VacA and CagA Status as Biomarker of Two Opposite End Outcomes of Helicobacter pylori Infection (Gastric Cancer and Duodenal Ulcer) in a Moroccan Population

Abstract

Helicobacter pylori (H. pylori) infection induces inflammation of the gastric mucosa, which may progress to precancerous lesions leading to gastric cancer. Pathological determinism is associated to some virulence genes of the bacterium, notably the vacA and cagA genes. The present study aimed to determine the H. pylori genotypes distribution and their association with sex, age and gastric diseases in a Moroccan population. Gastric biopsy was taken from 1079 consenting patients. The specimens were processed by PCR to identify H. pylori and to determine the genotypic profile by PCR characterizing vacA s, vacA m and vacA i regions directly from biopsies H. pylori positives. VacA genotyping revealed the predominance of vacA m2 (53.2%), vacA s2 (52.9%) and vacA i2 (52%). The most virulent vacA alleles (s1, i1 and m1) are more predominant in men (47.3%, 41.9% and 46.1% respectively) than in women (38.3%, 33.3% and 37% respectively). However, the association between vacA genotypes and age did not reach a statistical significant value. Logistic regression analysis results show that vacA i1m1 and vacA i1m2 genotypes were strongly associated with the risk of GC, the Odds Ratio (95% confidence interval) was 29.73 [5.08–173.73] and 9.17 [2.06–40.82] respectively, while vacAs1/cagA+ seems to be a risk factor for DU since it is inversely associated with GC (OR was 0.13 [0.02–0.75]. The results of this study suggest that vacA i1 genotype independently to vacAm status may be of a clinical usefulness and will help to identify patients at a high risk of GC development.

VacA genotypes and cagA‐EPIYA‐C motifs of Helicobacter pylori and gastric histopathological lesions

“…pylori vacAi1 as a possible marker in the identification of patients at high risk of gastric cancer developing. The association of this allele with pre-neoplastic lesions confirms our previous result 10 and also the results obtained in a study conducted in Iran. 44 However, the results obtained for intestinal metaplasia lesions should be taken with caution, since H. pylori is hardly detectable in these lesions.…”

“…The biopsies of these patients were previously used to characterize vacA-s, vacA-m, vacA-i regions and cagA 3 0 region polymorphism. 10,11 Therefore, in the present study, the correlation between vacA and cagA genotypes with histological lesions was established. Thus, all consenting patients had a personal interview before endoscopy, and were asked about individual characteristics.…”

“…15 Two sets of primers were used to determine the vacAi polymorphisms. 10 To increase the ability of cagA detection, four additional primers pairs (cag5c-F/cag3c-R; F1/B1, AB7628/AB7629 and Cag-TF/Cag-TR in addition to cag PAI empty site primers as previously described 11 ) were used. CagA was considered positive if it shows positive results by at least one of the four primers pairs and PCR negative with cag PAI empty site primers.…”

What is the Relationship Between Helicobacter Pylori CagA Genotypes and Gastrointestinal Diseases in the Iranian Population? A Systematic Review and Meta-Analysis

“…We observed that there was a signi cant relationship between EPIYA-ABCCC and gastric cancer in Iranian population. Overall, it can be concluded that the higher number of EPIYA-C copy numbers leads to the higher risk of gastric cancer (55,88). Therefore, according to our results, it seems that the presence of EPIYA-ABCCC strains of H. pylori should be considered as an appropriate marker in prevention of gastric cancer in Iranian population.…”

“…Based on our statistical analysis, frequency of cagA gene in Iranian population was evaluated about 71.34%, which con rmed previous ndings. In addition, the presence of cagA has a meaningful relationship with gastrointestinal diseases such as peptic ulcer, gastric atrophy, and gastric cancer (54)(55). In our project, also, abundance of cagA positive strains in peptic ulcer and gastric cancer patients was very high, and we also saw a meaningful relationship between the presence of cagA gene and gastric cancer (ORs: 2.277; p-value: 0.00).…”