Liver and intrahepatic bile ducts - nontumor
Biliary tract disease
Cholestasis

Editor-in-Chief: Debra Zynger, M.D.
Raul S. Gonzalez, M.D.

Topic Completed: 13 September 2019

Revised: 13 September 2019

Copyright: 2002-2019, PathologyOutlines.com, Inc.

PubMed Search: Cholestasis[TI] liver[TI] free full text[sb]


Raul S. Gonzalez, M.D.
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Cite this page: Gonzalez R S. Cholestasis. PathologyOutlines.com website. http://www.pathologyoutlines.com/topic/livercholestasis.html. Accessed December 13th, 2019.
Definition / general
  • Decrease in bile flow due to hepatocellular dysfunction or biliary obstruction
Essential features
  • Microscopically visible bile, usually in hepatocyte cytoplasm or canaliculi
  • Seen in most forms of biliary pattern injury
Terminology
  • Bland cholestasis refers to cholestasis as an isolated microscopic finding
  • Cholestatic hepatitis refers to microscopic cholestasis alongside inflammatory findings (that is, hepatitis)
  • Histologic cholestasis sometimes referred to as bilirubinostasis
ICD coding
  • ICD-10: K71.0 - toxic liver disease with cholestasis
Pathophysiology
  • Bile is produced in hepatocytes and flows as follows: hepatocyte canaliculi → canals of Hering → bile ductules → interlobular bile ducts → larger bile ducts → duodenum
  • Injury or obstruction at any point along biliary flow can lead to cholestasis
Etiology
Clinical features
  • Patients with cholestasis may have jaundice, pruritus (due to bile acid deposition in skin), skin xanthomas (due to hyperlipidemia), deficiencies of fat soluble vitamins (A, D, E, K)
  • Clinical cholestasis may not correlate with histologic cholestasis
Laboratory
  • Elevated serum alkaline phosphatase (present in bile duct epithelium and hepatocyte canalicular membrane), elevated serum bilirubin
Treatment
  • Varies depending on etiology
  • Ursodeoxycholic acid and obeticholic acid can improve symptoms of cholestatic liver disease (Hepatology 2002;36:525 GR)
Microscopic (histologic) description
  • Bile pigment (yellow / green / brown) visible histologically within hepatic parenchyma, usually perivenular
  • May be present within hepatocyte cytoplasm, hepatocyte canaliculi, ductule lumens or large duct lumens
  • Chronic cholestasis leads to cholate stasis / feathery degeneration of periportal hepatocytes – enlarged, swollen cells with clear / granular cytoplasm
Microscopic (histologic) images

Contributed by Raul S. Gonzalez, M.D.

Bland cholestasis

Cholestatic hepatitis

Ductular cholestasis

Cholate stasis

Sample pathology report
  • Liver, biopsy:
    • Hepatic parenchyma with mild chronic inflammation and lobular cholestasis (see comment)
    • Comment: The findings suggest cholestatic hepatitis. Possible etiologies, depending on clinical findings, include primary biliary cirrhosis, drug induced liver injury, viral hepatitis, and primary sclerosing cholangitis.
Differential diagnosis
  • Other brownish pigments that can mimic bile histologically include lipofuscin (may be present in cytoplasm but not canaliculi) and hemosiderin (darker, duskier brown)
  • Differential for bland cholestasis: drug induced liver injury (eg. anabolic steroids), early duct obstruction, benign recurrent intrahepatic cholestasis, acute cholestasis of pregnancy
  • Differential for cholestatic hepatitis: primary sclerosing cholangitis (inflammation usually minimal), primary biliary cholangitis, viral hepatitis, large duct obstruction, progressive familial intrahepatic cholestasis
  • Differential for ductular cholestasis: sepsis, cirrhosis (any cause), dehydration, extrahepatic biliary atresia, ductal plate malformations
Board review question #1
Which of the following typically causes bland cholestasis as seen on liver biopsy



  1. Amoxicillin / clavulanate injury
  2. Anabolic steroid injury
  3. Chronic large duct obstruction
  4. Primary biliary cholangitis
  5. Primary sclerosing cholangitis
Board review answer #1
Board review question #2
Liver injury with cholestasis typically results in an increase of what laboratory value

  1. Alanine aminotransferase
  2. Albumin
  3. Alkaline phosphatase
  4. Aspartate aminotransferase
Board review answer #2
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