Gastric atrophy (GA) and intestinal metaplasia of the gastric mucosa (GIM) are collectively known as chronic atrophic gastritis (CAG). These early conditions can lead to the development of gastric adenocarcinoma (GC). This review focuses on the current evidence and guidelines in diagnosis, management, and surveillance of chronic atrophic gastritis to identify those at risk of progression to gastric adenocarcinoma.
Chronic atrophic gastritis is considered a precursor lesion for gastric cancer, which is the fifth most common cancer globally and carries third-highest cancer-related mortality in the world. This aggressive cancer presents late in most countries with no screening program and leads to numerous deaths due to late diagnosis.
The common etiologies of this premalignant lesion are Helicobacter pylori (H. pylori) and autoimmune gastritis. Chronic inflammation leads to the loss of gastric mucosa leading to an acid depleted environment hypothesized as an early precursor to distal gastric cancer.
H. pylori is a microaerophilic gram-negative bacterial pathogen. Its role has been implicated in not only atrophic gastritis but also peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma (MALT). Identification and eradication of the pathogen have a significant role in reducing the risk of CAG.
It is of utmost importance to identify the precancerous lesions by identifying those at risk. It is also crucial to follow-up with surveillance endoscopy and, if needed, endoscopically intervening to avoid major resection surgery in advanced stage gastric cancer.
The popular Correa Cascade suggested the linear progression from chronic atrophic gastritis (CAG) with metaplastic intestinal epithelium to low-grade dysplasia (LGD), high-grade dysplasia (HGD), and eventually gastric adenocarcinoma.
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