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      Hepatitis C Virus Infection Associated With an Increased Risk of Deep Vein Thrombosis : A Population-Based Cohort Study

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      Author(s): , MD, , MD, PhD, , MS, , MD, MS, PhD, , MD
      Editor(s):
      Publication date (Electronic):
      Journal: Medicine
      Publisher: Wolters Kluwer Health

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          Abstract

          The association between the hepatitis C virus (HCV) infection and the risk of myocardial infarction (MI) and stroke has been previously investigated. However, the association between the HCV infection and the risk of venous thromboembolism (VTE) has not been extensively discussed.

          Using the Longitudinal Health Insurance Database 2000 (LHID2000), we selected 3686 patients with newly diagnosed HCV infection. We randomly selected 14,744 people with no HCV or hepatitis B virus (HBV) infection as comparison group and frequency matched them with patients with HCV infection according to their age, sex, and index year. The incidence density rates and hazard ratios (HRs) of deep vein thrombosis (DVT) and pulmonary embolism (PE) were calculated until the end of 2011.

          The mean follow-up duration of 5.14 years for the HCV cohort and 5.61 years for the non-HCV cohort, the overall incidence density rates of DVT were 7.92 and 3.51 per 10,000 person-years in the non-HCV group, and the HCV groups, respectively (crude HR = 2.25; 95% confidence interval [CI] = 1.21–4.21). After adjusted for age, sex, and comorbidities, the risk of DVT remained significantly higher in the HCV group than in the non-HCV group (adjusted HR = 1.96; 95% CI = 1.03–3.73). The overall incidence density rates of PE in the HCV and non-HCV groups were not significantly different (crude HR = 2.20; 95% CI = 0.94–5.14).

          HCV infection is associated with the risk of DVT in a long-term follow-up period.

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          Risk of venous thromboembolism in patients with liver disease: a nationwide population-based case-control study.

          Kirstine Kobberøe Søgaard, Hendrik Vilstrup, Erzsébet Horváth-Puhó … (2008)
          It is known that liver disease can cause an imbalance in the coagulation system, but available data on liver disease and risk of venous thromboembolism are conflicting. We examined the risk of venous thromboembolism in patients hospitalized with liver diseases. We conducted a nationwide Danish case-control study of incident cases of venous thromboembolism from 1980 to 2005 using population-based data from the National Registry of Patients, and from the Civil Registration System. We used conditional logistic regression to compute the relative risk of venous thromboembolism in patients with liver disease compared to population controls. We then excluded patients with known malignancy (diagnosed either before or up to 3 months after the venous thromboembolism) or fractures, trauma, surgery, or pregnancy within 90 days before the venous thromboembolism to estimate the risk associated with unprovoked venous thromboembolism. A total of 99,444 patients with venous thromboembolism and 496,872 population controls were included in the study. Patients with liver disease had a clearly increased relative risk of venous thromboembolism, varying from 1.74 (95% CI, 1.54-1.95) for liver cirrhosis to 1.87 (95% CI, 1.73-2.03) for non-cirrhotic liver disease. The risks were higher for deep venous thrombosis compared with pulmonary embolism. In the analysis, restricted to 67,519 patients with unprovoked venous thromboembolism and 308,614 population controls, we found slightly higher relative risks: 2.06 (95% CI, 1.79-2.38) for liver cirrhosis and 2.10 (95% CI, 1.91-2.31) for non-cirrhotic liver disease. Patients with liver disease have a substantially increased risk of venous thromboembolism.
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            Coagulopathy does not fully protect hospitalized cirrhosis patients from peripheral venous thromboembolism.

            Patrick Northup, Jodi L. Berg, Stephen H. Caldwell … (2006)
            Despite the endogenous coagulopathy of cirrhosis, some patients with cirrhosis experience thrombophilic states. This study aims to determine the incidence and predictors of venous thromboembolism (VTE), such as deep vein thrombosis (DVT) and pulmonary embolism, in hospitalized patients with cirrhosis. A retrospective case-control study was performed in a tertiary-care teaching hospital over an 8-yr period. A total of 113 hospitalized patients with cirrhosis with a documented new VTE were compared to controls. Risk factors for VTE were determined using univariate and multivariate statistical analyses. Approximately 0.5% of all hospitalized patients with cirrhosis had a VTE. Traditional markers of coagulation such as INR and platelet count were not predictive of VTE. In the univariate analysis, serum albumin level was significantly lower in cases than controls (2.85 vs. 3.10 g/dL, respectively, p = 0.01). In the multivariate analysis, serum albumin remained independently predictive of VTE, with an odds ratio of 0.25 (95% CI 0.10-0.56). Approximately 0.5% of admissions involving cirrhosis patients resulted in a new thromboembolic event. Low serum albumin was strongly predictive of increased risk for developing VTE, independent of international normalized ratio or platelet count. Serum albumin deficiency may indicate low levels of endogenous anticoagulants.
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              Venous thromboembolism: disease burden, outcomes and risk factors.

              J A Heit (2005)
              The epidemiology of venous thromboembolism (VTE) in the community has important implications for VTE prevention and management. This review describes the disease burden (incidence), outcomes (survival, recurrence and complications) and risk factors for deep vein thrombosis and pulmonary embolism occurring in the community. Recent comprehensive studies of the epidemiology of VTE that reported the racial demography and included the full spectrum of disease occurring within a well-defined geographic area over time, separated by event type, incident vs. recurrent event and level of diagnostic certainty, were reviewed. Studies of VTE outcomes had to include a relevant duration of follow-up. VTE incidence among whites of European origin exceeded 1 per 1000; the incidence among persons of African and Asian origin may be higher and lower, respectively. VTE incidence over recent time remains unchanged. Survival after VTE is worse than expected, especially for pulmonary embolism. Thirty percent of patients develop VTE recurrence and venous stasis syndrome. Exposures can identify populations at risk but have a low predictive value for the individual. An acquired or familial thrombophilia may predict the subset of exposed persons who actually develop symptomatic VTE. In conclusion, VTE is a common, lethal disease that recurs frequently and causes serious long-term complications. To improve survival and prevent complications, VTE occurrence must be reduced. Better individual risk stratification is needed in order to modify exposures and target primary and secondary prophylaxis to the person who would benefit most.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Wolters Kluwer Health
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: September 2015
                Publication date (Electronic): 25 September 2015
                Volume: 94
                Issue: 38
                Electronic Location Identifier: e1585
                Affiliations
                From the Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan (C-CW); Division of Cardiology, Department of Internal Medicine, Taichung Tzuchi Hospital, The Buddhist Tzuchi Medical Foundation (C-CW); College of Medicine, China Medical University (C-TC, C-LL); Division of Nephrology, China Medical University Hospital (C-TC); Management Office for Health Data, China Medical University Hospital, Taichung (C-LL); Department of Family Medicine, Changhua Christian Hospital, Changhua (I-CL); School of Medicine, Chung Shan Medical University, Taichung (I-CL); Department of Nuclear Medicine and PET Center, China Medical University Hospital (C-HK); and Graduate Institute of Clinical Medical Science, College of Medicine, China Medical University, Taichung, Taiwan (C-HK).
                Author notes
                Correspondence: Chia-Hung Kao, Graduate Institute of Clinical Medical Science, College of Medicine, China Medical University, No. 2, Yuh-Der Road, Taichung 40447, Taiwan (e-mail: d10040@ 123456mail.cmuh.org.tw ).
                Article
                Accession ID: 01585
                DOI: 10.1097/MD.0000000000001585
                PMC ID: 4635760
                PubMed ID: 26402820
                SO-VID: f5d72b2d-ec3e-4157-b7e9-34dd154d8f4a
                Copyright © Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
                License:

                This is an open access article distributed under the Creative Commons Attribution-NoDerivatives License 4.0, which allows for redistribution, commercial and non-commercial, as long as it is passed along unchanged and in whole, with credit to the author. http://creativecommons.org/licenses/by-nd/4.0

                History
                Date received : 21 April 2015
                Date revision received : 19 August 2015
                Date accepted : 24 August 2015
                Categories
                Subject: 4500
                Subject: Research Article
                Subject: Observational Study
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