Clinical Citations: Acute infection: Risk of deep venous thrombosis and pulmonary embolism

September 1, 2006

Acute infection has been known to increase the risk of arterial cardiovascular events, but the effects of acute infections on venous thromboembolic disease have not been well established. Using the self- controlled case-series method, British researchers studied data obtained from general practitioners between 1987 and 2004 to investigate whether acute respiratory and urinary tract infections transiently increased the risk of initial incidents of deep venous thrombosis (DVT) in 7278 persons and pulmonary embolism (PE) in 3755.

Acute infection has been known to increase the risk of arterial cardiovascular events, but the effects of acute infections on venous thromboembolic disease have not been well established. Using the self- controlled case-series method, British researchers studied data obtained from general practitioners between 1987 and 2004 to investigate whether acute respiratory and urinary tract infections transiently increased the risk of initial incidents of deep venous thrombosis (DVT) in 7278 persons and pulmonary embolism (PE) in 3755.

Acute respiratory infections included, for example, pneumonia, acute bronchitis, and influenza. In an analysis that adjusted for age, the researchers compared patients who had been exposed to at least 1 infection during follow-up with those who had not.

After a urinary tract infection, the incidence ratios were 2:10 for DVT (compared with 0:5 per 1000 person-years in the general population) and 2:11 for PE. These rates were approximately double the rates at baseline in the first 2 weeks after exposure, and they gradually fell over subsequent months, returning to baseline at approximately 1 year.

These findings demonstrate that acute infection in a community setting is linked to a transient increase in the risk of both DVT and PE, suggesting that acute infections may have a causal role. The similar patterns observed with respiratory and urinary tract infections indicate that the effect of infections on the risk of venous thromboembolism may be generic rather than type-specific.