1. Optimizing Diagnosis From the Medical Liver Biopsy
Albert J. Czaja, Herschel A. Carpenter 
Clinical Gastroenterology and Hepatology 
Volume 5, Issue 8, Pages (August 2007)
DOI: /j.cgh
Copyright © 2007 AGA Institute Terms and Conditions

2. Figure 1
Interface hepatitis. Lymphocytic infiltrates extend from the portal tracts into acinar tissue with destruction of the limiting plate. Findings are consistent with autoimmune hepatitis, drug reaction, or viral infection.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

3. Figure 2
Portal plasma cell infiltration. Plasma cells, characterized by a cytoplasmic halo around the nucleus, are present commonly in autoimmune hepatitis, but they also occur in chronic hepatitis B and C infections and drug reactions.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

4. Figure 3
Portal lymphoid aggregates and minimal steatosis. The findings are consistent with a quiescent chronic hepatitis C infection.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

5. Figure 4
Ground-glass hepatocyte. Enlarged hepatocytes with homogeneous cytoplasm have prominent endoplasmic reticulum filled with hepatitis B surface antigen or reactive to certain drugs (eg, chlorpromazine, barbiturates, phenytoin, and azathioprine).
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

6. Figure 5
Cytomegalovirus infection. Findings of an enlarged endothelial cell with swollen nucleus and intranuclear inclusion (arrow) that resembles an owl’s eye typifies the viral infection.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

7. Figure 6
Herpes simplex infection at edge of focal hemorrhagic necrosis. Eosinophilic, near-purple, nuclear inclusion with clear surrounding halo typifies an infected hepatocyte.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

8. Figure 7
Macrovesicular fatty infiltration of hepatocytes with ballooning and hyalin bodies (arrows). These findings are consistent with nonalcoholic steatohepatitis or alcoholic hepatitis.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

9. Figure 8
Sinusoidal inflammation with little liver cell injury or liver plate alteration. This inflammatory pattern is consistent with an immune response to a systemic infection or lymphoproliferative disorder.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

10. Figure 9
Nonzonal foci of parenchymal necrosis. The foci of parenchymal necrosis (arrows) are typically associated with a viral infection (herpes simplex, herpes zoster, or adenovirus).
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

11. Figure 10
Multinucleated giant hepatocytes. This injury response is consistent with a viral infection, drug reaction, or toxic exposure. Electron microscopy may disclose widely scattered foci of viral-like inclusions.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

12. Figure 11
Bile ductular proliferation, bile duct tortuosity, and cholestasis. Findings indicate biliary obstruction associated with mechanical, toxic, or drug reaction.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

13. Figure 12
Granulomatous destructive cholangitis with bile duct loss (florid duct lesion). This feature is characteristic of primary biliary cirrhosis, but also may occur in sarcoidosis.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

14. Figure 13
Ductopenia. Arteriole within the portal tract lacks an adjacent bile duct. Findings are consistent with small-duct primary sclerosing cholangitis.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

15. Figure 14
Fibro-obliterative cholangitis. The rim of fibrosis encircling an obliterated bile duct (arrow) is a finding that is characteristic of primary sclerosing cholangitis.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

16. Figure 15
Nonnecrotizing granulomatous reaction. A discrete nonnecrotizing epithelioid granuloma is consistent with a drug reaction or sarcoidosis.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

17. Figure 16
Sinusoidal congestion and red blood cell extravasation. The vascular pattern of injury reflects venous outflow obstruction, and it may be caused by hepatic vein thrombosis, pulmonary hypertension, constrictive pericarditis, or veno-occlusive disease.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

18. Figure 17
Veno-occlusive disease with sinusoidal congestion and endothelial proliferation and obstruction of the central vein. Endothelial proliferation and obstruction of the central vein (arrow) distinguishes veno-occlusive disease from hepatic vein thrombosis. It is associated with toxicity to pyrrolizidine alkaloids (bush tea toxicity), hepatic radiation, or drug reaction (chemotherapeutic agents or azathioprine).
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions

19. Figure 18
Nodular regenerative hyperplasia. The nodular pattern (arrows) is associated with compression and atrophy of the perivenular hepatic plate and the absence of fibrosis. The finding is associated with obstruction of small portal veins as a result of myeloproliferative disorders, hypercoagulable states, toxic or drug reactions, or autoimmune conditions.
Clinical Gastroenterology and Hepatology 2007 5, DOI: ( /j.cgh )
Copyright © 2007 AGA Institute Terms and Conditions