Anti-cardiolipin autoantibodies and pulmonary embolism - A case for a common cause

A patient with primary Sjogren's syndrome developed pulmonary embolism foll owing infection with influenza A virus. IBM anti-cardiolipin autoantibodies (aCL) evolved two weeks after hospitalisation, synchronously with antibodi es against influenza A. Ige aCL developed three weeks after hospitalization , peaked during the recovery period, and gradually declined to undetectable levels 12 months after admission. Antibodies against beta2 glycoprotein I were not detected. Our results assign a high likelihood to the hypothesis t hat influenza A virus caused the patient's thromboembolic disease as well a s development of aCL. aCL may have contributed to tissue pathology by formi ng immunecomplexes with cardiolipin and rheumatoid factor.