Clinical and histological associations of cagA and vacA genotypes in Helicobacter pylori gastritis.

Abstract

Aims-To determine the relation among the cytotoxin associated gene (cagA) and vacuolating cytotoxin gene (vacA) status of Helicobacter pylori isolates, the associated clinical diseases, and the severity and pattern of chronic gastritis. Methods-Helicobacter pylori was cultured from gastric biopsies obtained from dyspeptic patients. DNA was extracted from the isolates and the cagA and vacA status determined by the polymerase chain reaction (PCR). The prevalence of the diVerent cagA and vacA genotypes in three clinical groups, duodenal ulcer, gastric ulcer, and non-ulcer dyspepsia was compared. The histological features in sections from two antral and two corpus biopsies were graded by one blinded observer. The grades were compared with age and sex matched groups with different cagA and vacA genotypes, and with duodenal ulcers, or non-ulcer dyspepsia. Results-Isolates from 161 patients were included. One hundred and nine (68%) harboured a cagA+ strain and 143 (89%) harboured a vacA s1 strain. The prevalence of cagA+ strains in duodenal ulcer patients (94%) was highly significantly greater than in those with non-ulcer dyspepsia (56%). However, of the patients infected with a cagA+ strain, almost equal numbers had non-ulcer dyspepsia or peptic ulceration. Chronic inflammation, polymorph activity, surface epithelial degeneration, atrophy, and intestinal metaplasia were all significantly more severe in the cagA+ than in the cagA− group, whereas only corpus epithelial degeneration was significantly more severe in the vacA s1 group compared with the vacA s2 group. Patients infected with cagA+ strains were almost four times more likely to have antral intestinal metaplasia than cagA− patients. An antral predominant gastritis was present in duodenal ulcer patients compared with matched nonulcer dyspepsia patients, but this was not attributable to cagA or vacA status. Conclusions-Helicobacter pylori strains showing cagA positivity and the vacA s1 genotype are associated with more severe gastritis but these virulence factors do not appear to determine the overall pattern. The pattern is closely linked to clinical disease. Therefore, it is likely that the nature of the disease complicating chronic infection is determined by host and environmental factors, while bacterial factors determine the magnitude of the risk of developing such disease. (J Clin Pathol 1998;51:55-61)

Serum Antibodies Positivity to 12 Helicobacter pylori Virulence Antigens in Patients with Benign or Malignant Gastroduodenal Diseases – Cross-sectional Study

“…Protein CagA is the most investigated H. pylori virulence factor, but its connection with the presence of various mucosal histological changes is still controversial and there are many studies with contradictory results (30)(31)(32)(33). Our results are consistent with previous observations, in which CagA elicited high neutrophil accumulation, measured as inflammation activity in gastric mucosa (29).…”

Prevalence of vacA, cagA and babA2 genes in Cuban Helicobacter pylori isolates

“…Here, 73.2% of the H pylori strains were cagA-positive, a prevalence similar to that reported in many studies from Western countries (e.g. USA, 60% [7] ; Spain, 66% [26] ; and England, 68% [27] ) but lower than that reported in some East Asian studies, which encountered over 90% of cagApositive isolates (Table 4) [25,28] . In addition, a highly significant correlation was observed between cagA status and vacAs1 and vacAs1m1 genotypes (Table 2), which is commonly linked to an increase in H pylori virulence [13,14,29,30] .…”

“…Moreover, a high frequency of cagA-positive strains was observed in DU patients ( Table 3), indicating that a statistical association could be reached by increasing the number of patients in future studies. [14,23,26,27] 66-73 [14,23,26,27] 34-72 [13,14,34] America 57-68 16-48 37-44 29-63 [19,20,24] 57-75 [7,19,24] 46-69 [24,32] East Asia 100 0 41-94 5-55 [12,25,28] 90-100 [12,25,28,35] 80-100 [12,21,35] Torres…”

Correlation of Helicobacter pylori Genotypes with Gastric Histopathology in the Central Region of a South-European Country

“…Our study population is rather young but, even so, we demonstrated that glandular atrophy, neutrophil activity, and OLGA stages were significantly higher in older patients. Infection generally occurs during childhood and development of more severe histopathological manifestations, such as intestinal metaplasia and glandular atrophy, are linked to prolonged infection and consequently to patients' age [25,26]. A study performed in the northern part of the country also revealed that patients with atrophic gastritis were significantly older than the ones with no atrophy [5].…”