Measurement of bile acids in fasting gastric aspirates: an objective test for bile reflux after gastric surgery.

Abstract

SUMMARYWe measured the concentration of bile acids in gastric aspirates from patients who had had operations for peptic ulcer. Some patients were asymptomatic and some had postoperative symptoms of the type that have been attributed to duodenogastric reflux. Samples were obtained via a nasogastric tube when the patients were fasting, after food, after pentagastrin, and overnight. We related the concentration and amount of bile acid and the volume aspirated to the presence or absence of symptoms and compared the results with radiological and endoscopic assessments of duodenogastric reflux. The most useful index to discriminate between symptomatic and asymptomatic patients was the amount of bile reflux in half an hour's aspiration from the fasting stomach; this we have termed 'fasting bile reflux' (FBR) and expressed as ,umol bile acids refluxing/hour. A figure greater than 120 ,umol/h was present in 17 of 22 symptomatic patients and in all who complained of bile regurgitation or bile vomiting. The FBR was less than 120 ,tmol/h in all of 20 asymptomatic patients, although some of them had reflux detected radiologically and endoscopically.

Reflux Gastritis Syndrome

“…However, this viewpoint has not been supported by others [35,43], Measuring the natural markers in the gas tric aspirate, as a biochemical index of enterogastric reflux, has often been used to sup port the diagnosis of reflux gastritis syn drome. Bilirubin concentrations of greater than 1 mg/dl was observed in 80% of symp tomatic patients, as was reported by Keigh ley et al [ 14], In another study [16], 17 o f the 22 symptomatic patients had fasting total bile acids reflux in excess of 120 mol/h. Technetium-labelled HIDA scintigraphy, as a technique to quantitate enterogastric re flux, is now widely available [52].…”

“…Duodenogastric reflux has been suggested in the patho genesis of gastric ulcer [7] and gastritis [8]. It may also be seen in smokers without gastric ulcer [9], in patients with chronic heartburn and gastroesophageal reflux [10], in gallstone disease [11], and after cholecystectomy [ 12,13], Excessive enterogastric reflux in the re flux gastritis syndrome has been largely dem onstrated through indirect methods measur ing the concentration of natural markers such as bilirubin [14], bile acids [15][16][17][18], sodium [19], and trypsin [20] in the gastric aspirates. The gastric concentrations of bile acids have been shown to be significantly higher in a number of symptomatic patients.…”

“…Several studies have focused on the rela tionship between the intragastric concentra tion of natural markers, such as bilirubin [14] and bile acids [16], and the severity of symptoms. A recent study [43], however, in dicates that the amount of bile acid refluxed, the rate of gastric emptying, and the gross and microscopic appearance of the gastric mucosa cannot discriminate the symptom atic patients.…”

Mechanism by which bile salt disrupts the gastric mucosal barrier in the dog.

“…This increased H+ back-diffusion can cause tissue injury ranging in animal models from gastritis to frank ulceration (4)(5)(6)(7). In man these events may contribute to development of the gastritis that accompanies reflux of bile salt into the stomach after surgical interruption of the pyloric sphincter (8)(9)(10).…”

Pre- and Postcholecystectomy Duodenogastric Reflux

“…The method has shown a coeffi cient of variation of 3.1 % between series. The concentration of bile acids in each sample of gastric juice (the first sample was excluded) was multiplied by the volume of each aspirate; by summing up the 4 values, the fasting bile reflux (FBR) expressed in micromoles per hour was obtained, thus measuring the absolute amount of bile acids flowing back into the stomach over 1 h [16]. (c) Esophagogastroduodenoscopy with biopsies were taken from the antral mucosa and the main body, 4 from each site.…”