95: Liver biopsy and histopathological diagnosis


CHAPTER 95
Liver biopsy and histopathological diagnosis


Sugantha Govindarajan


USC Keck School of Medicine, Los Angeles, CA, USA


Evaluation of liver biopsy requires that the pathologist recognize the architecture and identify the pathological changes, and correlate the changes with clinical and laboratory data (Figures 95.195.99). Although some histological diagnosis can be made without the help of the clinical or laboratory data, most meaningful information is obtained with a proper clinical–pathological correlation.


Special stains, such as Masson trichrome, demonstrate fibrosis or cirrhosis of the liver, an indication of a chronic process. Other routine stains include stains for iron, reticulin, and diastase‐resistant periodic acid–Schiff‐positive material. Granulomas of the liver require special stains for the etiological agent, such as acid‐fast organisms and fungi. Shikata or orcein stain identifies hepatitis B surface antigen as well as copper‐binding protein, metallothionein. Immunoperoxidase stains detect viral and nonviral protein in the biopsy material using specific antibodies directed against the proteins.


Routine hematoxylin and eosin‐stained sections are the most valuable tools in the diagnosis. Well‐embedded (3 μm) sections with good H&E stain will provide great cellular details of hepatocytes, such as inclusions in the cytoplasm or the nuclei, as well as features such as fat, cholestasis, or dysplasia.


Initial assessment of the architecture is followed by a closer review of the portal tract or the fibrous septa if cirrhosis is present. Elements to be examined are the bile ducts, epithelial abnormalities or their absence or proliferation, cellular types of the inflammatory infiltrates, and the infiltrates’ involvement of the bile ducts, the parenchymal limiting plate, or the vessels (vasculitis). The portal tracts or the fibrous septa should also be examined under polarized light for foreign material in the macrophages, which is usually seen in patients with a history of intravenous drug addiction.


The parenchyma is examined for cord sinusoidal pattern; normal one‐cell thickness is altered in hepatocellular carcinoma to 3–4 or more cells that thicken the trabeculae. Parenchymal cytoplasmic inclusions such as Mallory bodies, mega‐mitochondria, and αl‐antitrypsin, or ground‐glass cytoplasmic appearance are identified under higher magnifications in the review process. Areas of hepatocytolysis often appear as focal punched‐out or spotty necrosis with an accumulation of Kupffer cells and lymphocytes, or as large areas of collapsed reticulin with loss of hepatocytes. Hepatocytolysis is often localized in the perivenular zones. Individual cell necrosis is seen as acidophil bodies or apoptotic cells.


Attention also should be paid to the sinusoidal lining cells, Ito cells, and the space of Disse. In alcoholic liver disease, there is collagen deposition of the sinusoidal space, which stands out on Masson trichrome stain. Amyloid is also seen in this space, either as reticular or globular type, and is demonstrated by Congo red stain.


In addition to histology to confirm the clinical diagnosis, liver biopsy has become a very important prognostic tool to assess the responses to treatment of chronic viral hepatitis B and C. The Histology Activity Index (HAI) is measured using several standardized methods on pretreatment and 1–2‐year follow‐up biopsies. This quantitative measurement of necroinflammation and fibrosis by either Knodell or Ishak scoring (Table 95.1) has been applied to many long‐term therapeutic protocols. Standardization of scoring has been helpful in studies that compare different treatment modalities. Its application for individual cases also helps the clinician with patient follow‐up and monitoring of other serological viral markers.


Liver biopsies are also extremely valuable in post‐liver transplant settings. Standard protocols of liver biopsies help confirm clinical diagnoses from rejection to opportunistic infections. Post‐liver transplantation management of patients is largely dependent on the liver biopsy interpretations in conjunction with other laboratory studies.


With proper indications and carefully chosen technique, a needle biopsy of the liver is an invaluable tool. Most often, the biopsy provides the final diagnosis when the pathology interpretation is made using the combined expertise of the pathologist and the hepatologist.

Photo depicts cirrhosis of liver with fibrous septa and regenerative nodules.

Figure 95.1 Cirrhosis of liver with fibrous septa and regenerative nodules. (Masson stain; original magnification ×40.)

Photo depicts alpha 1-Antitrypsin globules in the periportal hepatocytes – diastase-resistant, PAS-positive.

Figure 95.2 α1‐Antitrypsin globules in the periportal hepatocytes – diastase‐resistant, PAS‐positive. (Di‐PAS stain; original magnification ×200.)

Photo depicts perls iron stain demonstrating bright-blue granules in hepatocytes and duct epithelial cells in hemochromatosis.

Figure 95.3 Perls iron stain demonstrating bright‐blue granules in hepatocytes and duct epithelial cells in hemochromatosis. (Original magnification ×100.)

Photo depicts immunoperoxidase for HBsAg in the hepatocytes in chronic hepatitis B.

Figure 95.4 Immunoperoxidase for HBsAg in the hepatocytes in chronic hepatitis B. (Original magnification ×400.)

Photo depicts rubeanic acid stain demonstrating dark-green granules of copper in periseptal hepatocytes in Wilson disease.

Figure 95.5 Rubeanic acid stain demonstrating dark‐green granules of copper in periseptal hepatocytes in Wilson disease. (Original magnification ×400.)

Photo depicts nodular regenerative hyperplasia demonstrating regeneration of parenchyma compressing the surrounding parenchyma without fibrous septa formation.

Figure 95.6 Nodular regenerative hyperplasia demonstrating regeneration of parenchyma compressing the surrounding parenchyma without fibrous septa formation. (H & E stain; original magnification ×40.)

Photo depicts submassive hepatic necrosis with collapsed perivenular reticulum network.

Figure 95.7 Submassive hepatic necrosis with collapsed perivenular reticulum network. (H & E stain; original magnification ×40.)

Photo depicts portal area with prominent neutrophils in close proximity to the dilated interlobular bile duct in acute cholangitis.

Figure 95.8 Portal area with prominent neutrophils in close proximity to the dilated interlobular bile duct in acute cholangitis. (H & E stain; original magnification ×200.)

Photo depicts portal area with prominent eosinophils among the inflammatory infiltrates in a case of Dilantin-induced hepatotoxicity.

Figure 95.9 Portal area with prominent eosinophils among the inflammatory infiltrates in a case of Dilantin‐induced hepatotoxicity. (H & E stain; original magnification ×200.)

Photo depicts portal area with increased number of eosinophils in a case of early rejection of orthotopic liver transplantation.

Figure 95.10 Portal area with increased number of eosinophils in a case of early rejection of orthotopic liver transplantation. (H & E stain; original magnification ×400.)

Photo depicts prominent plasma cells among the infiltrates in the portal tract of autoimmune hepatitis.

Figure 95.11 Prominent plasma cells among the infiltrates in the portal tract of autoimmune hepatitis. (H & E stain; original magnification ×400.)

Photo depicts a portal area under polarizing light to demonstrate polarizable crystals in an intravenous drug user.

Figure 95.12 A portal area under polarizing light to demonstrate polarizable crystals in an intravenous drug user. (H & E stain; original magnification ×200.)

Photo depicts lamellar periductal fibrosis in chronic bile duct obstruction.

Figure 95.13 Lamellar periductal fibrosis in chronic bile duct obstruction. (H & E stain; original magnification ×200.)

Photo depicts arachnoid portal fibrosis with periportal extension of collagen in alcoholic liver disease.

Figure 95.14 Arachnoid portal fibrosis with periportal extension of collagen in alcoholic liver disease. (Masson trichrome stain; original magnification ×200.)

Photo depicts portal area with marked cholangiolar proliferation in mechanical duct obstruction.

Figure 95.15 Portal area with marked cholangiolar proliferation in mechanical duct obstruction. (H & E stain; original magnification ×200.)

Photo depicts primary sclerosing cholangitis with evidence of periductal fibrosis and chronic inflammatory infiltrate.

Figure 95.16 Primary sclerosing cholangitis with evidence of periductal fibrosis and chronic inflammatory infiltrate. (H & E stain; original magnification ×100.)

Photo depicts primary biliary cholangitis with granuloma.

Figure 95.17 Primary biliary cholangitis with granuloma. (Original magnification ×200.)

Photo depicts a few dilated duct structures with abnormal epithelium surrounded by loose collagen representing Meyenburg complex.

Figure 95.18 A few dilated duct structures with abnormal epithelium surrounded by loose collagen representing Meyenburg complex. (H & E stain; original magnification ×200.)

Photo depicts biliary fibrosis and ductular proliferation in a 3-month-old infant with extrahepatic biliary atresia.

Figure 95.19 Biliary fibrosis and ductular proliferation in a 3‐month‐old infant with extrahepatic biliary atresia. (H & E stain; original magnification ×200.) Source: An Atlas and concise guide. New York: Demos Medical Publishing; 2011. Reproduced with permission.

Photo depicts increased number of thin-walled vascular structures representing portal venous radicles reflective of portal hypertension.

Figure 95.20 Increased number of thin‐walled vascular structures representing portal venous radicles reflective of portal hypertension. (H & E stain; original magnification ×200.)

Photo depicts severe necrotizing inflammatory reaction around hepatic arteriole in polyarteritis nodosa.

Figure 95.21 Severe necrotizing inflammatory reaction around hepatic arteriole in polyarteritis nodosa. (H & E stain; original magnification ×100.)

Photo depicts increased number of abnormal vascular structures in a portal tract in Osler–Weber–Rendu syndrome.

Figure 95.22 Increased number of abnormal vascular structures in a portal tract in Osler–Weber–Rendu syndrome. (H & E stain; original magnification ×100.)

Photo depicts marked perivenular fibrosis in alcoholic liver disease.

Figure 95.23 Marked perivenular fibrosis in alcoholic liver disease. (Masson trichrome stain; original magnification ×200.)

Photo depicts endothelialitis showing inflammatory changes of a terminal hepatic venule in acute rejection of orthotopic liver transplantation.

Figure 95.24 Endothelialitis showing inflammatory changes of a terminal hepatic venule in acute rejection of orthotopic liver transplantation. (H & E stain; original magnification ×200.)

Photo depicts Budd–Chiari syndrome with perivenular hemorrhage, necrosis, and sinusoidal dilation.

Figure 95.25 Budd–Chiari syndrome with perivenular hemorrhage, necrosis, and sinusoidal dilation. (H & E stain; original magnification ×200.)

Photo depicts confluent necrosis in the perivenular zone due to anoxia.

Figure 95.26 Confluent necrosis in the perivenular zone due to anoxia. (H & E stain; original magnification × 00.)

Photo depicts massive hepatic necrosis involving the entire parenchyma with islands of portal tracts remaining.

Figure 95.27 Massive hepatic necrosis involving the entire parenchyma with islands of portal tracts remaining. (H & E stain; original magnification ×200.)

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Nov 27, 2022 | Posted by in GASTROENTEROLOGY | Comments Off on 95: Liver biopsy and histopathological diagnosis
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