Human biliary β‐glucuronidase activity before and after relief of bile duct obstruction: Is it the major role in the formation of pigment gallstones?

Abstract

An increase in the activity of hBG may be a secondary response, developed after bile duct inflammation because it was elevated only when the bile duct obstruction was associated with infection.

Proliferating cell nuclear antigen shRNA treatment attenuates chronic proliferative cholangitis in rats

“…In any case, it can be affirmed that the inhibitory effect of PCNA shRNA treatment on b-glucuronidase helps prevent stone recurrence. 11,12,29,30 Overall, our generally favorable results confirm the inhibitory effect of PCNA shRNA on the hyperplasic behavior and lithogenic potential of CPC. Up until now, there are still no effective medications to treat CPC and thereby prevent stone recurrence after choledochoscopic lithotomy.…”

“…An alternative, and perhaps more likely explanation, is associated with its inhibitory effect on biliary epithelium and submucosal gland proliferation, which leads to a decrease in the endogenous β‐glucuronidase secreted from the diseased bile duct. In any case, it can be affirmed that the inhibitory effect of PCNA shRNA treatment on β‐glucuronidase helps prevent stone recurrence 11,12,29,30 …”

The Practical Value of Applying Chemical Biliary Duct Embolization to Chemical Hepatectomy for Treatment of Hepatolithiasis

“…The exact mechanism of CBDE inhibition of endogenous ␤-G is still unknown. One potential explanation may be related to the controlling effects of CBDE on biliary infection, which reduces the direct stimulatory effects of inflammatory cells and exogenous ␤-G on endogenous ␤-G. An alternative and perhaps more likely explanation is associated with the massive death of hepatocytes, which leads to the decreased secretion of endogenous hepatic ␤-G [17,32,35,36]. In any case, it can be affirmed that the inhibitory effect of CBDE on ␤-G must be to help prevent stone recurrence.…”

Significance of Controlling Chronic Proliferative Cholangitis in the Treatment of Hepatolithiasis

“…Third, the increase of acidic mucoglycoprotein in the diseased bile duct, causing a decrease in the pH value of bile and providing a favorable microenvironment that facilitates the lithogenic role of bacterial β‐glucuronidase in the deconjugation of bilirubin diglucuronide [7–10, 13]. In addition to the increase of bacterial β‐glucuronidase activity, the activity of endogenous β‐glucuronidase from leukocytes and bile duct epithelium is also obviously increased owing to the presence of cholangitis, thus leading to a further increase in the amount of unconjugated bilirubin and an acceleration of the stone formation process [15, 50, 52]. Thus, recurrent CPC causes repeatd cycles of bile infection, bile stasis, and bile composition alteration, conditions that combine to contribute to the initiation and growth of intrahepatic stones.…”