Assessment of Fibrosis and Cirrhosis in Liver Biopsies

An Update

Giacomo Germani, M.D.; Prodromos Hytiroglou, M.D.; Anastasia Fotiadu, M.D.; Andrew K. Burroughs, F.Med.Sci.; Amar P. Dhillon, M.D.


Semin Liver Dis. 2011;31(1):82-90. 

In This Article

Hepatic Fibrosis and Cirrhosis: Definitions

Hepatic fibrosis is the deposition of excess extracellular matrix that is rich in fibril-forming collagens. In the vast majority of cases, hepatic fibrosis is the result of chronic liver diseases, including viral hepatitis, alcoholic and nonalcoholic steatohepatitis, biliary diseases, and metabolic disorders. The major effectors of fibrosis are the hepatic stellate cells and the portal fibroblasts, which are activated by soluble mediators produced by activated hepatic resident cells, most importantly Kupffer cells, and by inflammatory cells infiltrating the liver in the course of chronic hepatic diseases.[1]

Cirrhosis is a pathologic condition of diverse etiology, characterized by architectural distortion of the liver, including diffuse parenchymal nodularity, fibrosis, and vascular changes of variable severity.[2] The nodules are surrounded by fibrous septa and may be small (i.e., <3 mm across—micronodular cirrhosis), large (>3 mm—macronodular cirrhosis), or of mixed size (mixed macro- and micronodular cirrhosis). Vascular changes commonly seen in cirrhotic livers include obliteration of afferent and efferent venules, and formation of microscopic portosystemic and arteriovenous shunts.[3] The sinusoids are also significantly altered in cirrhosis and exhibit loss of fenestrations and acquisition of basement membrane.[4]

There is a wide range of morphologic variation in cirrhosis that is related to the etiology, the activity, and the duration of the disease process causing hepatic injury and architectural distortion, and to secondary vascular changes resulting in further parenchymal cell loss, fibrosis, and remodeling. This morphologic variation is reflected in clinical manifestations of variable severity, such as those of portal hypertension, hepatic encephalopathy, and liver failure. Objective assessment of portal hypertension by means of hepatic venous pressure gradient (HVPG) is currently emerging as a means of classifying cirrhosis in clinically meaningful stages of severity.[5]


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