How can portal vein cavernous transformation cause chronic incomplete biliary obstruction?

World J Gastroenterol. 2012 Jul 14;18(26):3375-8. doi: 10.3748/wjg.v18.i26.3375.

Abstract

Biliary disease in the setting of non-cirrhotic portal vein thrombosis (and similarly in portal vein cavernous transformation) can become a serious problem during the evolution of disease. This is mostly due to portal biliary ductopathy. There are several mechanisms that play a role in the development of portal biliary ductopathy, such as induction of fibrosis in the biliary tract (due to direct action of dilated peribiliary collaterals and/or recurrent cholangitis), loss of biliary motility, chronic cholestasis (due to fibrosis or choledocholithiasis) and increased formation of cholelithiasis (due to various factors). The management of cholelithiasis in cases with portal vein cavernous transformation merits special attention. Because of a heterogeneous clinical presentation and concomitant pathophysiological changes that take place in biliary anatomy, diagnosis and therapy can become very complicated. Due to increased incidence and complications of cholelithiasis, standard treatment modalities like sphincterotomy or balloon sweeping of bile ducts can cause serious problems. Cholangitis, biliary strictures and hemobilia are the most common complications that occur during management of these patients. In this review, we specifically discuss important issues about bile stones related to bile duct obstruction in non-cirrhotic portal vein thrombosis and present evidence in the current literature.

Keywords: Cholelithiasis; Hemobilia; Portal biliopathy; Portal ductopathy; Portal vein cavernous transformation.

Publication types

  • Review

MeSH terms

  • Animals
  • Bile / metabolism
  • Bile Ducts
  • Biliary Tract Diseases / diagnosis
  • Biliary Tract Diseases / etiology
  • Cholelithiasis / metabolism
  • Cholestasis / etiology*
  • Cholestasis / physiopathology
  • Fibrosis / pathology
  • Gallbladder / metabolism
  • Hemobilia / metabolism
  • Humans
  • Portal Vein / physiopathology*
  • Recurrence
  • Ultrasonography / methods