Histopathologic Evaluation of Liver Biopsy for Cirrhosis

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Advances in anatomic pathology (Impact Factor: 3.23). 07/2012; 19(4):220-30. DOI: 10.1097/PAP.0b013e31825c6bab
Source: PubMed


In current medical practice, the clinical diagnosis of cirrhosis is rendered when a patient has suggestive imaging findings or features of portal hypertension (pHTN). Liver biopsy may be considered to assess potential underlying cause(s). Cirrhosis, however, is not the only etiology of pHTN; in fact, schistosomiasis remains a significant factor worldwide. pHTN results from obstruction of hepatic blood flow; it is classified clinically based on either the anatomic location of obstruction or hepatic venous pressure gradient measurements. The clinical categories carry clinicopathologic significances. Histopathologically, pHTN is manifest with either cirrhotic or noncirrhotic features. Noncirrhotic pHTN results from a heterogeneous group of disease processes, all of which result in vascular remodeling with variable parenchymal nodularity and fibrosis. This review summarizes liver biopsy findings of cirrhosis and possible etiologies and provides a stepwise approach for the histologic differential diagnosis of a liver biopsy done for "cirrhosis."

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    • "Cirrhosis is considered to be the final stage of any chronic liver disease, characterized by the replacement of the normal hepatic tissue by extensive fibrosis, regenerative nodules formation, and bridging fibrosis leading to distortion of the normal hepatic architecture. [9] The radiological findings of cirrhosis include diffuse nodularity, and a lobulated and relatively small liver. Moreover, signs of portal hypertension, such as splenomegaly, ascites and portosystemic shunts [7] may be seen. "

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    • "Cirrhosis is the end result of liver injury characterized by distortion of the hepatic architecture by extensive fibrosis and formation of regenerative nodules [5]. Cirrhosis is defined by its typical pathological features: 1) presence of regenerating nodules of hepatocytes and 2) presence of bridging fibrosis between these nodules [5]. "
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    ABSTRACT: OBJECTIVE: To evaluate the efficacy and safety of entecavir (ETV) in patients with advanced schistosomiasis and hepatitis B virus (HBV) co-infection. METHODS: Sixty-seven patients with advanced schistosomiasis and HBV co-infection were enrolled in this study. The patients were randomly divided into the ETV treatment group (n=35) and the control group (n=32). The patients in the control group adopted routine supportive therapy for 52 weeks, and those in the ETV treatment group received ETV at a dose of 0.5mg once daily on the basis of routine supportive therapy for 52 weeks. Hepatic fibrosis markers (hyaluronic acid, type III procollagen, type IV collagen, laminin, and fibronectin), Ishak fibrosis score, alanine transaminase (ALT), HBV DNA, and Child-Pugh score were compared between the two groups. The intention to treat (ITT) population was used for the analysis. The measurement data and count data were analyzed by t-test and Chi-square test, respectively. RESULTS: After 52 weeks of treatment, the hepatic fibrosis markers (hyaluronic acid, type III procollagen, type IV collagen, laminin, and fibronectin) were significantly improved in the ETV treatment group compared to the control group (all p<0.05). A ≥1-point improvement in the Ishak fibrosis score was found in 25.7% (9/35) of the ETV group, and the mean change from the baseline in the Ishak fibrosis score was a 0.3-point reduction. The control group showed disease progression in the Ishak fibrosis score. More patients in the ETV group than in the control group had undetectable serum HBV DNA levels (82.9% vs. 3.1%, p<0.05) and ALT normalization (68.6% vs. 18.3%, p<0.05). The ETV treatment group demonstrated an improvement in Child-Pugh score at week 52 (-3.7 vs. 0.3, p<0.05). In addition, no obvious adverse reactions were observed during ETV treatment. CONCLUSION: ETV is safe and effective in patients with advanced schistosomiasis and HBV co-infection.
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