Alkaline Reflux Gastritis

Abstract

In 1977, a controlled, prospective trial was initiated to test the hypothesis that excessive enterogastric (EG) reflux was responsible for a unique postgastrectomy syndrome, "alkaline reflux gastritis." Late (42 +/- 3 months) follow-up on all treated patients (N = 14; Rx = 45 cm Roux Y limb) is reported. The following parameters were assessed in symptomatic (N = 11 nonrefluxers, 15 refluxers) and asymptomatic postgastrectomy patients (N = 9): CCK-stimulated scintographically determined EG reflux (EGRI %), intragastric (IG) concentration of bile acids (BA, mM), net bile acid reflux/hr (microM), maximum acid output (mEq/hr), intragastric pH, gastric emptying of 99Tc-labeled solids (T 1/2; minutes), gastritis score (GS = 0-15), and specific symptomotology. A significant linear relationship was noted between intragastric BA concentration and the severity of histologic gastritis in the residual gastric pouch. As a group, excessive refluxers demonstrated significantly greater IG BA concentration, net BA reflux/hour, and EGRI than did either nonrefluxers or controls. Gastritis score in this group was also greater, intragastric pH higher, and maximal acid output (MAO) lower. Gastric emptying was not different between groups. Following Roux (N = 14), reflux was eliminated early and late, pH fell, MAO increased, and gastritis improved. Early marked delays in emptying occurred but normalized late and were rarely a clinical problem. Early symptomatic results were pain eliminated in 14/14, nausea in 8/14, vomiting 11/14, bilious vomiting in 14/14. Complications were one marginal ulcer (no vagotomy), two severe delays in emptying (simultaneous Roux + vagotomy). Late symptomatic results were recurrent or persistent pain in 4/14, nausea in 7/14, vomiting in 5/14. Bilious vomiting remains eliminated.

Effects of endotoxin on gastric injury from luminal irritants in rats: potential roles of nitric oxide

“…Given this possibility, our findings could have clinical significance. For example, during sepsis, there is often an associated ileus (3), and duodenogastric reflux of bile in this clinical scenario is not an uncommon event (19). In the critical care setting, in which the septic patient often requires ventilatory support and is prone to develop erosive stress gastritis (4), the patients frequently have nasogastric decompression of gastric juices.…”

Unusual Case of Biliary Peritonitis in a Dog Secondary to a Gastric Perforation

“…Bile acids and lysolecithin are the major components that destroy the barrier on the surface of gastric mucosa by dissolving phospholipids and cholesterol, which allows for back diffusion of hydrogen ions. As a consequence, gastritis, characterized by hyperemia, oedema, and erosion, occurs [ 30 , 31 ] and, histologically, foveolar hyperplasia occurs. Moreover, duodenal reflux liquids contain gut microbiome that can result in the imbalance of microbial flora in the stomach [ 32 ].…”

Bile Reflux Gastropathy and Functional Dyspepsia

“…All of these agents can cause chemical injury to the mucosa leading to a reactive or chemical gastropathy. 4 Such a gastropathy has long been recognized as a post-gastric surgery problem, and has been reported following Billroth II gastrectomy. 5 However, whether bile reflux causes dyspeptic symptoms in a normal, non-operated stomach is unclear, and there are conflicting reports in the literature.…”