Intestinal metaplasia (IM)

Intestinal metaplasia (IM) is a histological transformation where the normal epithelial lining of the stomach or esophagus is replaced by cells resembling the intestinal mucosa, characterized by the presence of goblet cells, absorptive cells, and Paneth cells (StatPearls, 2023). This condition is primarily a response to chronic mucosal injury and inflammation, such as that caused by Helicobacter pylori infection in the stomach or chronic acid reflux in the esophagus, the latter being the hallmark of Barrett's esophagus (NIH, 2023). It is widely recognized as a precancerous lesion in the Correa sequence of gastric carcinogenesis, significantly increasing the risk of developing adenocarcinoma (Correa, 1988). IM is often classified into complete (Type I) or incomplete (Type II/III) types, with the incomplete type carrying a higher risk of malignancy (PubMed, 2020). Because IM is a tissue-level pathological state rather than a specific protein or receptor, it is not a direct therapeutic target; instead, clinical management focuses on treating the underlying causes and performing regular endoscopic surveillance (ASGE, 2020). Biomarkers like CDX2, MUC2, and TFF3 are frequently used to identify and characterize the extent of the metaplastic change during pathological evaluation (PubMed, 2021). Eradication of H. pylori may regress early stages of metaplasia, but the point of no return in the carcinogenic sequence remains a subject of clinical debate (StatPearls, 2023).

Other names

Gastric intestinal metaplasiaGoblet cell metaplasiaBarrett's esophagus (specialized intestinal metaplasia)

Not applicable as this is a histological condition rather than a molecular target.