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Results for “hypercoagulable state”

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PubMed2006

Postoperative dural sinus thrombosis in a patient in a hypercoagulable state. Case report.

Spontaneous cerebral venous sinus thrombosis is a rare problem that may be encountered in patients with underlying thrombophilic disorders. It has also been reported as a postoperative complication following suboccipital, transpetrosal, and transcallosal approaches. The authors report on a 67-year-old man with two prior episodes of lower-extremity deep venous thrombosis who underwent transcallosal resection of a colloid cyst and in whom sagittal sinus thrombosis developed 2 weeks thereafter. Results of a subsequent hematological workup revealed both a factor V Leiden mutation and the presence of antiphospholipid antibodies, two thrombophilic risk factors that likely contributed to the development of delayed postoperative sinus thrombosis. Although the safety of low-molecular-weight heparin (LMWH) after craniotomy has not been established in a randomized, controlled study, there is sufficient evidence to justify its use for prophylactic anticoagulation therapy in patients at high risk for postoperative cerebral venous thrombosis. The authors propose using LMWH prophylaxis in patients with thrombophilic disorders who undergo neurosurgical procedures in proximity to dural sinuses in an effort to prevent catastrophic venous infarction.

Aged↗
PubMed2000

Evaluation of the hypercoagulable state. Whom to screen, how to test and treat.

Venous thromboembolism is a common disease that causes significant morbidity and mortality. In recent years, the ability to diagnose inherited genetic defects and common acquired conditions predisposing to thrombosis has greatly increased. Venous thromboembolism is now understood to be a complex interaction of genetic and environmental factors leading to thrombosis. Integrating the various factors to individually assess thrombotic risk still poses a challenging clinical problem that will likely become easier as more data accumulate. As the ability to accurately assess risk increases, the data can then be translated into tailored treatment regimens. Until then, only general guidelines regarding evaluation and management are available. In the future, it is likely that other prothrombotic conditions will be elucidated, adding to the pool of data.

Anticoagulants↗
PubMed1999

The use of soluble fibrin in evaluating the acute and chronic hypercoagulable state.

Soluble fibrin detected in clinical plasma samples includes a variety of complexes consisting of fibrin monomer units, fibrinogen, and various proteolytic derivatives of fibrinogen and fibrin. The advantage of measuring soluble fibrin over fibrinopeptide A to detect thrombin action on fibrinogen is the considerably longer half-life of soluble fibrin in the circulation. Soluble fibrin can be detected by a variety of methods, including paracoagulation and precipitation assays, adsorption of fibrin monomer to insolubilized fibrinogen, functional assays based on the cofactor activity of some soluble fibrin compounds in t-PA-induced plasminogen activation, and by using fibrin-specific antibodies. Fibrin-specific antibodies may react with epitopes generated directly by fibrinopeptide A or B release or with epitopes generated by fibrin polymerization. Epitopes dependent on fibrinopeptide A release are often not accessible in native fibrin complexes and require the disaggregation of fibrin compounds to be reactive, whereas epitopes dependent on fibrinopeptide B release or fibrin polymerization are accessible to the monoclonal antibodies in nondenatured fibrin. Since soluble fibrin assays detect different structural or functional properties of soluble fibrin, no common calibrator for all soluble fibrin assays and, often, little correlation between different assay systems in clinical evaluations exist. Clinical applications of soluble fibrin assays include diagnosis and treatment monitoring of intravascular coagulation processes and prethrombotic states, monitoring anticoagulant treatment, and biocompatibility investigations. Some soluble fibrin assays have been demonstrated to be extremely sensitive indicators of acute fibrin formation. For the exclusion of venous thrombosis, D-dimer assays appear to be more sensitive than current soluble fibrin assays, since D-dimer assays detect freshly formed fibrin and proteolytic fragments of particulate clots. Further clinical studies are needed to establish the clinical utility of specific, soluble fibrin assays. The development of rapid, quantitative soluble fibrin assays for clinical routine use should be encouraged.

Acute Disease↗
PubMed2000

[Antiphospholipid antibodies and thrombosis: the putative mechanisms of hypercoagulable state in patients with anticardiolipin antibody].

Antiphospholipid antibodies are well recognized as associated with serious clinical complications such as arterial and venous thrombosis and recurrent spontaneous abortion. These complications are collectively called antiphospholipid syndrome(APS). The mechanisms responsible for the thrombosis are unclear. We reported three mechanisms. beta 2-glycoprotein I(beta 2GPI) inhibited activated protein C(APC) activity and, furthermore, APC activity decreased by the addition of monoclonal aCL and beta 2GPI. Monoclonal anticardiolipin antibodies(aCL) seemed to enhance the inhibition of APC procoagulant activity caused by beta 2GPI. Monoclonal aCL in the presence of beta 2GPI also increased the activity of plasminogen activator inhibitor(PAI)-1 in the mixture of tissue-plasminogen activator(t-PA) and PAI-1 by inhibiting the function of beta 2GPI, which increased the remaining t-PA activity in the mixture. The formation of thrombin-antithrombin complexes(TAT) in APS was impaired. The level of TAT in APS did not increase, however the level of prothrombin fragment 1 + 2 (F1 + 2) increased. Therefore, free thrombin present in patients' blood may contribute to thrombosis in APS. These reports indicate that thrombosis in APS may be caused by several thrombogenic factors that stimulate aCL.

Antibodies, Anticardiolipin↗
PubMed2001

Vascular-bed-specific hemostasis and hypercoagulable states: clinical utility of activation peptide assays in predicting thrombotic events in different clinical populations.

This chapter summarizes the new paradigm for arterial thrombosis. This new paradigm emphasizes the heterogeneity of endothelial cells and the signaling pathways that control endothelial cell gene expression in surrounding tissue. It is suggested that genetic alterations in the signaling pathways are probably responsible for localized thrombosis, as manifested by heart attacks and strokes. A discussion of two clinical studies supporting the new arterial thrombosis paradigm is also included in this chapter. These studies, carried out by genetic engineering in mice, employ activation peptides to help predict the occurrence of thrombotic events in humans.

Animals↗