORI INFECTION A REAL RISK FACTOR FOR GASTRIC-CARCINOMA [J].
DZIERZANOWSKA, D ;
SIEMINSKA, J ;
BOGDANSKA, M ;
VOGT, E ;
EHRMANN, A ;
MUSZYNSKI, J .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 1995, 30 (07) :647-651
[8]   Helicobacter pylori infection and extradigestive diseases [J].
Gasbarrini, A ;
Ponzetto, A ;
Franceschi, F ;
Pellicano, R ;
Gasbarrini, G .
CURRENT OPINION IN GASTROENTEROLOGY, 1998, 14 :S65-S69
[9]   EVALUATION OF A COMMERCIALLY AVAILABLE 2ND-GENERATION IMMUNOGLOBULIN-G ENZYME-IMMUNOASSAY FOR DETECTION OF HELICOBACTER-PYLORI INFECTION [J].
GOOSSENS, H ;
GLUPCZYNSKI, Y ;
BURETTE, A ;
VANDENBORRE, C ;
BUTZLER, JP .
JOURNAL OF CLINICAL MICROBIOLOGY, 1992, 30 (01) :176-180
[10]  
GRAHAM DY, 1990, AM J GASTROENTEROL, V85, P394