Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

Kyi T. Tham, Richard M. Peek, John C. Atherton, Timothy L. Cover, Guillermo I. Perez-Perez, Yu Shyr, Martin J. Blaser

研究成果: Article

38 引文 斯高帕斯(Scopus)

摘要

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P < .001) and epithelial degeneration (P = .004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non-Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and non-steroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. This is a US Government work. There are no restrictions on its use.

原文English
頁(從 - 到)264-273
頁數10
期刊Human Pathology
32
發行號3
DOIs
出版狀態Published - 2001 一月 1

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

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    Tham, K. T., Peek, R. M., Atherton, J. C., Cover, T. L., Perez-Perez, G. I., Shyr, Y., & Blaser, M. J. (2001). Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease. Human Pathology, 32(3), 264-273. https://doi.org/10.1053/hupa.2001.21136