H.Pylor related chronic atrophic gastritis and Gastric Cancer

Helicobacter pylori (H. pylori)-related chronic atrophic gastritis (CAG) is a condition where long-term infection by H. pylori bacteria leads to damage in the stomach lining. This damage includes inflammation, loss of stomach gland cells (atrophy), and replacement of normal stomach tissue with intestinal-like cells, known as intestinal metaplasia (IM). CAG caused by H. pylori significantly increases the risk of developing gastric cancer.

H. pylori is classified as a Class I carcinogen due to its strong link to stomach cancer. The bacteria release harmful proteins, such as CagA and VacA, which disrupt normal cell functions, trigger chronic inflammation, and cause DNA damage. This persistent inflammation accelerates the progression of Correa’s cascade, a step-by-step process from gastritis to IM, dysplasia (abnormal cell growth), and eventually gastric cancer. Additionally, H. pylori can evade the immune system, allowing the infection to persist and promote cancer development.

Epigenetic changes, such as DNA methylation, play a major role in this process. H. pylori silences tumor-suppressor genes and activates cancer-promoting pathways like WNT and NF-κB. Co-infection with Epstein–Barr virus (EBV) further increases cancer risk through combined effects on cellular growth and signaling.

While early eradication of H. pylori can prevent progression, advanced stages of IM or dysplasia may become irreversible. Treatment typically involves antibiotics combined with proton pump inhibitors, with newer therapies like vonoprazan showing promise. Regular monitoring after eradication is essential, as early detection and intervention can significantly reduce the risk of gastric cancer.