Reductions in tissue plasminogen activator and thrombomodulin in blood draining veins damaged by venous access devices.
A frequent complication of venous access devices (VADs) is axillary-subclavian venous thrombosis. To study this problem we have compared blood drawn through VADs with peripheral blood samples in a group of oncology patients with venographically demonstrated venous damage (N = 14) and a group with normal venograms (N = 21). The samples were assayed for a battery of proteins believed to be involved in thrombogenesis. After approximately six weeks of catheterization the venographically abnormal patients had significantly less thrombomodulin (P = 0.0055) and significantly higher PAI:tPA (P = 0.022) in catheter-drawn samples as compared with the venographically normal group. Although the data are inconclusive, it is hypothesized that these changes resulted from local endothelial injury.
D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000008:administration & dosage; D001367:Axillary Vein / Q000293:injuries; D002405:Catheterization, Central Venous / Q000009:adverse effects; D002408:Catheters, Indwelling / Q000009:adverse effects*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009369:Neoplasms / Q000097:blood / Q000150:complications / Q000188:drug therapy; D013350:Subclavian Vein / Q000293:injuries; D018180:Thrombomodulin / Q000378:metabolism*; D013924:Thrombophlebitis / Q000097:blood / Q000209:etiology; D010959:Tissue Plasminogen Activator / Q000097:blood*
D000970:Antineoplastic Agents; D018180:Thrombomodulin; D010959:Tissue Plasminogen Activator