Barrett’s Esophagus: Epithelial Metaplasia

The mucosal layer of the human esophagus is lined with cells known as stratified squamous epithelium. This epithelium is ideal for areas with lots of abrasion and use (ie: swallowing food and drink) because it is easily shed and replaced.

However, in Barrett’s esophagus the squamous epithelium is replaced by another cell type known as columnar epithelium interspersed with goblet cells (ie: cells that secrete mucous). This type of epithelium normally lines the intestine. This abnormal change in esophageal cell type is called "metaplasia".

Long standing acid reflux is responsible for the metaplasia that occurs in the esophagus. Poorly controlled reflux allows stomach acid to regurgitate into the lower esophagus. After many years of this the esophagus responds by changing its lining to be more like an intestinal cell type; this is referred to as “intestinal metaplasia”. The intestinal cell types, including goblet cells, secrete mucous and bicarbonate ions to neutralize the refluxed acid. This change is believed to help prevent damage to the esophagus.

Why is Barrett’s esophagus a bad thing? Occasionally, the metaplastic cells undergo a process known as dysplasia in which they assume pre-cancerous characteristics. Many patients do not progress past low grade dysplasia, and therefore their risk of developing esophageal cancer is minimal. However, a small percentage of patients will go on to develop high grade dysplasia, which puts them at significant risk for developing esophageal cancer.

Signs and Symptoms

Barrett’s esophagus does not cause any symptoms per se. Rather the symptoms are usually related to gastroesophageal reflux disease (GERD). Most patients with GERD have “heart burn” symptoms, especially after eating spicy foods. Heart burn refers to a burning pain behind the sternum. In addition, patients with GERD frequently have nausea and mild amounts of regurgitation.

Interestingly, patients who develop Barrett’s esophagus often have improvement in GERD symptoms. This is because the intestinal type cells are able to neutralize the acid more effectively.

Diagnosis

Diagnosis of Barrett’s esophagus usually occurs after years of uncontrolled GERD symptoms. Patient’s with severe reflux can undergo upper endoscopic visualization of the esophagus (aka: swallowing a "roto-rooter" with a camera on the end of it). At this time biopsies can be taken to look for metaplasia and dysplasia. A pathologist reviews the biopsy samples and is able to tell if Barrett’s esophagus is present.

Treatment

Treatment is highly variable and depends on the severity of dysplasia seen. For simple metaplasia and low grade dysplasia treating the acid reflux with medications such as H2-blockers (ie: ranitidine, famotidine, etc.) and proton pump inhibitors (omeprazole, lansoprazole, etc.) can often reverse the changes.

In patients with high grade dysplasia numerous options exist including surgery, radiofrequency ablation of the esophageal lining, and close endoscopic monitoring with frequent repeat biopsies. Treatment is highly tailored to the individual patient.

Overview

Barrett’s esophagus is intestinal metaplasia of the cells lining the esophagus. It normally occurs after years of uncontrolled acid reflux. The metaplastic cells can undergo a pre-cancerous change, which can ultimately lead to esophageal cancer in a certain subset of individuals. Treatment is highly individualized and is dictated by the degree of dysplasia and risk of developing esophageal cancer.

References and Resources

  • Shaheen NJ, Sharma P, Overholt BF, et al. Radiofrequency Ablation in Barrett’s Esophagus with Dysplasia. N Engl J Med 360:22, p2277-88. May 28, 2009.
  • Flynn JA. Oxford American Handbook of Clinical Medicine (Oxford American Handbooks of Medicine). First Edition. Oxford University Press, 2007.
  • Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.
  • Blackbourne LH. Surgical Recall, Fifth North American Edition (Recall Series). Fifth Edition. Philadelphia: Lippincott Williams and Wilkins, 2009.