NYMC Faculty Publications

Association of Hepatitis C With Markers of Hemostasis in HIV-Infected and Uninfected Women in the Women's Interagency HIV Study (WIHS)

Author Type(s)

Faculty

DOI

10.1097/QAI.0b013e31827fdd61

Journal Title

Journal of Acquired Immune Deficiency Syndromes

First Page

301

Last Page

310

Document Type

Article

Publication Date

3-1-2013

Department

Biostatistics

Second Department

Public Health

Keywords

Adult, Biomarkers, Coinfection, Cross-Sectional Studies, Factor VIII, Female, Fibrin Fibrinogen Degradation Products, HIV Infections, Hemostasis, Hepatitis C, Humans, Plasminogen Activator Inhibitor 1, Prospective Studies, Protein S, Regression Analysis, United States

Disciplines

Medical Biomathematics and Biometrics | Medicine and Health Sciences | Other Public Health | Women's Health

Abstract

BACKGROUND: Coinfection with HIV and hepatitis C virus (HCV) is common. HIV infection and treatment are associated with hypercoagulability; thrombosis in HCV is underinvestigated. Proposed markers of hemostasis in HIV include higher D-dimer, Factor VIII%, and plasminogen activator inhibitor-1 (PAI-1) antigen and lower total Protein S% (TPS) but have not been examined in HCV. We assessed the independent association of HCV with these 4 measures of hemostasis in a multicenter, prospective study of HIV: the Women's Interagency HIV Study.

METHODS: We randomly selected 450 HCV-infected (anti-HCV+ with detectable plasma HCV RNA) and 450 HCV-uninfected (anti-HCV-) women. HCV was the main exposure of interest in regression models.

RESULTS: Four hundred forty-three HCV+ and 425 HCV- women were included. HCV+ women had higher Factor VIII% (124.4% ± 3.9% vs. 101.8% ± 3.7%, P < 0.001) and lower TPS (75.7% ± 1.1% vs. 84.3% ± 1.1%,

CONCLUSIONS: HCV was independently associated with higher Factor VIII% and lower TPS consistent with hypercoagulability. Higher Factor VIII% and D-dimer and lower TPS were also strongly associated with HIV infection and levels of HIV viremia, independent of HCV infection. Further investigation is needed to determine if there is increased thrombotic risk from HCV. Studies examining hemostasis markers in HIV infection must also assess the contribution of HCV infection.

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