Changes in plasma bile acids are associated with gallbladder stones and polyps

Abstract

Background The development of gallbladder disease (GBD) is related to bile acid (BA) metabolism, and the rate of BA circulation increases the risk of biliary cancer. However, it is unclear whether patterns of circulating bile acids (BAs) change in patients with benign GBDs such as gallbladder stones and polyps. Herein, we compared and characterised plasma BA profiles in patients with cholecystolithiasis and non-neoplastic polyps with healthy controls, and explored relationships between plasma BA profiles, demographics, and laboratory test indices. Methods A total of 330 subjects (13 healthy controls, 292 cholecystolithiasis and 25 non-neoplastic polyps) were recruited and plasma BA profiles including 14 metabolites from patients with pathologically confirmed cholecystolithiasis and non-neoplastic polyps were compared with controls. BAs were quantitated by liquid chromatography and mass spectrometry, and statistical and regression analyses of demographics and laboratory test indices were performed. Results Females displayed a higher burden of GBD than males (63.36% cholecystolithiasis, 60% non-neoplastic polyps). Cholecystolithiasis and non-neoplastic polyps were associated with increased plasma total secondary BAs, while levels of primary BAs were lower than in healthy controls. Plasma ursodeoxycholic acid (UDCA), tauroursodeoxycholic acid (TUDCA), glycyurdeoxycholic acid (GUDCA), taurochenodeoxycholic acid (TCDCA) and glycochenodeoxycholic acid (GCDCA) were decreased significantly in GBDs, and ursodeoxycholic acid (UDCA) was negatively correlated with white blood cell count and neutrophil percentage. Conclusions Secondary BA levels were higher in patients with cholecystolithiasis and non-neoplastic polyps. White blood cell count and percentage of neutrophil in peripheral blood were negatively correlated with UDCA, indicating an anti-inflammation effect of UDCA.

Association of egg consumption with colorectal polyp prevalence: findings from the Lanxi Pre-Colorectal Cancer Cohort (LP3C) in China

“…Dietary cholesterol could increase LDL-C concentrations, 41 which contributed to gallstone formation. 42,43 Patients with gallstones have a higher level of secondary bile acids, 44 which was correlated with promoting cancerogenesis. 45 An individual with higher dietary cholesterol intake has a higher risk of dyslipidemia, 40 which may bring about the imbalance between inflammatory cytokines and anti-inflammatory cytokines in the body.…”

Small Intestinal Bacterial Overgrowth in Patients with Gallbladder Polyps: A Cross-Sectional Study

“…In turn, SIBO can reduce the absorption of fat-soluble vitamins, such as vitamin D, 19 and research has shown that vitamin D deficiency may further aggravate the cholestasis, 20 thus starting a vicious cycle. In addition, the formation of GBPs may be associated with a disturbance of the bile acid pool 21 ,which is common in SIBO. Previous studies have found that compared to SIBO-negative patients, the levels of unconjugated bile acids were higher in SIBO-positive patients.…”

Predictive value of bile acids as metabolite biomarkers for gallstones: A protocol of systematic review and meta-analysis

“…A Swedish study showed that the shortage of bile acids was a major reason why bile was supersaturated with cholesterol in gallstones patients [ 34 ]. While secondary bile acids were higher in patients with gallstones compared with healthy controls [ 35 ], and higher overall concentrations of fecal bile acids with lower microbial diversity had been found in gallstones [ 36 ]. A prospective cohort study proved that the disorder of bile acids metabolism had already occurred at the beginning of the disease [ 37 ].…”

“…Therefore, an increasing number of metabolomics studies have focused on the bile acids profile in gallstones, and demonstrate that the levels of some bile acids are significantly associated with the development of gallstones [19][20][21]. However, there is still lack of a consistent and comprehensive conclusion and the biological samples they detect are diverge.…”