Acute infections and venous thromboembolism

• Autores: M. Schmidt, E. Horváth Puhó, R.W. Thomsen, L. Smeeth, H. T. Sorensen
• Localización: Journal of Internal Medicine, ISSN-e 1365-2796, Vol. 271, Nº. 6, 2012, págs. 608-618
• Idioma: inglés
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• Resumen

  • Abstract.  Schmidt M, Horvath-Puho E, Thomsen RW, Smeeth L, Sørensen HT (Department of Clinical Epidemiology, Institute of Clinical Medicine, Aarhus University Hospital, Aarhus, Denmark; and Department of Non-Communicable Epidemiology, London School of Hygiene and Tropical Medicine, London, UK). Acute infections and venous thromboembolism. J Intern Med 2012; 271: 608–618.

    Background.  Data on the association between acute infections and venous thromboembolism (VTE) are sparse. We examined whether various hospital-diagnosed infections or infections treated in the community increase the risk of VTE.

    Methods.  We conducted this population-based case–control study in Northern Denmark (population 1.8 million) using medical databases. We identified all patients with a first hospital-diagnosed VTE during the period 1999–2009 (n = 15 009). For each case, we selected 10 controls from the general population matched for age, gender and county of residence (n = 150 074). We identified all hospital-diagnosed infections and community prescriptions for antibiotics 1 year predating VTE. We used odds ratios from a conditional logistic regression model to estimate incidence rate ratios (IRRs) of VTE within different time intervals of the first year after infection, controlling for confounding.

    Results.  Respiratory tract, urinary tract, skin, intra-abdominal and bacteraemic infections diagnosed in hospital or treated in the community were associated with a greater than equal to twofold increased VTE risk. The association was strongest within the first 2 weeks after infection onset, gradually declining thereafter. Compared with individuals without infection during the year before VTE, the IRR for VTE within the first 3 months after infection was 12.5 (95% confidence interval (CI): 11.3–13.9) for patients with hospital-diagnosed infection and 4.0 (95% CI: 3.8–4.1) for patients treated with antibiotics in the community. Adjustment for VTE risk factors reduced these IRRs to 3.3 (95% CI: 2.9–3.8) and 2.6 (95% CI: 2.5–2.8), respectively. Similar associations were found for unprovoked VTE and for deep venous thrombosis and pulmonary embolism individually.

    Conclusions.  Infections are a risk factor for VTE.