HISTOPATHOLOGIC FINDINGS IN CHRONIC HEPATITIS-C

Citation
Hp. Fischer et al., HISTOPATHOLOGIC FINDINGS IN CHRONIC HEPATITIS-C, Journal of hepatology, 24, 1996, pp. 35-42
Citations number
37
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
01688278
Volume
24
Year of publication
1996
Supplement
2
Pages
35 - 42
Database
ISI
SICI code
0168-8278(1996)24:<35:HFICH>2.0.ZU;2-R
Abstract
Evaluation of liver biopsies in hepatitis C is aimed at confirming the clinical and serologic diagnosis, grading of necroinflammatory activi ty, staging of consecutive fibrosis, ruling out or confirming liver di seases of different etiology, and assessment of therapeutic effects. U sually, the course of chronic hepatitis C virus (HCV) infection is slo w with mild inflammatory changes. Nevertheless, even in mild asymptoma tic chronic hepatitis C episodes of higher inflammatory activity assoc iated with extensive piecemeal necrosis and porto-central bridging, ne crosis 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 predict ive 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 d amage 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 identi fication of viral proteins by immunohistochemistry. Immunostaining for hepatitis B antigens, for alpha-l-antitrypsin and copper staining are helpful in detecting hepatitis B and congenital liver diseases (Wilso n's disease, alpha-l-antitrypsin deficiency) as possible causes of chr onic progressive inflammatory liver disease. Centrilobular Mallory's h yalin, identified by immunostaining for ubiquitin in combination with perivenular fibrosis, is helpful in diagnosing concomitant alcoholic l iver disease. In our own biopsy material (n = 100) and autopsy materia l (n = 58), HIV/HCV-coinfected patients have a significantly higher ra te 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. (C) European Associ ation for the Study of the Liver.