Bile reflux gastropathy is a noninflammatory gastric mucosal injury caused by long-term exposure to bile acids and exacerbated by pancreatic enzymes and the formation of lysolecithin. It typically occurs after Billroth II gastrectomy but may also follow cholecystectomy or other causes of duodenogastric reflux. Bile reflux gastropathy may present with dyspepsia, abdominal pain, nausea, vomiting, and weight loss, but it is often asymptomatic. The symptoms that prompt investigation may also be due to the preceding surgery or the underlying disease.
Diagnosis is based on endoscopic findings confirmed by histologic findings of a reactive (chemical) gastropathy, characterized by foveolar hyperplasia, mucin cell depletion, and paucity of inflammatory cell infiltrates. Endoscopy shows characteristic hyperemia and erythema of the gastric mucosa (often described as a "beefy red stomach" or "red-green stomach") and, occasionally, mucosal encrustation with bile crystals. Despite the dramatic appearance, there is poor correlation between the endoscopic appearance and the patient’s symptoms, so histologic assessment is warranted to confirm the diagnosis and exclude concomitant Helicobacter pylori infection, which is also associated with an inflammatory infiltrate and requires eradication therapy.
In the absence of prior surgery, medical therapy with proton pump inhibitors (PPIs) or mucosal protectants (eg, alginic acid or sucralfate) may be helpful, but the results are variable. There is no published evidence to support the use of prokinetic agents for bile reflux gastritis. Bile acid sequestrants (eg, cholestyramine) are generally not effective. There is some limited evidence to suggest that ursodeoxycholic acid may be helpful and, possibly, more effective than PPI therapy. Rarely, surgical reconstruction (Roux-en-Y gastric bypass) may be considered for patients who have had prior partial gastrectomy, provided that other causes have been excluded.