A Follow-up Study on the Effect of Helicobacter pylori Eradication on the Severity of Gastric Histology

Abstract

Helicobacter pylori genetic diversity and geographic distribution affect the severity of gastric histology; while eradication heals gastritis, the improvement of atrophy and intestinal metaplasia (IM) is still controversial. We investigated whether H. pylori infection and genotypes (cagA-vacA) influence the histological changes and whether eradication resolves these changes. Twenty-one patients (11 duodenal ulcer, 2 gastric ulcer, 8 gastritis) received treatment. Biopsies for CLO, PCR, histology, and culture were collected before and at 1 and 12 months after treatment, and serum samples at 0, 1, 2, 6, and 12 months. H. pylori eradication was achieved in 71% of the patients. Histological scores for H. pylori densities were significantly higher in the antrum and incisura angularis. Scores for mononuclear cell and neutrophil infiltration were significantly higher in regions with a high H. pylori density and improved progressively after eradication. Eight patients with atrophy including five with IM showed no significant changes 12 months after eradication. The cagA gene, detected in 13 (62%), the vacA-s1a gene, in 20 (95%), and the vacA-m1 gene, in 12 (57%) of 21 patients were significantly associated with duodenal ulcer. A gradual decline in antibody titer reached an average of 67% 12 months after eradication. H. pylori infection and the associated genotypes (cagA of Western type) affect the severity of the gastric histology (mild forms of atrophy and IM) and the disease outcome. Eradication of H. pylori resulted in healing of gastritis, but with no significant improvement in atrophy or IM.

Helicobacter pylori and Gastric Cancer

“…The data about the actual regression of IM or glandular atrophy are controversial. Several authors report an improvement only of the degree of inflammation within one year after eradication but no effect on metaplasia or atrophy [219,220]. Rokkas et al [221] presented a meta-analysis on the long-term effect of eradication therapy on gastric histology.…”

Participation of Capsaicin-Sensitive Afferent Nerves in the Gastric Mucosa of Patients with Helicobacter pylori-Positive or-Negative Chronic Gastritis

“…Nowdays, the importance of Helicobacter pylori infection is increasing as the main causative factor in gastric diseases in humans. This bacterium is highly prevalent in many countries [3] and it increases the risk for development of gastric and duodenal ulcer disease, gastric cancer, and gastric mucosa-associated lymphoid tissue lymphoma [4][5][6][7][8][9].…”

“…Capsaicin-sensitive afferent nerves take part in gastric mucosal protection in animals [1][2][3][4][5][6][7][8][9][10][11][12] and in healthy human subjects [13][14][15], and the presence of these fibers is proved to play a role in the development of human gastrointestinal disorders including gastritis, peptic ulcer, polyp without and with dysplasia, tumor, and inflammatory bowel diseases [16,17]. The mechanisms by which these neurons express their effects are complex but widely [20][21][22].…”

Gastric carcinogenesis

“…Several authors report an improvement only of inflammation within 1 year after eradication but no effect on the degree of metaplasia or atrophy [139,140]. Rokkas and colleagues presented a meta-analysis on the long-term effect of eradication therapy on gastric histology [141].…”