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Markers of endothelial and haemostatic function in the treatment of relapsed myeloma with the immunomodulatory agent Actimid TM (CC‐4047) and their relationship with venous thrombosis
Author(s) -
Streetly Matthew,
Hunt Beverley J.,
Parmar Kiran,
Jones Richard,
Zeldis Jerome,
Schey Steve
Publication year - 2005
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.2004.00393.x
Subject(s) - medicine , fibrinolysis , coagulation , platelet , multiple myeloma , thrombosis , thalidomide , d dimer , platelet activation , venous thrombosis , gastroenterology , endothelium , endothelial activation , immunology
We evaluated the serum/plasma levels of cytokines [interleukin (IL)‐6, vascular endothelial growth factor (VEGF), transforming growth factor (TGF)‐ β 2] and markers of coagulation, fibrinolysis, endothelial and platelet activation during the first 4 wk of treatment with the thalidomide analogue Actimid TM (CC‐4047) in 15 patients with relapsed/refractory myeloma. There was evidence of activation of endothelium (soluble vascular cell adhesion molecule, sVCAM), coagulation (prothrombin fragment 1 + 2, PF1 + 2) and fibrinolysis (D‐dimers) but no evidence of platelet activation or endothelial cell damage in myeloma patients. These parameters were not affected by the use of CC‐4047. Three of four patients with baseline D‐dimers levels >500 μ g/L subsequently developed deep vein thrombosis (DVT). The hypothesis that D‐dimer level >500 μ g/L may predict for those patients most at risk of thromboembolism with multiple myeloma undergoing treatment is worthy of further study.