2022년 The 28th National Congress of Digestive Diseases (Digestive and Liver Disease 54S2 (2022) S85. OC.07.3)
Background and aim: Autoimmune atrophic gastritis (AAG) is a chronic immune-mediated disease characterized by corpus-predominant atrophy. Several studies support Helicobacter pylori (HP) as a pathogenetic agent in AAG since it might induce autoimmunity through a molecular mimicry. However, only a few data are available on how HP could influence AAG evolution, the phenotype of the disease, and the neoplastic risk. In this study, we aimed to compare AAG patients with a history of HP infection to AAG patients without HP history regarding clinical, histological, and serological characteristics over time.
Materials and methods: We enrolled patients with AAG histological diagnosis between 2000 and 2021. Two groups were identified: patients with HP history and/or antral atrophy AAG (HP-AAG), and primary AAG with neither HP history, nor antral atrophy (considered as a stigma of a previous HP infection). We recorded clinical, serological, and histological data at diagnosis (T0) and at the time of the last available follow up (T1). Results were considered significant if p<0,05.
Results: In total 214 AAG patients were enrolled: 120 primary AAG and 94 HP-AAG. Mean follow-up was 7.4 ± 4.8 y. At T0 HP-AAG patients had higher OLGA stage (p<0.001), instead, total gastrin level was higher in primary AAG (p=0.003). From T0 to T1 PGI and PGII were significantly reduced (p=0.030, p=0.00). Corpus atrophy was stable in 50% of patients over time, but got worse in 38%, and improved in 12% (p=0.001), and it was similar in both groups. OLGA stage did not change over time (p = 0.136), especially it was stable in primary AAG (67%) than HP-AAG (40%) (p=0,001). Past HP infection was found to be a risk factor for OLGA progression (OR 2.41 CI 95% 1.31-4.43 p=0.005). NET prevalence was 4.5% at T0 and 3.7% at T1 (p=0.8), with no difference between the two groups. We found only 2 cases of gastric cancer among our patients, with a prevalence of 0.6% and an incidence of 0.1 case/person-year. Both cases were in the HP-AAG group, and one also had Familial Adenomatous Polyposis.
Conclusions: In AAG natural history, corpus atrophy tends to worsen or be stable in the majority of AAG patients, an improvement being rare. A history of HP infection is a risk factor for OLGA progression; however, this staging system does not seem to reliably describe the AAG evolution over time. We observed a significant reduction of both PGI and PGII, in time. While we confirm the relatively high risk of NET in AAG patients, we found a very low incidence of gastric cancer.
2022년 The 28th National Congress of Digestive Diseases (Digestive and Liver Disease 54S2 (2022) S85. OC.07.3)
Background and aim: Autoimmune atrophic gastritis (AAG) is a chronic immune-mediated disease characterized by corpus-predominant atrophy. Several studies support Helicobacter pylori (HP) as a pathogenetic agent in AAG since it might induce autoimmunity through a molecular mimicry. However, only a few data are available on how HP could influence AAG evolution, the phenotype of the disease, and the neoplastic risk. In this study, we aimed to compare AAG patients with a history of HP infection to AAG patients without HP history regarding clinical, histological, and serological characteristics over time.
Materials and methods: We enrolled patients with AAG histological diagnosis between 2000 and 2021. Two groups were identified: patients with HP history and/or antral atrophy AAG (HP-AAG), and primary AAG with neither HP history, nor antral atrophy (considered as a stigma of a previous HP infection). We recorded clinical, serological, and histological data at diagnosis (T0) and at the time of the last available follow up (T1). Results were considered significant if p<0,05.
Results: In total 214 AAG patients were enrolled: 120 primary AAG and 94 HP-AAG. Mean follow-up was 7.4 ± 4.8 y. At T0 HP-AAG patients had higher OLGA stage (p<0.001), instead, total gastrin level was higher in primary AAG (p=0.003). From T0 to T1 PGI and PGII were significantly reduced (p=0.030, p=0.00). Corpus atrophy was stable in 50% of patients over time, but got worse in 38%, and improved in 12% (p=0.001), and it was similar in both groups. OLGA stage did not change over time (p = 0.136), especially it was stable in primary AAG (67%) than HP-AAG (40%) (p=0,001). Past HP infection was found to be a risk factor for OLGA progression (OR 2.41 CI 95% 1.31-4.43 p=0.005). NET prevalence was 4.5% at T0 and 3.7% at T1 (p=0.8), with no difference between the two groups. We found only 2 cases of gastric cancer among our patients, with a prevalence of 0.6% and an incidence of 0.1 case/person-year. Both cases were in the HP-AAG group, and one also had Familial Adenomatous Polyposis.
Conclusions: In AAG natural history, corpus atrophy tends to worsen or be stable in the majority of AAG patients, an improvement being rare. A history of HP infection is a risk factor for OLGA progression; however, this staging system does not seem to reliably describe the AAG evolution over time. We observed a significant reduction of both PGI and PGII, in time. While we confirm the relatively high risk of NET in AAG patients, we found a very low incidence of gastric cancer.