Helicobacter pylori vacA genotypes and cagA gene in a series of 383 H-pylori-positive patients

Citation
J. Rudi et al., Helicobacter pylori vacA genotypes and cagA gene in a series of 383 H-pylori-positive patients, Z GASTROENT, 38(7), 2000, pp. 559-564
Citations number
46
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
ZEITSCHRIFT FUR GASTROENTEROLOGIE
ISSN journal
00442771 → ACNP
Volume
38
Issue
7
Year of publication
2000
Pages
559 - 564
Database
ISI
SICI code
0044-2771(200007)38:7<559:HPVGAC>2.0.ZU;2-H
Abstract
Background: Only 10-15 % of all patients infected with Helicobacter pylori develop peptic ulcer disease (PUD) or gastric cancer. Apart from immunologi cal factors in the host, virulence determinants of H. pylori such as the va cuolating cytotoxin (VacA) or the cytotoxin-associated protein A (CagA) mig ht represent a predisposition for the development of PUD. Methods: We studied antral biopsies of 383 H. pylori-positive patients with peptic ulcer disease (PUD) or other H.pylori-related diseases for H. pylor i vacA genotypes and the presence of the cagA gene by PCR. Results: VacA genotypes and cagA status could be completely determined in 3 57 (93.2%) of the patients. In 91 (93.8%) of 97 patients with PUD, the vacA sl genotype (sl mi. 45; s1m2, 46 patients) was present. The vacA s2m2 geno type was found in only 6 (6.2%) of 97 patients with PUD. In contrast, 180 ( 75.3%) of 239 patients (s1m1, 89; s1m2, 91 patients) without PUD and withou t gastric malignancies harbored strains with the vacA s1 genotype. The vacA genotype s2m2 was found in 59 (24.7%) of these patients. The presence of t he cagA gene was closely associated with the vacA genotype sl and found in 124 (88.6%) and in 113 (80.7%) of patients with the s1m1 or s1m2 genotypes, respectively, whereas strains with the genotype s2m2 were almost exclusive ly cagA negative. Conclusion: Most H. pylori strains found in patients with PUD possess the v acA sl genotype and the cagA gene. Patients with this type of H. pylori str ain but without PUD might be at higher risk of developing PUD. In contrast, the risk for PUD might be significantly decreased in those patients who ar e infected by H. pylori strains with the vacA s2 genotype lacking the cagA gene.