Helicobacter pylori cagA status, vacA genotypes and ulcer disease.
Stephens, Jonathan C. a; Stewart, James A.D. b; Folwell, Andrew M. c; Rathbone, Barrie J. b
European Journal of Gastroenterology & Hepatology.
10(5):381-384, May 1998.
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Objective: Helicobacter pylori is the causative organism of peptic ulcer disease and has two putative virulence determinants: the cagA gene which encodes a protein of unknown function in 60% of strains, and the vacA gene, which is present in all strains, although active cytotoxin is produced in only about 50% of these. The relationship between genotypes of both cagA and vacA and resultant gastroduodenal pathology is unclear. The objective of this study was to correlate vacA genotype and cagA status with gastroduodenal pathology.
Methods: One hundred and six dyspeptic patients were studied (average age 56 years, range 19-86 years, 56 men) referred for routine endoscopy. Macroscopic evidence of gastroduodenal disease was noted and antral biopsies taken for culture and genotyping of H. pylori. The polymerase chain reaction (PCR) was used to detect the cagA and vacA genes of H. pylori using specific primers.
Results: Seventy eight of the 106 (73.6%) patients were cagA positive. Of those who had peptic ulcer disease 29/32 (90.6%) were cagA positive. The presence of the cagA gene was significantly associated with peptic ulcer disease (P = 0.006). The presence of the vacA s1 genotype was also significantly associated with peptic ulcer disease (P = 0.01). The presence of the cagA gene was significantly associated with the vacA s1 genotype (P < 0.001). There was no significant difference in the distribution of the s1/m1 and s1/m2 strains between ulcer and non-ulcer patients.
Conclusion: There is a significant association of the cagA gene and vacA s1 signal sequence with gastroduodenal ulcer disease. The relationship of the various other vacA genotypes to gastroduodenal ulcer disease is less clear.
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