INFLAMMATION AND SPECIALIZED INTESTINAL METAPLASIA OF CARDIAC MUCOSA IS A MANIFESTATION OF GASTROESOPHAGEAL REFLUX DISEASE

Objective The purpose of the study was to lest the hypothesis that car diac mucosa, carditis, and specialized intestinal metaplasia at an end oscopically normal-appearing cardia are manifestations of gastroesopha geal reflux disease. Summary Background Data In the absence of esophag eal mucosal injury, the diagnosis of gastroesophageal reflux disease c urrently rests on 24-hour pH monitoring. Histologic examination of the esophagus is not useful. The recent identification of specialized int estinal metaplasia at the cardia, along with the observation that it o ccurs in inflamed cardiac mucosa, led the authors to focus on the type and condition of the mucosa at the gastroesophageal junction and its relation to gastroesophageal reflux disease. Methods Three hundred thi rty-four consecutive patients with symptoms of foregut disease, no evi dence of columnar-lined esophagus, and no history of gastric or esopha geal surgery were evaluated by 1) endoscopic biopsies above, al, and b elow the gastroesophageal junction; 2) esophageal motility; and 3) 24- hour esophageal pH monitoring. The patients were divided into groups d epending on the histologic presence of cardiac epithelium with and wit hout inflammation or associated intestinal metaplasia. Markers of gast roesophageal reflux disease were compared between groups (i.e., lower esophageal sphincter characteristics, esophageal acid exposure, the pr esence of endoscopic erosive esophagitis, and hiatal hernia). Results When cardiac epithelium was found, it was inflamed in 98% of the patie nts. The presence of cardiac epithelium and carditis was associated wi th deterioration of lower esophageal sphincter characteristics and inc reased esophageal acid exposure. Esophagitis occurred more commonly in patients with carditis whose sphincter, on manometry, was structurall y defective. Specialized intestinal metaplasia at the cardia was only seen in inflamed cardiac mucosa, and its prevalence increased both wit h increasing acid exposure and with the presence of esophagitis. Concl usion The findings of cardiac mucosa, carditis, and intestinal metapla sia in an endoscopically normal-appearing gastroesophageal junction ar e histologic indicators of gastroesophageal reflux disease. These find ings may be among the earliest signs of gastroesophageal reflux and co ntribute to the authors understanding of the pathophysiology of the di sease process.