Biliary strictures as a cause of primary intrahepatic bile duct stones

Abstract

We collected 51 cases of stricture in the upper portion of the biliary tract and discussed the pathogenesis and the clinical significance of the strictures. All 51 patients had congenital cystic dilatation of the common bile duct (CCDB): 2 had infant-type cysts which involved the choledochus and/or the common hepatic duct, and 49 had adult-type cysts which included the entire extrahepatic bile duct and/or the main intrahepatic bile ducts. Thirty-five of the latter 49 had intrahepatic bile duct stones proximal to the stricture. Considering the location and the clinical features, the strictures may have been formed congenitally. Furthermore, adult-type cysts of the common bile duct with strictures in the upper portion of the biliary tract are thought to be the basis for the formation of primary intrahepatic bile duct stones.

Suppression of proliferative cholangitis in a rat model with direct adenovirus-mediated retinoblastoma gene transfer to the biliary tract

“…In 6 of 7 cases, bile ducts containing stones, as well as adjoining ducts, showed fibrous thickening of their walls, fibrosis in the periductal tissue, and numerous glandular elements within the ductal walls and in the periductal tissue 4,5 (Fig. 1).…”

“…In the pathogenesis of hepatolithiasis, cholestasis and biliary infection have been widely accepted as indispensable factors. [1][2][3][4][5] The most characteristic pathological feature is proliferative cholangitis (PC), which shows the peribiliary gland hyperplasia and the proliferation of the biliary epithelium and fibrous tissue, resulting in considerable thickening of the bile duct wall. [3][4][5] PC frequently induces residual and/or recurrent stones, [1][2][3][5][6][7] which are the largest problem after repeated treatments for hepatolithiasis.…”

“…[1][2][3][4][5] The most characteristic pathological feature is proliferative cholangitis (PC), which shows the peribiliary gland hyperplasia and the proliferation of the biliary epithelium and fibrous tissue, resulting in considerable thickening of the bile duct wall. [3][4][5] PC frequently induces residual and/or recurrent stones, [1][2][3][5][6][7] which are the largest problem after repeated treatments for hepatolithiasis. [1][2][3] In the present study, gene therapy using the adenovirus vector encoding nonphosphorylatable, constitutively active form of retinoblastoma gene product (AdRb) was introduced to reduce proliferation caused by PC.…”

“…Cholestasis and biliary infection are considered to play important roles in the formation of intrahepatic stones and to remain even after treatments for hepatolithiasis. [1][2][3][5][6][7] We assumed that inhibition of the formation of proliferative changes in this model could lead to some new adjuvant treatment modality for reducing recurrence of PC and stones after treatments. Therefore, we investigated in the current study whether the adenovirus-mediated overexpression of human Rb into the biliary tract could control the formation of proliferative changes in this model.…”

Paclitaxel Interrupts TGF-β1 Signaling Between Gallbladder Epithelial Cells and Myofibroblasts

“…This condition is characterized by hyperplasia of bile duct epithelium and inflammatory cell infiltration. The resulting bile stasis can lead to recurrent bacterial cholangitis, intrabiliary lithiasis, and secondary biliary cirrhosis [10,11]. The histologic features of PC can be reproduced in an in vivo rat model, in which the pathological process is initiated by insertion of a thread into the bile duct [12].…”