Liver and intrahepatic bile ducts - nontumor
General
Diagnostic patterns - differential diagnosis

Author: Komal Arora, M.D. (see Authors page)

Revised: 23 October 2017, last major update April 2012

Copyright: (c) 2002-2017, PathologyOutlines.com, Inc.

PubMed Search: Liver diagnostic patterns differential diagnosis[title]

Table of Contents
Definition / general
Cite this page: Arora, K. Diagnostic patterns - differential diagnosis. PathologyOutlines.com website. http://pathologyoutlines.com/topic/liverdiagnosticpatterns.html. Accessed November 17th, 2017.
Definition / general
  • Adopted from Mills: Sternberg's Diagnostic Surgical Pathology, 5th Edition, 2009 and earlier editions

  • Lobular lymphocytic infiltrate: acute viral hepatitis (A, B, C, delta virus, CMV, EBV), autoimmune hepatitis, extramedullary hematopoiesis (not actually lymphocytes), leukemia, lymphoma, mastocytosis, primary biliary cirrhosis

  • Lobular neutrophilic infiltrate: alcoholic hepatitis, postsurgical, viral hepatitis, sepsis

  • Portal lymphoplasmacytic infiltrate with minimal lobular inflammation or degeneration / necrosis: resolving acute hepatitis, autoimmune hepatitis, chronic bile duct obstruction, graft versus host disease, leukemia / lymphoma, area adjacent to granuloma or neoplasm, primary biliary cirrhosis, primary sclerosing cholangitis, graft rejection, hepatitis B or C, Wilson disease, steatohepatitis
    • Variable involvement of portal tracts suggests primary biliary cirrhosis, hepatitis C, steatohepatitis
    • Extensive piecemeal necrosis suggests autoimmune hepatitis; lack of eosinophils or plasma cells makes hepatitis C or Wilson disease less likely
    • Exclusive lymphocytic infiltrate favors hepatitis C
    • Bile duct loss and bile ductular proliferation favor primary biliary cirrhosis or primary sclerosing cholangitis
    • Granulomas favor primary biliary cirrhosis

  • Portal neutrophilic infiltrate with minimal lobular inflammation or degeneration / necrosis: ascending cholangitis, acute biliary tract obstruction, hyperalimentation, medication reaction, viral hepatitis

  • Hepatocellular necrosis with minimal inflammation: ischemia, fulminant hepatitis, drug / toxin reaction, trauma, acute hepatitis in immunocompromised, hepatic venous outflow obstruction, epithelioid hemangioendothelioma

  • Congestion / hemorrhage: venous outflow disease, Budd-Chiari syndrome, congestive heart failure, angiosarcoma or epithelioid hemangioendothelioma, nodular regenerative hyperplasia, peliosis hepatis

  • Pigments: bile (green brown, usually in bile ducts or bile canaliculi, usually centrilobular), iron (gold brown, usually periportal but centrilobular with congestive liver disease, in hepatocytes in primary hemochromatosis, in Kupffer cells secondary to hemolysis, iron overload or hepatocyte necrosis; highlighted with Prussian blue stain), lipofuscin (brown, in centrilobular hepatocytes, highlighted with Fite stain), gold (brown black in Kupffer cells in arthritis patients), thorium dioxide / Thorotrast (gray blue in Kupffer cells)

  • Inclusions: adenovirus, alpha-1-antichymotrypsin, alpha-1-antitrypsin deficiency, amylopectin, CMV, glycogen nuclei, herpes, Mallory hyaline, macrovesicular steatosis, microvesicular steatosis

  • Fatty change with no / mild necrosis: alcoholic steatohepatitis, fatty liver of pregnancy, biopsy associated, hepatocellular adenoma or carcinoma, drug / toxin reaction, metabolic disease (features defined by specific disease), nonalcoholic steatohepatitis, nonspecific, Wilson disease

  • Nearly normal biopsy: hepatoportal sclerosis, drug / toxin reaction, missed lesion, nodular regenerative hyperplasia, metabolic diseases

  • Loss of bile ducts: mild to moderate if less than 0.9 bile ducts per portal tract; severe if less than 0.6 bile ducts per portal tract
    • Causes include chronic biliary tract obstruction, primary biliary cirrhosis, primary sclerosing cholangitis, paucity in neonates, idiopathic adult ductopenia, drug reaction (Augmentin), ischemia, chronic graft versus host disease, chronic graft rejection (Pathol Res Pract 2005;201:565)

  • Loss of central veins: sampling error, cirrhosis, hepatocellular adenoma or carcinoma, nodular regenerative hyperplasia (central veins present but difficult to see)
  • Loss of hepatocytes: massive hepatic necrosis / fulminant hepatitis
  • Loss of portal tracts: sampling error, cirrhosis, hepatocellular adenoma or carcinoma
  • Loss of portal veins but portal tracts present: hepatoportal sclerosis
  • Loss of sinusoids: metabolic storage diseases, cirrhosis