Duodenogastric reflux of bile acids, gastrin and parietal cells, and gastric acid secretion before and 6 months after cholecystectomy

Lorusso, D.; Misciagna, Giovanni; Mangini, V; Messa, Caterina; Cavallini, A; Caruso, Maria Lucia; Giorgio, Piero; Guerra, Vito

doi:10.1016/s0002-9610(06)80069-3

Cited by 22 publications

(8 citation statements)

References 30 publications

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“…It has been suggested that both gallstones and previous cholecystectomy contribute to the occurrence of duodeno-gastric reflux [16,[34][35][36][37][38][39]. The underlying mechanism is thought to be a dysfunction of the antroduodenal motor unit that favors the reflux of duodenal contents into the stomach [37].…”

Section: Discussionmentioning

confidence: 99%

Gallstones increase the prevalence of Barrett’s esophagus

et al. 2009

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Section: Discussionmentioning

confidence: 99%

Gallstones increase the prevalence of Barrett’s esophagus

et al. 2009

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“…Many studies have investigated whether duodenogastric reflux (DGR) is elevated after cholecystectomy. In aspiration studies, a three-to tenfold increase of bile acid levels in the stomach has been described following cholecystectomy [16,20,34]. Scintigraphic studies have produced conflicting results.…”

Section: Discussionmentioning

confidence: 99%

Effect of Cholecystectomy on Gastric and Esophageal Bile Reflux in Patients with Upper Gastrointestinal Symptoms

et al. 2007

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Epidemiologic data have shown that cholecystectomy is associated with a moderately increased risk of esophageal adenocarcinoma. The study objective was to evaluate the role of refluxed bile. A total of 696 patients with upper gastrointestinal symptoms were included in the study, of whom 55 had a history of cholecystectomy (CHE). Bilirubin exposure was measured in percent time above absorbance 0.25 in the stomach and above 0.14 in the esophagus. Total gastric and esophageal bilirubin exposure was similar in both groups. Supine gastric bile reflux was slightly increased after cholecystectomy (30.6 +/- 30.2 vs. CHE: 37.1 +/- 29.5, P < 0.05). In patients with erosive esophagitis or Barrett's esophagus, there were differences in total gastric exposure (24.3 +/- 22.6 vs. CHE: 36.7 +/- 26.8, P < 0.05) but not in esophageal exposure. Cholecystectomy slightly augments bile reflux into the stomach without detectable differences in the esophagus. Therefore, increased esophageal bile reflux following cholecystectomy as a potential cause for the associated cancer risk could not be substantiated.

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“…In investigations regarding patients after cholecystectomy (CHE), an increased DGR was shown with scintigraphy, aspiration and analysis of gastric contents, 24-hour pH monitoring and the Bilitec device [7,16,17,18,19,20,21,22,23]. Still, some studies failed to show any increased DGR after CHE, again utilizing scintigraphy [7, 24] or the Bilitec device [25].…”

Section: Introductionmentioning

confidence: 99%

Relation of Gallbladder Function and <i>Helicobacter pylori</i> Infection to Gastric Mucosa Inflammation in Patients with Symptomatic Cholecystolithiasis

Stathopoulos

Zündt²,

Spelsberg³

et al. 2006

Digestion

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Background: Inflammatory alterations of the gastric mucosa are commonly caused by Helicobacter pylori (Hp) infection in patients with symptomatic gallstone disease. However, the additional pathogenetic role of an impaired gallbladder function leading to an increased alkaline duodenogastric reflux is controversially discussed. Aim: To investigate the relation of gallbladder function and Hp infection to gastric mucosa inflammation in patients with symptomatic gallstones prior to cholecystectomy. Patients: Seventy-three patients with symptomatic gallstones were studied by endoscopy and Hp testing. Methods: Gastritis classification was performed according to the updated Sydney System and gallbladder function was determined by total lipid concentration of gallbladder bile collected during mainly laparoscopic cholecystectomy. Results: Fifteen patients revealed no, 39 patients mild, and 19 moderate to marked gastritis. No significant differences for bile salts, phospholipids, cholesterol, or total lipids in gallbladder bile were found between these three groups of patients. However, while only 1 out of 54 (<2%) patients with mild or no gastritis was found histologically positive for Hp, this infection could be detected in 14 (74%) out of 19 patients with moderate to marked gastritis. Conclusion: Moderate to marked gastric mucosa inflammation in gallstone patients is mainly caused by Hp infection, whereas gallbladder function is not related to the degree of gastritis. Thus, an increased alkaline duodenogastric reflux in gallstone patients seems to be of limited pathophysiological relevance.

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Duodenogastric reflux of bile acids, gastrin and parietal cells, and gastric acid secretion before and 6 months after cholecystectomy

Cited by 22 publications

References 30 publications

Gallstones increase the prevalence of Barrett’s esophagus

Gallstones increase the prevalence of Barrett’s esophagus

Effect of Cholecystectomy on Gastric and Esophageal Bile Reflux in Patients with Upper Gastrointestinal Symptoms

Relation of Gallbladder Function and <i>Helicobacter pylori</i> Infection to Gastric Mucosa Inflammation in Patients with Symptomatic Cholecystolithiasis

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