Therapy of hepatitis C: Patients with normal aminotransferase levels

P Marcellin, S Levy, S Erlinger – 30 December 2003 – An important group of patients with chronic hepatitis C have normal serum alanine aminotransferase (ALT) levels despite having hepatitis C virus (HCV) RNA detectable in serum. These patients are typically identified after donating blood and being found to be positive for antibody to HCV (anti‐HCV). A strict definition of this patient population is needed, which should include presence of anti‐HCV, HCV RNA detectable by polymerase chain reaction (PCR), and persistently normal ALT levels.

Therapy of hepatitis C: Overview

K L Lindsay – 30 December 2003 – Based on the first decade of research on α interferon in viral hepatitis, one can conclude that up to 40% of patients with compensated chronic hepatitis C and elevated alanine aminotransferase (ALT) levels will respond at least transiently to interferon. Four forms of α interferon have been evaluated in large numbers of patients with chronic hepatitis C: alfa‐2b, alfa‐2a, alfa‐n1, and consensus interferon (CIFN).

Diagnosis of hepatitis C

A S Lok, N T Gunaratnam – 30 December 2003 – Currently, the second‐ and third‐generation enzyme immunoassays (EIA‐2 and EIA‐3) for hepatitis C virus antibody (anti‐HCV) are the most practical screening tests for the diagnosis of HCV infection. The need for and the choice of supplementary or confirmatory tests depend on the clinical setting and the likelihood of a true‐positive EIA result. Detection of HCV RNA in serum by polymerase chain reaction (PCR) assay is the gold standard for the diagnosis of HCV infection.

Antibodies to tumor necrosis factor alfa attenuate hepatic necrosis and inflammation caused by chronic exposure to ethanol in the rat

Y Iimuro, R M Gallucci, M I Luster, H Kono, R G Thurman – 30 December 2003 – Tumor necrosis factor (TNF)α, a pivotal cytokine involved in inflammation, is produced primarily by Kupffer cells in the liver. It has been shown that inactivation of Kupffer cells prevents alcohol‐induced liver injury; therefore, the purpose of this study was to determine if neutralizing anti‐TNF‐α antibody is also effective. Male Wistar rats were exposed to ethanol (11 to 12 g · kg‐1 · d‐1) continuously for up to 4 weeks via intragastric feeding using an enteral feeding model.

Role of Kupffer cells in gut ischemia/reperfusion‐induced hepatic microvascular dysfunction in mice

Y Horie, R Wolf, J Russell, T P Shanley, D N Granger – 30 December 2003 – Kupffer cells (KCs) have been implicated in the leukocyte recruitment and microvascular dysfunction associated with liver inflammation. The overall objective of this study was to assess the role of KCs in the leukocyte adhesion and oxidative stress elicited in the liver by gut ischemia/reperfusion (I/R).

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case‐control study, pathological analysis, and pathogenetic hypothesis

R G Lee, A C Tsamandas, A J Demetris – 30 December 2003 – Large cell change (LCC), characterized by cellular enlargement, nuclear pleomorphism and hyperchromasia, and multinucleation of hepatocytes, is a common lesion in cirrhotic livers, but its nature, significance, and pathogenesis remain uncertain.

Enhanced apoptosis relates to bile duct loss in primary biliary cirrhosis

K Harada, S Ozaki, M E Gershwin, Y Nakanuma – 30 December 2003 – Primary biliary cirrhosis (PBC) is characterized by an immune‐mediated destruction of intrahepatic small bile ducts. Apoptosis, a unique pattern of cell death, has been suggested to be responsible for the biliary destruction in PBC. To address this issue, we attempted to detect the apoptosis of biliary epithelial cells by in situ nick‐end labeling and by the expression of apoptosis‐related proteins using immunohistochemistry in patients with various hepatobiliary diseases, including PBC.

Extracellular matrix remodeling at the early stages of liver regeneration in the rat

T Kim, W M Mars, D B Stolz, B E Petersen, G K Michalopoulos – 30 December 2003 – Previous studies have shown that activity of urokinase‐type plasminogen activator (u‐PA) increases very rapidly (within 1 minute) after partial hepatectomy. In view of the well‐recognized roles of u‐PA as one of the major initiators of the matrix proteolysis cascade and as an activator of plasminogen and hepatocyte growth factor (HGF), we studied matrix degradation in liver shortly after partial hepatectomy.

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