Patients with a wide range of autoimmune disorders have much greater risk of pulmonary embolism, and prophylaxis could be warranted

November 25, 2011

When patients have been admitted to hospital for an autoimmune disorder, they have a much greater risk of having a pulmonary embolism during the following 12 months. Thus prophylaxis could be warranted in these patients. These are the conclusions of an article published Online First by the Lancet, written by Dr Bengt Zöller, Center for Primary Health Care Research, Lund University and Clinical Research Centre, Malmo University Hospital, Sweden, and colleagues.

Venous thromboembolism is a major health problem, for which pulmonary embolism is a potentially lethal complication. Pulmonary embolism is a common cardiovascular and cardiopulmonary illness with a yearly incidence in the USA of more than one case per 1000 people and a mortality rate of more than 15% in the first 3 months after diagnosis, which is similar to that for acute myocardial infarction. Inflammation and venous thromboembolism are linked, with inflammation driving venous thrombosis.

The study analysed more than 500 000 patients admitted to hospital for any of 33 autoimmune disorders in Sweden between 1964 and 2008. The three most common autoimmune disorders were rheumatoid arthritis, Hashimoto's thyroiditis, and Graves' disease. Others include psoriasis, chronic rheumatic heart disease, and Crohn's disease.

Overall risk of pulmonary embolism during the first year after admission for an autoimmune disorder was 6 times that for patients without an autoimmune disorder. All the 33 autoimmune disorders were associated with a significantly increased risk of pulmonary embolism during the first year after admission. This overall risk was similar to the increased risk for rheumatoid arthritis and Grave's disease. However, some diseases had a particularly high risk of pulmonary embolism compared with patients without an autoimmune disorder -- eg, immune thrombocytopenic purpura (11 times increased risk), polyarteritis nodosa (13 times), polymyositis or dermatomyositis (16 times). Overall risk decreased over time from the 6 times increased risk within one year of hospital admission stated above, to a 50% increased risk at 1 years, down to a 15% increase risk at 5 years, and finally a 4% increased risk at 10 years and later. The risk was increased for both sexes and all age groups.

The authors note that the increased risk of venous thromboembolism could have different underlying causes in different autoimmune diseases and might indicate more severe cases of autoimmune disorders, because the patients in this study had been admitted to hospital.

The authors say: "Our results show that autoimmune disorders affect the risk of hospital admission for pulmonary embolism in men and women of all ages... 33 autoimmune diseases were associated with significantly increased risks of pulmonary embolism during the first year after admission."

They conclude: "Our findings show that autoimmune disorders in general should be regarded not only as inflammatory disorders, but also as hypercoagulable (blood clotting) disorders. Prophylaxis could be warranted in patients admitted with autoimmune disorders or at least for those disorders for which the risk of pulmonary embolism was very high. Further studies are needed to assess the potential usefulness of such treatment."

In a linked Comment, Dr Carani B Sanjeevi, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden, says: "The decrease in overall risk for pulmonary embolism over time for all 33 autoimmune diseases suggests that the decrease in inflammation could be due to reductions in inflammatory activity and treatment. Nevertheless, a clear link is shown between thrombosis and inflammation. Anti-inflammatory drugs and thromboprophylaxis should be considered to treat inflammation associated with autoimmune disorders, particularly in those admitted to hospital. However, prospective studies are needed to identify the predictive value of inflammatory markers for pulmonary embolism."
-end-
Dr Bengt Zöller, Center for Primary Health Care Research, Lund University and Region Skåne, Clinical Research Centre, Malmo University Hospital, Sweden. T) 46-70-66914-76 E) bengt.zoller@med.lu.se

Dr Carani B Sanjeevi, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. T) 46-70-7976632 E) sanjeevi.carani@ki.se

Lancet

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