Amalia Rizki, Miftahussurur Muhammad, Syam Ari Fahrial, Uchida Tomohisa, Alfaray Ricky Indra, Fauzia Kartika Afrida, Rezkitha Yudith Annisa Ayu, Akada Junko, Matsumoto Takashi, Yamaoka Yoshio
Department of Environmental and Preventive Medicine, Oita University Faculty of Medicine, Yufu, Japan.
Helicobacter pylori and Microbiota Study Group, Institute of Tropical Disease, Universitas Airlangga, Surabaya, Indonesia.
Helicobacter. 2025 Mar-Apr;30(2):e70035. doi: 10.1111/hel.70035.
Despite the low prevalence of Helicobacter pylori in Indonesia, the high incidence of gastritis, predominantly atrophic gastritis, suggests that factors such as autoimmune gastritis (AIG) contribute to this unusual pattern. This study aims to investigate the epidemiology of AIG, histopathology, and its association with H. pylori status in Indonesia.
A cross-sectional study was conducted in various regions in Indonesia between 2014 and 2017; 380 eligible sera and gastric biopsies were available when this study was conducted. As many as 138 sera samples were included in this study based on the initial examination by the updated Sydney system. The diagnosis of AIG was confirmed by serologic testing for parietal-cell antibodies (PCA) and detailed histopathological assessment with sparing of antrum histopathological features.
Among the included samples in this study, 78.99% (109/138) were PCA positive (≥ 10 RU/mL) and 0.72% (1/138) were considered to be diagnosed as AIG (spared from antrum histopathological features). The majority of PCA positive cases were H. pylori positive (61/109; 55.96%) with a significant correlation (p < 0.05, R = 0.31). Additionally, a significant association was found between H. pylori infection and PCA level with gastric histopathological features (p < 0.05).
This study demonstrates that the incidence of gastritis without H. pylori infection in Indonesia is not attributable to AIG, as only a single AIG-positive case was found. These findings underscore the important role of H. pylori as a pathogenic factor in chronic gastritis and highlight its mechanisms in triggering immune responses and driving disease progression and histopathological changes.
尽管印度尼西亚幽门螺杆菌感染率较低，但胃炎（主要是萎缩性胃炎）的高发病率表明，自身免疫性胃炎（AIG）等因素促成了这种不寻常的模式。本研究旨在调查印度尼西亚AIG的流行病学、组织病理学及其与幽门螺杆菌感染状况的关联。
2014年至2017年在印度尼西亚各地区进行了一项横断面研究；本研究开展时共有380份符合条件的血清和胃活检样本。根据更新后的悉尼系统进行初步检查，本研究纳入了138份血清样本。通过壁细胞抗体（PCA）血清学检测以及保留胃窦组织病理学特征的详细组织病理学评估来确诊AIG。
在本研究纳入的样本中，78.99%（109/138）的PCA呈阳性（≥10 RU/mL），0.72%（1/138）被认为诊断为AIG（胃窦组织病理学特征未受累）。大多数PCA阳性病例幽门螺杆菌呈阳性（61/109；55.96%），具有显著相关性（p<0.05，R=0.31）。此外，幽门螺杆菌感染与PCA水平和胃组织病理学特征之间存在显著关联（p<0.05）。
本研究表明，印度尼西亚无幽门螺杆菌感染的胃炎发病率并非由AIG所致，因为仅发现1例AIG阳性病例。这些发现强调了幽门螺杆菌作为慢性胃炎致病因素的重要作用，并突出了其触发免疫反应、推动疾病进展和组织病理学变化的机制。
