We read with interest the paper by Rugge et al on the long-term natural history in Helicobacter pylori (Hp)-negative patients with autoimmune gastritis (AIG)1 whose main findings were that (1) corpus-restricted inflammation, pseudopyloric (PPM) rather than intestinal metaplasia (IM), and enterochromaffin like (ECL)-cell hyperplasia and neoplasia were the main histopathological hallmarks associated with AIG; (2) patients with AIG seem not to have an increased gastric cancer (GC)-risk when previous/current Hp infection is thoroughly excluded, but surveillance for type-1 gastric neuroendocrine tumours (t1-gNETs) risk may be performed.

We fully agree that corpus-restricted inflammation, ECL-cell hyperplasia, t1-gNETs and PPM are findings commonly associated with AIG, although not exclusively present.

ECL-cell hyperplasia is the consequence of increased gastrin and a result of impaired gastric acid secretion due to oxyntic glands atrophy, over time possibly leading to …