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Abstract
BackgroundInfluenza infections have been associated with procoagulant changes. Whether influenza infections lead to an increased risk of pulmonary embolism remains to be established.MethodsWe conducted a nested case control study in a large cohort of patients with a clinical suspicion of having pulmonary embolism. Blood samples were collected to investigate the presence of influenza A and B by complement fixation assay (CFA). We compared case patients, in whom pulmonary embolism was proven (n = 102), to controls, in whom pulmonary embolism was excluded (n = 395). Furthermore, we compared symptoms of influenza-like illness in both patient groups 2 weeks prior to inclusion in the study, using the influenza-like illness (ILI) score, which is based on a questionnaire. We calculated the risk of pulmonary embolism associated with influenza infection.ResultsThe percentage of patients with influenza A was higher in the control group compared to the case group (4.3% versus 1.0%, respectively, odds ratio 0.22; 95% CI: 0.03–1.72). Influenza B was not detectable in any of the cases and was found in 3 of the 395 controls (0.8%). The ILI score was positive in 24% of the cases and 25% in the control persons (odds ratio 1.16, 95% CI: 0.67–2.01). We did not observe an association between the ILI score and proven influenza infection.ConclusionIn this clinical study, influenza infection was not associated with an increased risk of acute pulmonary embolism. The ILI score is non-specific in this clinical setting.
Highlights
Influenza infections have been associated with procoagulant changes
Symptoms of respiratory tract infection The influenza-like illness score was positive in 24% of the pulmonary embolism patients (24/102)
The adjusted odds ratio for the influenza-like illness score was 1.16; 95% confidence intervals (95% CI): 0.67–2.01
Summary
Whether influenza infections lead to an increased risk of pulmonary embolism remains to be established. Deep vein thrombosis and pulmonary embolism, collectively known as venous thromboembolism (VTE), have an annual incidence of approximately 2–3 per 1000 people [1]. Many risk factors of venous thromboembolism have been well established, including genetic predisposition, immobilization, surgery, pregnancy, oral contraceptives and malignancies. There are patients who develop venous thromboembolism in the absence of one of these risk factors. There is growing evidence that acute infections are associated with an increased risk of developing a venous thromboembolic event. Emmerich and others found an association between positive antibody titers for Chlamydia pneumoniae and venous thromboembolism [2,3,4]. Patients with HIV are at increased risk of developing venous thromboembolism [5]. In a population-based case-control study, subjects with elevated IL-8 levels had an increased risk of venous thrombosis, which indicates the role of inflammation (potentially as a consequence of infection) in the pathogenesis of venous thrombosis [6]
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