Although clinical and laboratory features yield clues to the extent of inflammatory processes (disease grade), the degree of scarring and architectural distortion (disease stage), and the nature of the disease process, the liver biopsy is felt to represent the gold standard for assessing the degree of liver injury and fibrosis. Examination of liver histology provides not only a basis for quantitative scoring of disease activity and progression but also a wealth of qualitative information that can direct and inform diagnosis and management.
A normal liver lobule consists of portal (zone 1), lobular (midzonal or zone 2), and central (zone 3) zones. The portal tract contains the hepatic artery (HA) and portal vein (PV), which represent the dual vascular supply to the liver, as well as the bile duct (BD). The lobular area contains cords of liver cells surrounded by vascular sinusoids, and the central zone consists of the central vein (CV), the terminal branch of the hepatic vein (see figure below).
Included in this atlas of liver biopsies are examples of common morphologic features of acute and chronic liver disorders, some involving the lobular areas (e.g., the lobular inflammatory changes of acute hepatitis, apoptotic hepatocyte degeneration in acute and chronic hepatitis, virus antigen localization in hepatocyte cytoplasm and/or nuclei, viral inclusion bodies, copper or iron deposition, other inclusion bodies), and others involving the portal tracts (e.g., the portal mononuclear infiltrate that expands and spills over beyond the border of periportal hepatocytes in chronic hepatitis C, autoimmune hepatitis, and liver allograft rejection) or centrizonal areas (e.g., acute acetaminophen hepatotoxicity). Other histologic features of importance include hepatic steatosis (observed in alcoholic liver injury, in nonalcoholic fatty liver disorders, in metabolic disorders—including mitochondrial injury—and in patients with chronic viral hepatitis); injury of bile ducts in the portal tract, an important diagnostic hallmark of primary biliary cirrhosis, primary sclerosing cholangitis, as well as of liver allograft rejection; cholestasis in intrahepatic or extrahepatic biliary obstruction or in infiltrative disorders; ductular proliferation in the setting of marked hepatocellular necrosis; plasma cell infiltration common in autoimmune hepatitis; portal inflammation affecting portal veins (“endothelialitis”) in liver allograft rejection; and mild-to-severe fibrosis, in varying distribution and pattern, as a consequence of liver injury common to many disorders. (All magnifications reflect the objective lens used.)
Acute hepatitis with lobular inflammation and hepatocellular ballooning (H&E, 10×).
Acute hepatitis, higher magnification, showing lobular inflammation, hepatocellular ballooning, and acidophilic bodies (arrows) (H&E, 20×).
Chronic hepatitis C with portal lymphoid infiltrate and lymphoid follicle containing germinal center (H&E, 10×).
Chronic hepatitis C with portal and lobular inflammation and steatosis (H&E, 10×).
Chronic hepatitis C with portal inflammation and interface hepatitis (erosion of the limiting plate of periportal hepatocytes by infiltrating mononuclear cells) (H&E, 20×).
Lobular inflammation with acidophilic body (apoptotic body) surrounded by lymphoid cells (H&E, 40×).
Chronic hepatitis B with hepatocellular cytoplasmic staining for hepatitis B surface antigen (immunoperoxidase, 20×).
Chronic hepatitis B with hepatocellular nuclear staining for hepatitis B core antigen (immunoperoxidase, 20×).
Autoimmune hepatitis with portal and lobular inflammation, interface hepatitis, and cholestasis (H&E, 10×).
Autoimmune hepatitis, higher magnification, showing dense plasma cell infiltrate in the portal and periportal regions (H&E, 40×).
Primary biliary cirrhosis with degenerating bile duct epithelium (“florid ductular lesion”) (arrow) surrounded by epithelioid granulomatous reaction and lymphoplasmacytic infiltrate (H&E, 40×).
Chronic hepatitis C with bridging fibrosis (arrow) (Masson trichrome, 10×).
Cirrhosis with architectural alteration resulting from fibrosis and nodular hepatocellular regeneration (Masson trichrome, 2×).
Acute cellular rejection of orthotopic liver allograft demonstrating a mixed inflammatory cell infiltrate (lymphoid cells, eosinophils, neutrophils) of the portal tract as well as endothelialitis of the portal vein (arrow) and bile duct injury (H&E, 10×).
Liver allograft with cytomegalovirus infection showing hepatocytes with nuclear inclusions (arrows) surrounded by a neutrophilic and lymphoid infiltrate (H&E, 10×).
Combined acetaminophen hepatotoxicity and alcoholic liver injury with extensive centrilobular areas of necrosis (H&E, 4×).
Combined acetaminophen hepatotoxicity and alcoholic liver injury at higher magnification showing necrotic centrilobular area with Mallory bodies (H&E 20×).
α1 antitrypsin deficiency with cytoplasmic periodic acid–Schiff (PAS)-positive, diastase-resistant globules in many ...
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