Role of Corpus Gastritis and cagA -Positive Helicobacter pylori Infection in Reflux Esophagitis

Abstract

Considering that the role of Helicobacter pylori infection in gastroesophageal reflux and reflux esophagitis (GERD) is still controversial and that the role of virulence markers of the bacterium has not been evaluated in most studies of GERD, we investigated the association among H. pylori infection with cagA-positive and -negative strains, corpus gastritis, and GERD in a large group of patients by controlling for confounding factors. We studied prospectively 281 consecutive adult patients: 93 with GERD and 188 controls. H. pylori infection status was diagnosed by culture, by the preformed urease test, with a carbolfuchsin-stained smear, and by histology. The cagA status was determined by PCR of H. pylori isolates and gastric biopsy specimens. H. pylori infection was diagnosed in 191 (68.0%) of 281 patients. Among the 93 patients with GERD, 84 presented with mild or moderate esophagitis and 9 presented with severe esophagitis. In the multivariate analysis, the age of the patients and the degree of oxyntic gastritis were associated with GERD. Among the strains isolated from patients with GERD and from the control group, 24.4 and 66.9%, respectively, were positive for cagA (P < 0.001). Compared to infection with cagA-negative strains, infection with cagA-positive H. pylori strains was associated with a more intense gastritis in the corpus (P ‫؍‬ 0.001). cagA status (odds ratio [OR] ‫؍‬ 0.16, 95% confidence interval [CI] ‫؍‬ 0.07 to 0.40), gastritis of the corpus (OR ‫؍‬ 0.69, 95% CI ‫؍‬ 0.48 to 0.99), and age (OR ‫؍‬ 1.04, 95% CI ‫؍‬ 1.01 to 1.07) were associated with GERD. In conclusion, the study provides evidence supporting the independent protective roles of cagA-positive H. pylori strains and the degree of corpus gastritis against GERD.

Clinical Relevance of the cagA,vacA and babA2 Virulence Factors ofHelicobacter pylori in Egyptian Patients with Gastroduodenal Diseases.

“…Several studies have provided evidence supporting the protecting role of cagA-positive H. pylori strains against GERD [59, [60], [61], [62]and [63], but these results were not confirmed by others [64], [65]. On the contrary,there was a significant increase in cagA-positive H. pylori strains in GERD (70%) [66].…”

Neither genotype nor the gastric colonization site of Helicobacter pylori are predictive factors for the development of erosive esophagitis in patients with peptic ulcer disease, 1 year after eradication

“…In Brazil, PEREIRA-LIMA et al (31) concluded that H. pylori gastric infection and especially H. pylori CagA-positive may play a protective role against the development of the most severe forms of GERD. On the other hand in this study, the patients had dyspepsia, peptic ulcer and erosive gastritis, differently that our study, in which all patients homogeneously had peptic ulcer disease.…”

Análise das impressões digitais de DNA e de fatores de virulência de linhagens de Helicobacter pylori

“…Recentemente, alguns trabalhos mostram que a infecção pelo H. pylori poderia ter um efeito protetor contra a doença (17,18,33,45,57) . De modo complementar, mostrou-se que pacientes infectados por linhagens mais virulentas (cagA+, vacAs1) estariam inversamente associados com o desenvolvimento da doença.…”

“…De modo complementar, mostrou-se que pacientes infectados por linhagens mais virulentas (cagA+, vacAs1) estariam inversamente associados com o desenvolvimento da doença. Deste modo, pacientes infectado por tais linhagens seriam protegidos contra complicações decorrentes do refluxo ácido (17,33,45,57) . Algumas hipóteses têm sido propostas para explicar tal fenômeno.…”

“…Algumas hipóteses têm sido propostas para explicar tal fenômeno. Por um lado, postula-se que este efeito deva-se à redução da secreção ácida gerada pela infecção por linhagens mais virulentas (51,57) , por outro acredita-se que, além dos fatores de virulência da bactéria, alguns fatores genéticos do hospedeiro devem contribuir nesta proteção (45) . Na presente série, detectou-se uma associação entre a presença de linhagens menos virulentas com esta doença ao se comparar o genótipo s2 do gene vacA da bactéria com o desenvolvimento de esofagite de refluxo, assim como observado por outros autores (18,32,44,57) .…”