Gallstone Formation Follows a Different Trajectory in Bariatric Patients Compared to Nonbariatric Patients
Sylke Haal,
Maimoena S. S. Guman,
Yair I. Z. Acherman,
Johannes P. G. Jansen,
Michel van Weeghel,
Henk van Lenthe,
Eric J. M. Wever,
Victor E. A. Gerdes,
Rogier P. Voermans,
Albert K. Groen
Affiliations
Sylke Haal
Department of Internal Medicine, Spaane Gasthuis, 2134 TM Hoofddorp, The Netherlands
Maimoena S. S. Guman
Department of Internal Medicine, Spaane Gasthuis, 2134 TM Hoofddorp, The Netherlands
Yair I. Z. Acherman
Department of Surgery, Spaarne Gasthuis, 2134 TM Hoofddorp, The Netherlands
Johannes P. G. Jansen
Department of Internal and Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, 1105 AZ Amsterdam, The Netherlands
Michel van Weeghel
Laboratory of Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, The Netherlands
Henk van Lenthe
Laboratory of Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, The Netherlands
Eric J. M. Wever
Laboratory of Genetic Metabolic Diseases, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam Cardiovascular Sciences, 1105 AZ Amsterdam, The Netherlands
Victor E. A. Gerdes
Department of Internal Medicine, Spaane Gasthuis, 2134 TM Hoofddorp, The Netherlands
Rogier P. Voermans
Department of Gastroenterology and Hepatology, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, 1105 AZ Amsterdam, The Netherlands
Albert K. Groen
Department of Internal and Vascular Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam Gastroenterology Endocrinology Metabolism, 1105 AZ Amsterdam, The Netherlands
Since obese patients form cholesterol gallstones very rapidly after bariatric surgery, in patients who did not form gallstones during preceding years, we hypothesized that gallstone formation follows a different trajectory in bariatric patients compared to nonbariatric patients. We therefore analyzed the lipid composition of gallbladder bile derived from 18 bariatric gallstone patients and 17 nonbariatric gallstone patients (median (IQR) age, 46.0 (28.0–54.0) years; 33 (94%) female) during laparoscopic cholecystectomy using an enzymatic and lipidomics approach. We observed a higher concentration of total lipids (9.9 vs. 5.8 g/dL), bile acids (157.7 vs. 81.5 mM), cholesterol (10.6 vs. 5.4 mM), and phospholipids (30.4 vs. 21.8 mM) in bariatric gallstone patients compared to nonbariatric gallstone patients. The cholesterol saturation index did not significantly differ between the two groups. Lipidomics analysis revealed an interesting pattern. Enhanced amounts of a number of lipid species were found in the gallbladder bile of nonbariatric gallstone patients. Most striking was a fivefold higher amount of triglyceride. A concomitant ninefold increase of apolipoprotein B was found, suggesting secretion of triglyceride-rich lipoproteins (TRLs) at the canalicular pole of the hepatocyte in livers from nonbariatric gallstone patients. These findings suggest that gallstone formation follows a different trajectory in bariatric patients compared to nonbariatric patients. Impaired gallbladder emptying might explain the rapid gallstone formation after bariatric surgery, while biliary TRL secretion might contribute to gallstone formation in nonbariatric patients.
