Atrophic gastritis and Helicobacter pylori infection in outpatients referred for gastroscopy

Abstract

Background-Atrophic gastritis has been shown to be one of the long term sequelae of Helicobacter pylori infection. Aims-To determine the prevalence of atrophic gastritis in outpatients, to study the accuracy of serological methods for revealing atrophy, and to define the association of H pylori infection with atrophic gastritis in these patients. Patients/methods-A total of 207 consecutive outpatients referred for gastroscopy were included. Biopsy specimens from the antrum and corpus were assessed histologically according to the Sydney system. Serum samples were studied for H pylori IgG and IgA antibodies by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence. Results-Histological examination revealed atrophic gastritis in 52 (25%) of 207 patients. H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with atrophic corpus gastritis. Low serum pepsinogen I was the most sensitive and specific indicator of moderate and severe atrophic corpus gastritis. All six patients with moderate atrophic corpus gastritis had H pylori infection but eight of 10 patients with severe atrophic corpus had increased parietal cell antibodies and nine had no signs of H pylori infection. Conclusions-Atrophic antral gastritis was strongly associated with CagA positive H pylori infection. Severe atrophic corpus gastritis was not determined by H pylori tests but low serum pepsinogen I, high gastrin, and parietal cell antibodies may be valuable in detecting these changes.

Relation of atrophic gastritis with Helicobacter pylori -CagA+ and interleukin-1 gene polymorphisms

“…It has been reported in sev- [4,23] . In the present study, infection with H pylori CagA + is associated with atrophic gastritis of the antrum, but not of the body, results which are in accordance with those reported by Oksanen et al, 2000 [24] . Indeed, in a stomach affected by ABG, the microenvironment is more hostile for the survival and growth of H pylori promoting spontaneous eradication of the bacteria and a progressive decline in concentrations of serum antibodies to H pylori [25][26][27] .…”

“…H pylori and its virulence factor CagA may be involved in processes during the early stages of inflammation of the antrum that lead to extension of atrophic gastritis towards the gastric body [29] . In concordance with other studies, infection with H pylori-CagA + is associated with low PGI/PGII ratios [24] . Several studies have reported an association of low PGI concentrations and low PGI/PGII ratios with precancerous lesions as well as with gastric cancer [30][31][32] .…”

Relationship Between Metabolic Parameters and Helicobacter Pylori Infections With Upper Gastrointestinal System Endoscopy and Gastric Histopathology Results in Patients With Dyspeptic Type 2 Diabetes Mellitus

“…Bunun da glukoz metabolizmasındaki değişikliklerin HP kolonizasyonunun hazırlanmasında bir rolü olduğuna bağlamışlardır. Diyabet ve obesite sırasında gözlenen azalmış gastrik motilite (59,60) ve musinlerin nonenzimatik reaksiyonu ile gastrik mukozadaki kimyasal değişiklikler(61) kolonizasyonu kolaylaştırabilir (62). Kimyasal değişiklikler sonrası mukus hücrelerinin apikal membranına adheze olan HP ultrastrüktürel değişiklikler yapar.…”

Disappearing Microbiota: Helicobacter pylori Protection against Esophageal Adenocarcinoma

“…First, gastric acidity begins to diminish after decades of carriage of H. pylori and the gradual agerelated development of atrophic gastritis (15,31). Therefore, the H. pylori-positive stomach produces a lower acid load and less damage to the distal esophagus when reflux arises.…”