Evaluation of liver biopsies in
hepatitis C is aimed at confirming the clinical and serologic diagnosis, grading of necroinflammatory activity, staging of consecutive
fibrosis, ruling out or confirming
liver diseases of different etiology, and assessment of
therapeutic effects. Usually, the course of
chronic hepatitis C virus (HCV)
infection is slow, with mild inflammatory changes. Nevertheless, even in mild asymptomatic
chronic hepatitis C episodes of higher inflammatory activity associated with extensive piecemeal
necrosis and porto-central bridging,
necrosis can accelerate the course of the disease. For this reason, the traditional, morphologically based classification of
chronic hepatitis and the term "
chronic persistent hepatitis" have lost their predictive usefulness, especially in
hepatitis C.
Chronic hepatitis should be characterized by etiologic designation as well as grade and stage of the disease. Portal lymphoid aggregates, some inflammatory bile duct damage and mild steatosis are the most characteristic features by which
hepatitis C can be differentiated from other progressive inflammatory
liver diseases.
Antibodies directed against HCV
antigens allow identification of
viral proteins by immunohistochemistry. Immunostaining for
hepatitis B antigens, for alpha-1-antitrypsin and
copper staining are helpful in detecting
hepatitis B and congenital
liver diseases (
Wilson's disease,
alpha-1-antitrypsin deficiency) as possible causes of chronic progressive inflammatory
liver disease. Centrilobular Mallory's hyalin, identified by immunostaining for
ubiquitin in combination with perivenular
fibrosis, is helpful in diagnosing concomitant
alcoholic liver disease. In our own biopsy material (n = 100) and autopsy material (n = 58), HIV/HCV-coinfected patients have a significantly higher rate of
fibrosis and
cirrhosis than HIV patients without HCV
infection.
Hepatitis C can apparently aggravate the course of
HIV infection. Our morphologic findings support the clinical observation that chronic HCV
infection seems to be the main cause of
liver failure, especially in the risk group of HCV/HIV-coinfected hemophiliacs.