摘要:

In 37 patients undergoing total hip replacement, a prophylactic treatment by a low-molecular-weight heparin (LMWH) was conducted for 2 weeks. They belonged to a group of 499 patients included in a multicenter clinically controlled trial comparing two LMWHs. Blood was collected 1 day before surgery (D-1) and at D+1 or D+2 and D+5 or D+6 as well as D+10 through D+14 after surgery for determinations of platelets counts and anti-Xa. Bilateral venography was performed between D+10 and D+14. A fatal heparin-associated-thrombocytopenia (HAT) occurred on D+9 in one patient and was associated with a positive platelet aggregation test. This finding was confirmed with a recent ELISA test which evidenced a high concentration of PF4-heparin dependent antibodies 72 h before the detection of thrombocytopenia. This led us to study retrospectively PF4-heparin ELISA results by testing the plasma samples of 36 other surgical patients treated under the same conditions and during the same period (four measurements per patient). Among these patients, seven had a venous thrombotic event as a treatment failure. Although some authors claimed that some post-operative thromboses may be facilitated by the presence of heparin-dependent antibodies associated with or without thrombocytopenia, no thrombocytopenia and no positive PF4-heparin ELISA test was observed in this group. Out of the 144 tests performed in these 36 patients for the detection of PF4-heparin complexes dependent antibodies, 15 results were borderline in ten patients and three results in two patients were positive. No relation was evidenced between a positive ELISA test and the occurrence of venous thrombosis. This study points out the possible usefulness of the PF4-heparin ELISA test for HAT-antibodies detection. A daily platelet count in a postoperative patient under heparin therapy, showing thrombocytopenia associated with the detection of heparin-dependent antibodies could allow an earlier and more reliable diagnosis of HAT.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

A simple, rapid and cheap method for the analysis of variable dinucleotide tandem repeat polymorphisms in introns 13 and 22 of the factor VIII gene has been established. The protocol uses blood spots stored on filter paper (Guthrie spots) and other DNA containing materials as sources of DNA. Following DNA amplification using a thermostable DNA polymerase, products are size fractionated on native polyacrylamide gels and visualized by silver staining. This simplified protocol obviates the use of DNA extraction, reducing time and costs and in addition, reduces the requirement for gel documentation equipment (i.e. photography), as silver staining can be visualized readily without additional equipment and the gels themselves can be stored. These alterations to the analysis enhance the universal applicability of these polymorphisms, as was demonstrated by a comparative study in Caucasian and Thai females.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

The effects of L-arginine and L-NG-nitro arginine methyl ester (L-NAME) on human blood coagulation and fibrinolysis were studiedin vitrousing computerized thromboelastography and native whole blood. L-Arginine (8–80 $mUM) prolonged the split point (SP), reaction time (R) and biKoatugulierung time (K); and diminished the angle (α), maximum amplitude (MA) and TEG index. L-NAME (0.5–50 $mUM) shortened SP, R and K and increased α, MA and the TEG index in a concentration-dependent manner. Neither L-arginine nor L-NAME had any effect on clot lysis. SP and R indicate the initiation of fibrin-strand formation, therefore L-arginine delayed, while L-NAME promoted the processes leading to fibrin formation. K and α reflect the rate of clot formation and involve fibrin build-up and platelets. Thus, L-arginine inhibited and L-NAME enhanced the rate of clot formation. MA (clot strength) involves the integrity of fibrin strands and platelet aggregation, and again L-arginine was inhibitory, while L-NAME enhanced this interaction. The TEG index indicates the coagulability of the sample; L-arginine was anticoagulant while L-NAME had procoagulant effects. These results are consistent with the inhibitory effects of NO on platelet function and of the platelet-aggregating properties of NOS inhibitors. In addition, NO may play an inhibitory role in the process leading to fibrin formation and also on the interactions between platelets and fibrin. Such effects may be important when considering the clinical use of drugs that affect the NO-cGMP pathway.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Dahlbäcket al.recently describedin vitroresistance to the anticoagulant response of activated protein C (APC), in the majority of cases associated with the Arg506to Gin point mutation in the factor V gene in thrombophilic patients. To determine to what extent this common gene mutation affects the risk of childhood stroke, its occurrence was prospectively investigated in a population of children with ischaemic stroke. Over a 2-year period the Arg506to Gln mutation, factor V, protein C, protein S, antithrombin, antiphospholipid antibodies and lipopoprotein (a) [Lp(a)] were measured in 14 infants and children with acute ischaemic stroke. Heterozygous factor V Leiden mutation (n= 4), homozygous factor V Leiden mutation (n= 1), protein C deficiency type I (n= 3) and increased Lp(a) (n= 2) were diagnosed in the children investigated. Seven of 14 patients showed an underlying disease and additionally risk factors were present in nine of 14 children. Data of this study indicate that deficiencies in the protein C anticoagulant pathway play an important role in the aetiology of childhood stroke. However, additional triggering factors may promote early manifestation of thromboembolism in children with inherited defects of clotting inhibitors.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

We have previously identified a group of blood donors with inherited deficiencies of either antithrombin (AT) or protein C who appear to have a relatively low thrombosis rate. In the 5 years that have elapsed since initial identification of these individuals, resistance to activated protein C (APC resistance), which is associated with the factor VLeidengene mutation, has emerged as an important and highly prevalent inherited thrombophilic risk factor. We have followed 28 donors/relatives with deficiency of AT (median age 48 years, range 16–77) and 23 with deficiency of protein C (median age 44 years, range 15–79) over a period of 5 years. During the study period only one individual, who was previously symptomatic, has suffered a thrombotic event which occurred spontaneously whilst on warfarin. We have now excluded coinheritance of APC resistance due to the factor VLeidenmutation in our cohort. Our findings demonstrate that individuals with single inherited thrombophilic defects are not uncommon and are frequently asymptomatic. The absence of the factor VLeidenmutation may in part explain the low thrombosis rate observed, and lends support to the hypothesis that multiple thrombophilic defects may be necessary for the development of thrombosis.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Abdominal aortic aneurysms have traditionally been thought to be a consequence of severe atherosclerosis of the arterial wall. To date, the role of haemostatic factors in aneurysmal disease has not been extensively researched. The aim of this study was to see if such factors were independently related to the occurrence of aortic aneurysm. Furthermore, were the associations maintained after taking into account the presence of underlying atherosclerotic disease? Using data from the Edinburgh Artery Study, a nested case-control design was used involving 40 cases of aortic aneurysm, each being matched to five controls by sex and within a 5-year age band. After adjustment for age and sex, both fibrinogen (P× 0.01) and fibrin D-dimer (P× 0.001) were each associated with a significant increased risk of aneurysm. Further adjustment for packyears, history of cardiovascular disease and the ankle brachial pressure index resulted in odds ratios of 1.51 (95% CI 1.05 to 2.16,P× 0.05) for fibrinogen and 3.75 (95% CI 1.80 to 7.82,P× 0.001) for fibrin D-dimer. These associations probably arise as a consequence of fibrin deposition and turnover within the aneurysmal sac, although further prospective studies are needed before thrombotic factors can be used in the identification of a group who are at high risk of developing an abdominal aortic aneurysm.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

To evaluate if the presence of anti-β2GPI antibodies (aβ2GPI) is associated with activated protein C resistance (APC-R) phenotype, we performed the APC-R APTT-based assay in 74 plasma samples from patients with antiphospholipid antibodies (aPL). Samples were diluted 1:5 in factor V-deficient plasma. Lupus anticoagulant (LA), anticardiolipin antibodies (aCL) and aβ2GPI (IgG and IgM) were also performed. A control group of 22 healthy volunteers was used. The prevalence of reduced APC-R ratio in patients with aPL was significantly higher than in normal controls (31.1vs4.5%,P< 0.05) and the mean APC-R ratio was lower (mean × SD; 2.32 × 0.40vs2.55 × 0.21,P< 0.02). There were no differences in the prevalence of APC-R and the ratio values between LA(+) and LA(-). Among the LA(+), the aCL(+) had a higher prevalence of APC-R than the aCL(-) (P< 0.01) and lower APC-R ratios (P< 0.01). The latter group was no different to normal controls. Anti-β2GPI antibodies were associated with a higher prevalence of APC-R (50.0vs19.6%,P< 0.001), and lower APC-R ratios (2.15 × 0.41vs2.42 × 0.35,P< 0.005), compared with a β2GPI(-). In conclusion, the acquired APC-R in patients with aPL seems to be associated with aCL and aβ2GPI rather than anin vitrointerference by LA.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

摘要:

Patients with homozygous heparin-binding-site (HBS) qualitative antithrombin deficiencies are at significant risk of venous and arterial thrombosis. We report on the eighth case of homozygous HBS deficiency, and the fourth case concerning the Arg 47-Cys mutation. The proposita is a 25 year old, without known thrombotic antecedent, despite an oral contraceptive therapy for 7 years. After 25 weeks of a first pregnancy, she presented an intrauterine fetal demise complicated with deep vein thrombosis and pulmonary embolism. Heparin therapy was inefficient (no clinical nor angiographic improvement, no biological hypocoagulability). Heparin cofactor activity was < 10%, antigen concentration was normal. The crossed immunoelectrophoresis of patient's plasma, with and without heparin, showed a typical profile of qualitative HBS antithrombin deficiency. The molecular analysis revealed an homozygous Arg 47-Cys mutation. Antithrombotic therapy was achieved with continuous infusion of antithrombin concentrates (80 IU/kg/day) and unfractionated heparin (500 IU/kg/day) during 12 days, leading to clinical improvement, and followed by treatment with vitamin K antagonists. This observation emphasizes the risk of intrauterine fetal demise and the inefficiency of heparin therapy without antithrombin infusion in type II HBS homozygous deficiency. The management of a future pregnancy will probably require repeated infusions of antithrombin.

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID

ISSN:0957-5235    

出版商:OVID    

年代:1996

数据来源: OVID