Helicobacter pylori in the biliary tract: Is it curiosity or culprit in hepatolithiasis?

Abstract

Background/Aims: There are growing evidences that Helicobacter spp. may be present in the biliary tract especially in areas where the prevalence of Helicobacterpylori (H. pylori) is high. However, it is uncertain whether they can colonize in the biliary epithelium or play a role in any kinds of biliary diseases. In Korea, the prevalence of both H. pylori and hepatolithiasis is rather high. Therefore, we hypothesized that H. pylori in the bile might play a role in the formation of hepatolithiasis. Thus, the aims of this study are to investigate whether H.pylori can be present in bile or biliary epithelium and to determine the possible pathogenetic role of H. pylori in the formation of hepatolithiasis. Methods: We analyzed 43 bile samples obtained by percutaneous transhepatic biliary drainage (PTBD grout,: hepatolithiasis 30, cholangiocarcinoma 9, others 4), 23 bile samples collected during cholecystectomy (CCT ~rouo: gallstones 16, gallbladder polyp 7), and 8 samples at incidental cholecystectomy (control group: stomach cancer 8). Furthermore, intrahepatic bile duct tissues were obtained by choledochoscopic biopsy and gallbladder tissues were taken at operation. The composition and pH of the bile were analyzed and H. pylori in the bile was examined by PCR with 26 k-Da protein primer. In addition, the presence of H. pylori in the biliary epithelium was investigated by H&E stain, WarthinStarry stain, CLO test, and PCR. In 7 cases of hepatolithiasis, gallstones were collected and DNA was extracted from the inner side of the stones for subsequent H. pylori PCR. Results: PCR was positive in 4/43 (9.3%) in biles from PTBD ~rouo. PCR positive cases were all H. pylori seropositive. However, H. pylori DNA was not detected in all the bile duct tissues including bile-PCR positive cases. Upon analysis of intrahepatic bile, pH was significantly lower in cases with H.pylori PCR positive than PCR negative cases (7.39 ± 0.52 vs. 7.72 ± 0.16, p<0.05), while cholesterol, total bile acid, and phospholipid were similar between both groups. Other examinations for H. pylori were all negative both in PTBD and CCT ~,rouns. PCR of bile and gallbladder tissue was all negative in CCT and control ~,rouo. H. pylori DNA was not detected in 7 intrahepatic stones by PCR. Conclusions: H. pylori DNA may be present in the intrahepatic bile when there is a certain environmental change such as lowered pH. Decreased inhibitory activity of bile against H. pylori caused by acidification might explain the presence of H. pylori DNA in the bile. However, they may not colonize the bile duct epithelium. We could not find a pathogenetic role of H. pylori in the formation of hepatolithiasis.