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The Effect of Hepatic Fibrosis and HCV viremia on Serum Inflammatory Mediators in HIV Infection - a Women's Interagency HIV Study
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Reported by jules Levin
CROI 2013
Sheila M. Keatinga,b, Jennifer Dodged, Philip J. Norrisa,b,c, Audrey Frenche, Marshall Glesbyf, Brian Edling, Patricia Lathamh, Ruth M. Greenblatti and Marion G. Petersc. aBlood Systems Research Institute, San Francisco, CA; bDepartment of Laboratory Medicine, University of California San Francisco, CA; cDepartment of Medicine, UCSF, San Francisco, CA; dDepartment of Surgery, UCSF, San Francisco, CA eCORE Center, Stroger Hospital of Cook County, Chicago, IL; fDepartment of Medicine, Division of Infectious Diseases, Weill Cornell Medical College, New York, NY; gDepartment of Medicine, SUNY Downstate, Brooklyn, NY; hDepartment of Pathology, Division of Infectious Diseases, Georgetown University, Washington, DC; iDepartment of Pharmacology, UCSF, San Francisco, CA
"In 3 of the groups there were positive correlations with cell adhesion molecules and increased fibrosis."
Wikipedia: Soluble cell adhesion molecules (sCAMs) are a class of cell adhesion molecule (CAMs - cell surface binding proteins) that may represent important biomarkers for inflammatory processes involving activation or damage to cells such as platelets and the endothelium.
They include soluble forms of the cell adhesion molecules ICAM-1, VCAM-1, E-selectin and P-selectin (distinguished as sICAM-1, sVCAM-1, sE-selectin and sP-selectin). The cellular expression of CAMs is difficult to assess clinically, but these soluble forms are present in the circulation and may serve as markers for CAMs.[1]
Research has focused on their role in cardiovascular (particularly atherosclerosis), connective tissue and neoplastic diseases, where blood plasma levels may be a marker of the disease severity or prognosis, and they may be useful in evaluating progress of some treatments.[2]
Many studies have postulated that increased production of cell adhesion molecules (CAMs) on the vascular endothelium (blood vessel lining) plays a role in the development of arterial plaque, with the suggestion from both in vitro and in vivo studies that the CAM production is increased by dyslipidemia (abnormal lipid levels in the blood).[3]
Research studies have used sCAMs as biomarkers to measure correlations with nutrients[4][5] or nutrient levels[6] as significant, or not.[7]
Certain melanoma cells can use VCAM-1 to adhere to the endothelium, and VCAM-1 may participate in monocyte recruitment to atherosclerotic sites. As a result, VCAM-1 is a potential drug target.
IP-10 correlates with hepatitis C viral load, hepatic inflammation and fibrosis and predicts hepatitis C virus relapse or non-response in HIV-HCV coinfection-Antiviral Therapy 2009
Pretreatment IP-10 levels correlated with HCV viral load, ALT levels, hepatic inflammation and fibrosis. An IP-10 cutoff level of 400 pg/ml might serve as a useful predictive marker for anti-HCV therapy in HIV-HCV-coinfected patients because it could discriminate patients with expected NR or HCV relapse after therapy from patients with an SVR before starting antiviral treatment......The IFN-induced increase of IP-10 was significantly stronger in patients with an SVR (P = 0.017). IP-10 levels were associated with HCV viral load, alanine aminotransferase (ALT) levels, hepatic inflammatory activity and fibrosis stage. Advanced fibrosis, high HCV viral load, hepatovenous pressure gradient and pretreatment IP-10 > 400 pg/ml predicted NR to antiviral therapy. In the multivariate analysis, IP-10 was identified as the strongest baseline predictor of SVR
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