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- Dahlbäck, Björn, et al.
(författare)
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Inherited resistance to activated protein C caused by presence of the FV:Q506 allele as a basis of venous thrombosis
- 1996
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Ingår i: Haemostasis. - 0301-0147. ; 26:SUPPL. 4, s. 301-314
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Tidskriftsartikel (refereegranskat)abstract
- Inherited resistance to activated protein C (APC) was recently discovered as a cause of familial thrombophilia and is now known to be the most common genetic risk factor for venous thrombosis. In a majority of cases, APC resistance is associated with a single point mutation in the factor V gene, which results in substitution of arginine (R) at position 506 by glutamine (Q) (FV:Q506). The mutation renders factor Va partially resistant to degradation by activated protein C (APC), which leads to a hypercoagulable state and a life-long 5-10-fold increased risk of venous thrombosis. The previously known inherited deficiencies of antithrombin, protein S or protein C, are in western societies together found in less than 10-15% of thrombosis patients, whereas APC resistance is present in 20 to 60% of the patients. A functional APC resistance test, which includes predilution of the patient plasma with factor V deficient plasma, is 100% sensitive and specific for the presence of FV:Q506. The FV:Q506 allele is common in populations of Caucasian origin (prevalence ranging between 1 and 15%), whereas it is not found in certain other ethnic groups such as in Japanese and Chinese. The thrombotic risk in individuals with APC resistant may be further increased by other genetic defects such as protein C or protein S deficiency and by exposure to circumstantial risk factors such as oral contraceptives, pregnancy, immobilisation and surgery.
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| 2. |
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| 3. |
- Schulman, S
(författare)
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Long-term prophylaxis in venous thromboembolism: LMWH or oral anticoagulation?
- 1998
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Ingår i: Haemostasis. - : S. Karger AG. - 0301-0147. ; 2828 Suppl 3, s. 17-21
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Tidskriftsartikel (refereegranskat)abstract
- Warfarin remains the standard drug for secondary prophylaxis following venous thromboembolism, however this treatment is not ideal. In patients for whom monitoring is problematic or who have a high risk of bleeding complications, other possible solutions have been explored. Unfractionated heparin has been used to a limited extent in these situations and requires dose adjustment in order to achieve an acceptable efficacy. Low-molecular-weight heparin (LMWH) is a valuable alternative to warfarin for these patients and for thromboprophylaxis during pregnancy. In several subgroups of patients with venous thromboembolism the use of a LMWH instead of warfarin could offer specific advantages. The combination of warfarin and LMWH is warranted in patients for whom it is predicted that warfarin treatment alone may fail. The optimal dose of LMWH in long-term prophylaxis has not been evaluated in a properly designed study and the optimal duration of prophylaxis with LMWH is thought to be similar to that for warfarin.
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| 5. |
- Strandberg, LE, et al.
(författare)
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Anticoagulant effects of low-molecular-weight heparin following thrombolytic therapy in acute myocardial infarction: a dose-finding study
- 1996
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Ingår i: Haemostasis. - : S. Karger AG. - 0301-0147. ; 26:5, s. 247-257
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Tidskriftsartikel (refereegranskat)abstract
- The aim of the present study was to gain clinical experience with different dose levels of dalteparin, a low-molecular-weight heparin, following thrombolytic therapy in acute myocardial infarction. Compared to heparin, dalteparin has a longer half-life and a greater and highly predictable bioavailability, which would suggest dalteparin to be a convenient alternative. Twenty patients with ECG signs of acute transmural myocardial ischemia received streptokinase (1.5 million IU for 60 min) and were allocated to a control group or to open treatment with 50, 75 or 100 IU of dalteparin/kg b.w. s.c. b.i.d., starting 4 h later, for 6 days. Each group consisted of 5 patients. Except for the control group, aspirin was withheld during dalteparin treatment. Anti-factor-Xa (anti-FXa) values increased dose-dependently during the first 24 h and were maintained throughout the study period. On day 6, anti-FXa levels after 100 IU/kg b.w. were 0.79 (0.59-1.00) IU/ml (median, min.-max.) 4 h after administration of dalteparin, and 0.51 (0.34-0.82) IU/ml before the subsequent dose of dalteparin. In conclusion, our results indicate that a dalteparin dose slightly higher than 100 IU/kg b.w. is required in order to obtain the presumed therapeutic range of anti-FXa (0.6-1.0 IU/ml).
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