Natural history of autoimmune atrophic gastritis: a prospective, single centre, long‐term experience

Abstract

Summary Background Autoimmune atrophic gastritis (AAG) is an immune‐mediated disorder characterised by destruction of gastric oxyntic mucosa Aim To explore gastric histopathological evolution in a cohort of AAG patients over a prolonged follow‐up Methods Single centre prospective study enrolling consecutive patients with histologically confirmed AAG between 2000 and 2018. All AAG patients undergoing endoscopic follow‐up every 1‐3 years were classified as having stages 1, 2 or 3 according to atrophy severity (mild, moderate and severe). AAG patients with either glandular or neuroendocrine dysplasia/neoplasia were classified as having stage 4. Disease stage progression, and changes in serum anti‐parietal cell antibody (PCA), chromogranin A and gastrin‐17 were assessed. Results In total, 282 AAG patients (mean age 60.3 years; F:M ratio 2.4:1; median follow‐up 3 years, interquartile range 1‐7) were enrolled. All patients with stages 1 or 2 progressed to stage 2 or 3 over time with a steady trend (P = .243) and regression from a severe to a milder stage was never noticed. Disease progression of patients with stages 1 or 2 occurred within the first 3 years. PCA positivity rate did not change over time. Stage 3 patients had higher gastrin‐17 levels compared to patients with stages 1 and 2 (median 606 vs 295 pg/mL; P < .001). In stage 3, the hazard ratio for the risk of developing stage 4 was 6.6 (95% CI 1.5‐29; P = .001). Conclusions AAG is a steadily progressive disease, in which stages 1 and 2 always progress to stage 3. The risk of developing a complicated disease stage is greater in patients with more severe gastric lesions.

Multiple Pseudopolyps Presenting as Reddish Nodules Are a Characteristic Endoscopic Finding in Patients with Early-stage Autoimmune Gastritis

“…In both cases, the nodular lesions shrank over time and were surrounded by atrophic mucosa, in agreement with the progression of gastric atrophy. Although a recent study reported that the histopathological progression of gastric atrophy from early-stage AIG occurred within three years, the relevant changes in the endoscopic appearances have not been determined (12). The findings in our cases indicate that the nodular lesions in non-atrophic areas of the gastric corpus are a manifestation of gastric inflammation and atrophy during the progress of early-stage AIG.…”

Helicobacter pylori-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions

“…In this scenario, the background of active H. pylori inflammation is likely to play a confounding role that may have hampered the accurate detection of gastric dysplasia. Nevertheless, the unexpected high baseline prevalence of dysplasia may be partially justified by the concomitant presence of AAG in a considerable number of our patients, in accordance with results from a recent study showing that in the presence of AAG the risk of developing more advanced stages on long-term follow-up is greater in patients with more severe gastric lesions[ 8 ]. The overlap between autoimmune and H. pylori -induced chronic gastritis may presumably be associated with a more severe gastric injury, especially in older subjects.…”

“…Helicobacter pylori ( H. pylori ) infection has been associated with premalignant gastric conditions (PGC), such as chronic atrophic gastritis and intestinal metaplasia (IM), which are strongly associated with dysplasia and Lauren intestinal-type of gastric carcinoma (GC)[ 1 - 7 ]. Autoimmune atrophic gastritis (AAG) is responsible for progressive mucosal atrophy (antrum-sparing) with or without IM[ 8 ]. Many studies have attributed gastric carcinogenesis to both genetic predisposition and H. pylori -induced gastric inflammation[ 9 - 13 ].…”

Cell Blood Count Alterations and Patterns of Anaemia in Autoimmune Atrophic Gastritis at Diagnosis: A Multicentre Study

“…Particularly, iron deficiency anaemia was more common in younger female patients, whereas pernicious anaemia was more common in older male patients. These findings may be explained by the slow evolution of AAG, that may take several years to progress [1,33,34]. It is reasonable to assume that iron deficiency characterises earlier disease stages, in which hypo-achlorhydria causes iron malabsorption, even if additional unknown immunological factors may have a role.…”