In cancer, the incidence of venous thromboembolism (VTE) is particularly high in patients with myeloma, especially when it is de novo and treated with thalidomide, lenalidomide or erythropoietin. Curiously, the prevention of VTE with LMWH (low-molecular-weight heparin) in myeloma seems no more effective than that achieved with aspirin, while the effectiveness of the latter in the primary prevention of VTE has never been demonstrated regardless of the type of population considered. Meanwhile, a biological study showed that prophylactic doses of LMWH in patients with different types of cancer did not always optimal reduction of thrombin peak during the 24 hours following the injection of LMWH. These clinical and biological studies lead to the conclusion that patients with myeloma may be resistant to the usual doses of preventive LMWH, which may explain the failure of prevention. Initially we intend to investigate whether this resistance to prophylactic doses of LMWH is present in patient's biology and if this resistance is specific to myeloma in hematological cancers. For this, we propose to study the evolution of thrombin generation by Thrombinography during 24 hours after subcutaneous injection of 4500 anti-Xa IU Tinzaparin in 6 patients with de novo myeloma whit high thrombo embolic risk ie treated with thalidomide, lenalidomide or erythropoietin. LMWH is Tinzaparin chosen because it does not accumulate in patients with impaired renal function, and has a greater anti-biological activity thrombotic than other LMWH. To assess whether the observed pattern of thrombin generation is particularly multiple myeloma, we will take the same study in 6 patients with aggressive lymphoma and 6 medical patients hospitalized for acute heart and respiratory failure.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
19
single subcutaneous injection of 4500 IU tinzaparin
blood sample taken at hours 0, 3, 8, 18 and 24 after subcutaneous injection of 4500 IU tinzaparin
CHU de Saint-Etienne
Saint-Etienne, France
Endogenous Thrombin Potential (ETP, nM.min) for all patients with de novo myeloma with high thrombotic risk
Endogenous Thrombin Potential (i.e. the aera under the thrombin generation curve, nM.min) is measured by Thromboplastin Generation Tests (TGTs) following a single injection of 4500 IU tinzaparin
Time frame: hours : 0, 3, 8, 18, 24
Endogenous Thrombin Potential (ETP, nM.min) for all patients with aggressive lymphoma treated with chemotherapy
Endogenous Thrombin Potential (i.e. the aera under the thrombin generation curve, nM.min) is measured by Thromboplastin Generation Tests (TGTs) following a single injection of 4500 IU tinzaparin
Time frame: hours : 0, 3, 8, 18, 24
Endogenous Thrombin Potential (ETP, nM.min) for all patients with over 40 years hospitalized for heart or respiratory failure
Endogenous Thrombin Potential (i.e. the aera under the thrombin generation curve, nM.min) is measured by Thromboplastin Generation Tests (TGTs) following a single injection of 4500 IU tinzaparin
Time frame: hours : 0, 3, 8, 18, 24
Differences of Endogenous Thrombin Potential (ETP, nM.min) between group 1 and group 2 et 3
Endogenous Thrombin Potential (i.e. the aera under the thrombin generation curve, nM.min) is measured by Thromboplastin Generation Tests (TGTs) following a single injection of 4500 IU tinzaparin
Time frame: hours : 0, 3, 8, 18, 24
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