Cure of Helicobacter pylori infection in atrophic body gastritis patients does not improve mucosal atrophy but reduces hypergastrinemia and its related effects on body ECL‐cell hyperplasia

Abstract

Cure of H. pylori infection in patients with atrophic gastritis reverses some adverse effects on gastric function and ECL cell hyperplasia. H. pylori infection may be cured in atrophic body gastritis patients with partial reversion of its negative consequences on acid secretion and body ECL cell hyperplasia.

Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands

“…The most common autoantibodies in H. pylori-infected patients are anticanalicular and appear to be directed against the Hϩ,K ϩ -ATPase (as are the classic anti-parietal cell antibodies) and are strongly associated with body atrophy. When H. pylori organisms are present along with AG, then treatment of the H. pylori infection is important and can even reduce the serum gastrin levels and cause regression of the ECL cell hyperplasia, though the atrophic changes do not appear to improve (24).…”

The long‐term effects of cure of Helicobacter pylori infection on patients with atrophic body gastritis

“…For this purpose, systematic sampling of the gastric mucosa, including four biopsies from the antrum and seven from the fundus ⁄ corpus, was carried out. 10,17 The absence of H. pylori at histology or a decrease of at least 50% in the initial titre of H. pylori immunoglobulin G, associated with a reduction in inflammatory cells, was accepted as a criterion for the successful cure of infection. 19 Acid secretory tests were repeated, and fasting gastrin and pepsinogen I levels were also assessed.…”

“…6 In 50% of patients with atrophic body gastritis, evidence of H. pylori infection, detected only at the serological level, has been found. 7 We and others have shown that, following the cure of H. pylori infection in patients with atrophic body gastritis, achlorhydria is partially reversed and histological corporal inflammation is improved; [8][9][10][11] however, it is still a matter of debate whether, following the cure of…”

“…Studies may be interpreted from two different points of view: 12 on the one hand, the data may indicate that the oxyntic mucosal damage is reversed after cure; [13][14][15] on the other, the glands may simply be concealed by the inflammatory infiltrate, and thus the body atrophy score and metaplastic changes are not modified by eradication. [9][10][11]16 Moreover, the level of agreement in terms of the diagnosis of body atrophy between experienced pathologists falls into a poor statistical range, 17 as the criteria for defining body atrophy are not well-established, particularly in the presence of active H. pylori infection. Indeed, a dense mononuclear cell infiltrate in the gastric body mucosa may suggest negligible or complete loss of glands, whereas only the coexistence of a loss of glands and replacement by intestinalized metaplastic epithelium represents true atrophy.…”

Molecular Epidemiology of Helicobacter pylori in Brazilian Patients with Early Gastric Cancer and a Review to Understand the Prognosis of the Disease

“…In the same way, other randomized studies identified that H. pylori eradication in intestinal metaplasia could be important in the regression of this precancerous lesion [76,[109][110][111]119,120]. Oppositely, other trials, both follow-up and randomized control, had not identified regression of intestinal metaplasia when H. pylori eradication was administrated [121][122][123][124][125][126][127][128][129].…”