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Inflammation, TNFα and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia
American journal of hematology, 2011-10, Vol.86 (10), p.835-840
Aue, Georg
Nelson Lozier, Jay
Tian, Xin
Cullinane, Ann M.
Soto, Susan
Samsel, Leigh
McCoy, Philip
Wiestner, Adrian
2011
Details
Autor(en) / Beteiligte
Aue, Georg
Nelson Lozier, Jay
Tian, Xin
Cullinane, Ann M.
Soto, Susan
Samsel, Leigh
McCoy, Philip
Wiestner, Adrian
Titel
Inflammation, TNFα and endothelial dysfunction link lenalidomide to venous thrombosis in chronic lymphocytic leukemia
Ist Teil von
American journal of hematology, 2011-10, Vol.86 (10), p.835-840
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2011
Link zum Volltext
Quelle
Electronic Journals Library
Beschreibungen/Notizen
Patients receiving lenalidomide are at an increased risk for deep venous thrombosis (DVT). Here, we prospectively investigated the DVT risk in patients with relapsed chronic lymphocytic leukemia (CLL) treated with lenalidomide (n = 32). Five patients developed six incidents of DVT over 1 year for an annual incidence of 16%. Three of these were considered drug‐related. Median time to DVT was 105 days (range 56–259 days). No pulmonary embolism was detected. Hypercoagulability screen before study entry was negative in all patients who subsequently developed DVTs. Compared to normal volunteers CLL patients had increased baseline levels of D‐dimer, thrombin‐antithrombin, soluble vascular endothelial adhesion molecule 1 (sVCAM‐1), and thrombomodulin (p < 0.001). After 1 week on lenalidomide D‐dimer, thrombomodulin, sVCAM‐1, factor VIII, TNFα, and C‐reactive protein were significantly increased while protein C was decreased (p < 0.001). In patients with lenalidomide‐related DVTs, TNFα, and sVCAM‐1 were more strongly upregulated than in all other patients (p < 0.05) and TNFα and sVCAM‐1 levels were significantly correlated (r = 0.65, p < 0.001). These data link lenalidomide associated DVTs with TNFα upregulation and endothelial cell dysfunction and suggest that aspirin may have a role for DVT prophylaxis in these patients. Am. J. Hematol., 2011. © 2011 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0361-8609
eISSN: 1096-8652
DOI: 10.1002/ajh.22114
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3414537
Format
–
Schlagworte
Adult
,
Aged
,
Biological and medical sciences
,
Blood and lymphatic vessels
,
Blood Coagulation
,
Cardiology. Vascular system
,
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
,
Endothelium, Vascular - drug effects
,
Endothelium, Vascular - pathology
,
Female
,
Hematologic and hematopoietic diseases
,
Humans
,
Inflammation - blood
,
Inflammation - pathology
,
Leukemia, Lymphocytic, Chronic, B-Cell - blood
,
Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy
,
Leukemia, Lymphocytic, Chronic, B-Cell - pathology
,
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
,
Male
,
Medical sciences
,
Middle Aged
,
Prospective Studies
,
Risk Factors
,
Thalidomide - administration & dosage
,
Thalidomide - adverse effects
,
Thalidomide - analogs & derivatives
,
Tumor Necrosis Factor-alpha - biosynthesis
,
Up-Regulation
,
Venous Thrombosis - blood
,
Venous Thrombosis - chemically induced
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