Fibronectin and Factor VIII-Related Antigen in Liver Cirrhosis and Acute Liver Failure

Höfeler, H.; Hg, Klingemann

doi:10.1515/cclm.1984.22.1.15

Cited by 2 publications

(4 citation statements)

References 11 publications

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“…Liver fibrosis is associated with the predictor variable HCV 1,62,63 and fibrosis/cirrhosis is also associated several of markers of hemostasis 12,16,64,65 . We calculated FIB-4 from the Sterling’s formula using aspartate aminotransferase (AST) and alanine aminotransferase (ALT) 56 : [Age (in years)*AST] / [platelet(10^9/L) * ALT^1/2].…”

Section: Methodsmentioning

confidence: 99%

“…HIV infection itself and HIV treatment with highly active antiretroviral therapy (HAART) have been associated with a hypercoaguable state 3,4 and increased risk for thrombotic events such as deep vein thrombosis (DVT) or pulmonary embolism (PE) 5–10 . However, thrombosis in HCV has been evaluated mainly in end-stage liver disease and cirrhosis 11–16 .…”

Section: Introductionmentioning

confidence: 99%

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

Kiefer¹,

Shi²,

Hoover³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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Coinfection with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is common. HIV infection and treatment are associated with hypercoaguability; thrombosis in HCV is under-investigated. Proposed markers of hemostasis in HIV include higher D-dimer, Factor VIII% and Plasminogen Activator Inhibitor-1 (PAI-1Ag), and lower total Protein S% (TPS), but have not been examined in HCV. We assessed the independent association of HCV with these four measures of hemostasis in a multicenter, prospective study of HIV: the Women’s Interagency HIV Study (WIHS). 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. 443 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, <0.001) than HCV−, independent of HIV infection and viral load; there was little difference in PAI-1Ag or log10 D-dimer. After adjustment for confounders, these inferences remained. HIV infection was independently associated with higher Factor VIII% and log10 D-dimer, and lower TPS. HCV was independently associated with higher Factor VIII% and lower TPS consistent with hypercoaguability. Higher Factor VIII % and D-dimer and lower total Protein S % 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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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Kiefer¹,

Shi²,

Hoover³

et al. 2013

JAIDS Journal of Acquired Immune Deficiency Syndromes

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“…65 Numerous clinical reports have confirmed a significant increase in plasma FVIII levels in cirrhotic patients, specifically during the advanced/late stages of cirrhosis. [79][80][81][82][83][84] Although the exact reason for FVIII increase in cirrhosis is not known, there are several hypotheses for how FVIII levels are changed during cirrhosis. Cytokine release from the necrotic tissue of cirrhotic livers can lead to increased FVIII synthesis.…”

Section: Factor VIII and Cirrhosismentioning

confidence: 99%

Section: Relevance Of Fviii In Cldmentioning

confidence: 99%

Exploring the Complex Role of Coagulation Factor VIII in Chronic Liver Disease

Pradhan‐Sundd

Gudapati²,

Kamiński³

et al. 2021

Cellular and Molecular Gastroenterology and Hepatology

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Chronic liver disease is one of the leading causes of death in the United States. Coagulopathy is often a sequela of chronic liver disease, however, the role and regulation of coagulation components in chronic liver injury remain poorly understood. Clinical and experimental evidence indicate that misexpression of the procoagulant factor VIII (FVIII) is associated with chronic liver disease. Nevertheless, the molecular mechanism of FVIII-induced chronic liver injury progression remains unknown. This review provides evidence supporting a pathologic role for FVIII in the development of chronic liver disease using both experimental and clinical models.

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Fibronectin and Factor VIII-Related Antigen in Liver Cirrhosis and Acute Liver Failure

Cited by 2 publications

References 11 publications

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

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

Exploring the Complex Role of Coagulation Factor VIII in Chronic Liver Disease

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