Exploring the potential of artificial intelligence in assessing the risk of gastric neoplastic lesions in patients with corpus atrophic gastritis
摘要
Corpus atrophic gastritis (CAG) requires endoscopic-histological surveillance due to the risk of developing gastric neoplastic lesions (GNL). This study aimed to identify variables associated with GNL development at long-term follow-up using a Fisher score-based feature-ranking-approach coupled with a One-Class Support-Vector-Machine (SVM) model.
MethodsA dataset containing 30 clinical, endoscopic, and histological variables from consecutive CAG patients (2001–2023) adhering to a surveillance-program was considered. GNL presence at the longest available follow-up was recorded. Gastric biopsies and histological evaluations followed the updated-Sydney-system. A Fisher score-based feature ranking method and a One-Class SVM were employed to select key variables linked to GNL development, and then validated with synthetically generated data.
ResultsOverall, 355 CAG patients were initially considered. Of these, 36 were excluded due to the presence of GNL at baseline gastroscopy, and 216 for missing data. Thus, a total of 103 patients were considered and grouped into: CAG patients with [22 patients (F 68.1%), median-age 68(35–83) years] and without GNL at follow-up [81 patients (F 72.8%) median-age 59(26–84) years]. After a median follow-up of 60(12–192) months, 13 epithelial GNL (gastric adenocarcinoma or high/low-grade dysplasia) and nine type-1 gastric-neuroendocrine-tumors (T1gNET) were recorded. Parietal-cell-antibodies and pepsinogen-I < 30 μg/l were associated with epithelial GNL and T1gNET. Antral inflammation and age > 60 were linked to epithelial GNL, while anti-thyroperoxidase-antibodies, smoking, and dyspeptic-symptoms were linked to T1gNET. Low-dose aspirin and H. pylori eradication therapy showed inverse associations with epithelial GNL and T1gNET, respectively.
ConclusionsThis is the first study in which an AI-model simultaneously considers clinical, endoscopic, and histological features from a dataset of CAG patients, showing the potential to identify variables associated with GNL development.