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Background/Aims Nonalcoholic steatohepatitis (NASH) is prevalent in both economically developed and developing countries. Twenty percent of NASH progresses to cirrhosis with/without hepatocellular carcinoma, and there is an urgent need to find biomarkers for early diagnosis and monitoring progression of the disease. Using immunohistochemical and immunoelectron microscopic examination we previously reported that expression of matrix metalloproteinase-1 (MMP-1) increased in monocytes, Kupffer cells and hepatic stellate cells in early stage NASH. The present study investigated whether serum MMP-1 levels reflect disease activity and pharmaceutical effects in NASH patients.
Methods We measured the serum levels of MMPs, tissue inhibitors of metalloproteinases (TIMPs), and several cytokines/ chemokines in patients with histologically proven early and advanced stages of NASH and compared them with those in healthy controls.
Results Serum MMP-1 levels in stage 1 fibrosis, but not in the more advanced fibrosis stages, were significantly higher than in healthy controls (P=0.019). There was no correlation between serum MMP-1 level and fibrosis stage. Serum MMP- 1 levels in NASH patients represented disease activity estimated by serum aminotransferase values during the followup period. In contrast, MMP-2, MMP-9 and TIMPs did not change with disease activity. Consistent with the finding that MMP-1 is expressed predominantly in monocytes and Kupffer cells, serum levels of monocyte chemotactic protein-1 and granulocyte-colony stimulating factor were significantly increased in NASH with stage 1 fibrosis.
Conclusions These results suggest that serum MMP-1 levels represent disease activity and may serve as a potential biomarker for monitoring the progression of NASH.
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Background /Purpose: Phospholipase A (PLAq) is an rate-limiting enzyme hydrolyzing arachidonic acid from the sn-2 position of membrane phospholipids. In vitro studies demonstrated that the enzyme could be secreted into extracellular mileu by pro-inflammatory cytokines and endotoxin which were reported to have important roles in chronic liver diseases. This study was performed to know whether the enzyme is involved in the pathophysiology of the diseases. Methods: The subjects were composed of 24 patients with chronic hepatitis B, 26 patients with liver cirrhosis and 14 healthy individuals. The PLAp activities wem measured in the sera of the subjects by detecting radioactivity of "C-fatty acid hydrolyzed from "C-labeled phosphotadylethanolamine by the enzyme. Results: The activities of PLA were increased in the patients with chronic liver diseases, especially in the chronic hepatitis B patients with acute exacerbation and in the decompensated cirrhosis patients. Furthermore, their activities were closely related with the levels of transaminase in hepatitis group and with the levels of serum albumin in cirrhosis group, respectively. Conclusions: These results suggest that extracellular PLA might be involved in the exacerbution and progression of the chronic liver diseases.
Oromucosal cytokine therapy allows large amounts of cytokines to be administered with improved outcome and without dose limiting toxicity. Orally administered cytokines exert their effects by a novel two pronged mechanism of action. Firstly, specific populations of immuno-competent effector cells are activated in the oral cavity and migrate to the site of virus replication. Secondly, chemokines produced in the lymphoid tissue of the oral cavity enter the peripheral circulation and redirect activated lymphocytes to eliminate virus infected cells. Oromucosal IFN therapy constitutes an alternative and improved means of therapy for diseases such as chronic viral hepatitis which are currently treated parenterally with IFNα. The oral route also has obvious advantages for ease of administration and improved patient compliance. Furthermore, the availability of a well tolerated form of IFN therapy will also allow Type I IFNs to be used for the treatment of diseases such as upper respiratory tract virus infections, for which parenteral IFN therapy is currently precluded due to unacceptable toxicity.(Korean J Hepatol 2002;8:125-131)
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