Private Endoscopy Clinic; Henry Dunant Hospital, Athens; Statistical Analysis; Athens Medical Group; GI Dept Athens Medical, Paleo Faliron Hospital
aPrivate Endoscopy Clinic (Stergios N. Kouvaras, Ioannis G. Koumarianos); bHenry Dunant Hospital, 1st Gastroenterology Clinic (Stergios N. Kouvaras, Konstantinos Ekmektzoglou, Theodoros Rokkas); cStatistical Analysis (George Kounis); eGI Dept Athens Medical, Paleo Faliron Hospital (Sotirios D.Georgopoulos); dAthens Medical Group, Pathology Department (Charikleia Spiliadi)
Ann Gastroenterol 2026; 39 (2): 279-280
The comments raised in the letter by Prof. Kountouras et al [1] are fully consistent with the findings of our study [2]. Nevertheless, several issues discussed in that letter were beyond the scope of our investigation. In this context, 3 points merit attention:
In addition to the inflammation induced by Helicobacter pylori (H. pylori), other bacteria—such as Porphyromonas gingivalis (Pg)—have been reported to accelerate the progression of the Correa cascade. In our study, the presence of Pg in the gastric mucosa was not investigated. However, this possible coexistence does not diminish the primary role of H. pylori as an etiopathogenic factor in the evolution of the Correa cascade. In our cohort, a strong correlation was observed between H. pylori infection and the development of gastric intestinal metaplasia (GIM), both complete and incomplete types (P<0.001). Our data also support the presence of bile salts in the gastric lumen as an additional pathogenic mechanism contributing to GIM [2-4].
Both the CagA and VacA cytotoxins of H. pylori play a central role in driving the inflammatory process that promotes gastric carcinogenesis, in accordance with Correa’s model [5]. However, the aim of our study was to assess the prevalence of H. pylori infection and GIM, rather than to determine the proportion of H. pylori strains expressing CagA or VacA.
Several studies have shown regression of GIM in the gastric body and antrum 3 to 5 years after successful eradication therapy [6]. The objective of our study, however, was to evaluate the prevalence of GIM in our population. The impact of H. pylori eradication on the epidemiology of GIM was not examined.
1. Kountouras J, Polyzos SA, Papanikolaou IS, Doulberis M, Liatsos C, Vardaka E. Impact of Helicobacter pylori eradication on the progression of Correa's cascade. Ann Gastroenterol 2026;39:279.
2. Kouvaras SN, Koumarianos IG, Ekmektzoglou K, et al. Prevalence of Helicobacter pylori infection and gastric intestinal metaplasia in Greek patients. Ann Gastroenterol 2025;38:604-609.
3. Wang M, Lou E, Xue Z. The role of bile acid in intestinal metaplasia. Front Physiol 2023;14:1115250.
4. He Q, Liu L, Wei J, et al. Roles and action mechanisms of bile acid induced gastric intestinal metaplasia:a review. Cell Death Discov 2022;8:158.
5. Kazakos EI, Petinaki E, Liatsos C, Papanikolaou IS, Anastasiadou K, Kountouras J. The potential role of Helicobacter pylori-related mast cell activation in the progression from gastroesophageal reflux to Barrett's esophagus and esophageal adenocarcinoma. Microorganisms 2025;13:1883.
6. Hwang YJ, Kim N, Lee HS, et al. Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years. Aliment Pharmacol Ther 2018;47:380-390.