Esophageal metaplasia is a cellular alteration in the esophagus where typical flat, squamous cells are replaced by cells resembling the intestine’s lining. This transformation responds to chronic irritation, representing a cellular change rather than a disease itself.
What Leads to Esophageal Metaplasia
Chronic gastroesophageal reflux disease (GERD) is the primary cause of esophageal metaplasia. GERD involves repeated backflow of stomach acid and digestive contents into the esophagus, causing ongoing irritation and inflammation. This persistent exposure damages the normal esophageal lining.
Constant injury prompts esophageal cells to adapt, replacing squamous cells with more resilient, intestinal-like cells. This cellular change protects against reflux. Other risk factors include obesity (especially abdominal), smoking, and a family history of Barrett’s esophagus.
How Esophageal Metaplasia Is Detected
Esophageal metaplasia often has no specific symptoms. It is typically identified during investigations for underlying conditions like chronic GERD, which may cause persistent heartburn or regurgitation. Diagnosis is primarily through an upper endoscopy (EGD).
During an EGD, a thin, flexible tube with a camera visualizes the esophagus, stomach, and upper small intestine. The doctor looks for characteristic salmon-pink areas. To confirm, small tissue samples (biopsies) are taken from suspicious areas. A pathologist examines these samples under a microscope to confirm intestinal metaplasia.
Why Esophageal Metaplasia Matters
Esophageal metaplasia is often the initial step toward Barrett’s esophagus, a pre-cancerous condition. While many never develop cancer, these altered cells increase the risk of esophageal adenocarcinoma. Progression typically follows a sequence: non-dysplastic metaplasia to low-grade dysplasia, then high-grade dysplasia, and finally to esophageal adenocarcinoma.
Dysplasia refers to abnormal cell changes, indicating a higher potential for malignant transformation. Low-grade dysplasia involves mild cellular abnormalities, while high-grade dysplasia indicates more advanced changes. The risk of progression to esophageal adenocarcinoma is low for non-dysplastic Barrett’s esophagus, but increases with dysplasia severity, making regular monitoring important.
Managing Esophageal Metaplasia Long-Term
Managing esophageal metaplasia involves addressing the underlying cause, often GERD, and monitoring for cellular progression. Key lifestyle modifications include dietary adjustments to avoid trigger foods like chocolate, coffee, fried foods, peppermint, and spicy items. Eating smaller, more frequent meals and avoiding food two to three hours before bedtime can reduce reflux episodes.
Weight management, especially reducing abdominal fat, helps alleviate stomach pressure worsening reflux. Quitting smoking is also recommended, as it increases stomach acid production and weakens the esophageal sphincter. Medications, like proton pump inhibitors (PPIs), reduce stomach acid, allowing the esophageal lining to heal and minimizing irritation.
Regular endoscopic surveillance with biopsies is standard practice to monitor for changes, such as dysplasia. Endoscopy frequency depends on the presence and grade of dysplasia. For high-grade dysplasia, advanced endoscopic procedures like radiofrequency ablation (RFA) or endoscopic mucosal resection (EMR) remove or destroy abnormal tissue. RFA uses heat energy to eliminate affected cells, while EMR physically removes suspicious lesions.