Spontaneous disappearance of Helicobacter pylori antibodies in patients with advanced atrophic corpus gastritis

Abstract

Background. Only a few reported studies focus on the natural history and course of advanced and severe chronic atrophic gastritis. Methods. In this study we followed 47 men (mean age 62 years) with advanced (moderate or severe) Helicobacter pylori-positive atrophic corpus gastritis. Duration of endoscopic follow-up was 6 years and follow-up based on serum levels of pepsinogen I and antibodies to H. pylori covered a period of 10 years. None of the patients was treated for H. pylori infection prior to end of follow-up. Results. The median H. pylori antibody titre declined (IgG from 4000 to 1300; IgA from 200 to 50) in the study population, and 11 men (23%) converted to seronegative (p=0.0005, Fisher's exact test). There was a small but significant (p=0.0004, Page's test) declining trend in mean atrophy score of the corpus during follow-up (from 2.5 to 2.2). However, no significant changes were observed in grade of atrophy or intestinal metaplasia of the antral mucosa or in grade of intestinal metaplasia in the corpus. The mean SPGI level remained at the initial low level during the entire follow-up. Conclusions. H. pylori antibodies disappear spontaneously within 10 years in almost one fourth of patients with advanced atrophic corpus gastritis. The disappearance of H. pylori antibodies is accompanied by no or more than a mild improvement of the gastric mucosa.

Value of Additional Corpus Biopsy for Diagnosis of Helicobacter Pylori in Atrophic Gastritis

“…Therefore, antrum based biopsy only in case of atrophic gastritis yields to more false negative results [22]. This finding was in concordance with Kang HY et al [23], Satoh K et al [24], Yoo et al [25,26], and Kokkola A et al [14]. This study clarified that the sensitivity of H. pylori detection is decreased in cases of antral atrophic gastritis more than corpus one in the same time as inversely correlated with degree of atrophy.…”

“…It is widely recommended by many authors that eradication of H. pylori is mandatory in case of atrophic gastritis since the atrophy may reverse after successful eradication therapy [12,13]. But, it's difficult and challenging to detect H. pylori in case of atrophic gastritis [14].…”

Preventive effects of etodolac, a selective cyclooxygenase‐2 inhibitor, on cancer development in extensive metaplastic gastritis, a Helicobacter pylori‐negative precancerous lesion

“…7,10 Moreover, patients with extensive intestinal metaplasia-that is, metaplastic gastritis-should not be treated with eradication therapy, as bacterial load decreases with the progression of intestinal metaplasia, eventually resulting in spontaneous eradication. 13,14 Alternative chemopreventive measures are thus needed for the prevention of stomach cancer in subjects with metaplastic gastritis.…”

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

“…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] . Atrophic gastritis has been considered as a consequence of prolonged gastritis caused by H pylori and the association between H pylori infection and gastric cancer appears stronger when the infection is recorded several years before the onset of cancer [28] .…”