Risk of deep vein thrombosis and pulmonary embolism after acute infection in a community setting

L Smeeth, C Cook, S Thomas, AJ Hall, R Hubbard… - The Lancet, 2006 - thelancet.com
L Smeeth, C Cook, S Thomas, AJ Hall, R Hubbard, P Vallance
The Lancet, 2006thelancet.com
Background Acute infection increases the risk of arterial cardiovascular events, but effects
on venous thromboembolic disease are less well established. Our aim was to investigate
whether acute infections transiently increase the risk of venous thromboembolism. Methods
We used the self-controlled case-series method to study the risk of first deep vein thrombosis
(DVT)(n= 7278) and first pulmonary embolism (PE)(n= 3755) after acute respiratory and
urinary tract infections. Data were obtained from records from general practices who had …
Background
Acute infection increases the risk of arterial cardiovascular events, but effects on venous thromboembolic disease are less well established. Our aim was to investigate whether acute infections transiently increase the risk of venous thromboembolism.
Methods
We used the self-controlled case-series method to study the risk of first deep vein thrombosis (DVT) (n=7278) and first pulmonary embolism (PE) (n=3755) after acute respiratory and urinary tract infections. Data were obtained from records from general practices who had registered patients with the UK's Health Improvement Network database between 1987 and 2004.
Findings
The risks of DVT and PE were significantly raised, and were highest in the first two weeks, after urinary tract infection. The incidence ratio for DVT was 2·10 (95% CI 1·56–2·82), and that for PE 2·11 (1·38–3·23). The risk gradually fell over the subsequent months, returning to the baseline value after 1 year. The risk of DVT was also higher after respiratory tract infection, but possible diagnostic misclassification precluded a reliable estimate of the risk of PE after respiratory infection.
Interpretation
Acute infections are associated with a transient increased risk of venous thromboembolic events in a community setting. Our results confirm that infection should be added to the list of precipitants for venous thromboembolism, and suggest a causal relation.
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