Autoimmune gastritis studies and gastric cancer: True renaissance or bibliometric illusion

Table 1 Etiology of chronic gastritis and risk of gastric neoplasia

Etiology	Initial gastritis topography	Topography of atrophic gastritis	Typical pre-neoplastic lesions/risk markers	Risk of the neoplasia	Typical age at presentation
Autoimmune	Parietal cells zone (fundus and partly body of the stomach)	Fundus and body of the stomach	Gastrin induced ECL-cells hyperplasia /dysplasia	Type 1 NETs1–high; GC-very low	70+
Autoimmune + H. pylori	Parietal cells zone + antrum	Pangastritis	Mixed	Type 1 NETs1-high; GC- low; Rarely both tumors in the same patient[13]	70+
H. pylori	Antrum	Antrum predominant	OLGA-III-IV atrophy, incomplete IM, dysplasia	GC-highest possible risk with trend to decline in countries with high prevalence	50-70+ (varies due to the prevalence of H. pylori)
Autoimmune + bacterial (Streptococcus anginosus)?	Pangastritis?	No data	No data	GC-very low with trend to increase	< 50, predominantly in women

¹Usually two-third of Type 1 neuroendocrine tumors classified as Grade 1 during the diagnosis, however grade 2 or grade 3 gastric neuroendocrine tumors are associated with a larger size, deeper invasion, and extragastric recurrence, which require active treatment.

GC: Gastric cancer; IM: Intestinal metaplasia; ECL-cell: Enterochromaffine like cell; Type 1 NET: Type 1 neuroendocrine tumor; H. pylori: Helicobacter pylori.