Abstract
The article by Svensson and Dahlback on resistance to activated protein C (APC) (Feb. 24 issue)1 postulates that there is a genetically determined defect in anticoagulation characterized by resistance to APC. The authors subsequently found the anticoagulant cofactor that corrects inherited APC resistance to be identical to unactivated factor V. I believe that these findings could also be due to hyperhomocysteinemia. It has been demonstrated that hyperhomocysteinemia is an independent risk factor for vascular disease2,3. It was previously demonstrated that homocysteine induced a vascular-endothelial-cell activator that led to the activation of factor V4. I feel that serum homocysteine levels should have been measured by Svensson and Dahlback, and that elevated homocysteine levels may explain their findings.