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1/6. venous thromboembolism, factor v Leiden, and methylenetetrahydrofolate reductase in a sickle cell anemia patient.

    Vaso-occlusive crisis is the most common cause of morbidity in patients with sickle cell anemia (SCA). central nervous system involvement that leads to hemiplegia is the most frequent neurological complication in those patients. Peripheral deep venous thromboembolism was not reported in SCA patients. activated protein c resistance is associated with an increased risk of thrombophilia. The authors report an SCA patient with recurrent cerebrovascular accident and deep venous thrombosis. activated protein c resistance due to factor v Leiden heterozygous and heterozygocity for the methylenetetrahydrofolate reductase were diagnosed and suspected to be the risk factors that contribute to the development of the deep vein thrombosis in this SCA patient.
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ranking = 1
keywords = thromboembolism
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2/6. Fatal pulmonary artery thrombosis in a patient with Behcet's disease, activated protein c resistance and hyperhomocystinemia.

    Behcet's disease (BD) is known for its tendency for thromboembolism, which is thought to be due to vascular injury. The important role of inherited thrombophilias is now becoming increasingly clear. However, conflicting data exist in terms of the contribution of these factors to the thrombotic risk in BD. In this case report, we describe a patient with BD who presented with severe cor pulmonale due to recurrent chronic venous thromboembolism and pulmonary artery thrombosis. The biochemical evaluation revealed that the patient was homozygotic for the factor v Leiden (R506Q) mutation and had increased levels of homocysteine. His condition deteriorated despite adequate anticoagulation treatment, and he died suddenly after 7 months of follow-up. We assume that the presence of thrombophilic risk factors augments and synergizes with the hypercoagulable state already existing in BD, leading to fatal thrombosis in this patient.
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ranking = 0.4
keywords = thromboembolism
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3/6. Increased incidence of venous thrombosis in patients with shortened activated partial thromboplastin times and low ratios for activated protein c resistance.

    A cohort of 69 hospital patients with shortened activated partial thromboplastin time (APTT) were prospectively identified and were further investigated for resistance to activated protein C (APC). This was quantified by APTT-based and Russel viper venom time (RVVT)-based methods. The prevalence of objectively confirmed venous thromboembolism (VTE) in this cohort was 19% (13/69). Of these 69 patients, 28 also had low APC resistance ratios and the incidence of VTE among these patients (group 1) was 36% (10/28). This was significantly higher (P=0.003) than that in the remaining 41 patients (group 2) with shortened APTT and normal APC resistance (7%, 3/41). dna analysis confirmed 13 of the group 1 patients were FV Leiden positive. The incidence of VTE in the FV Leiden group (group 1a, n=13) was 38% (5/13) and in the group whose abnormal resistance to APC was independent of FV Leiden (group 1b, n=15) was 33% (5/15). These results suggest that a shortened APTT, coexisting with a low APC resistance ratio, regardless of FV Leiden carriership status, is a marker for VTE. Increased resistance to the anticoagulant activity of APC is multifactorial as reflected by evidence of abnormal resistance differing in the two assays.
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ranking = 0.2
keywords = thromboembolism
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4/6. Recurrent thromboembolism in a patient with beta-thalassemia major associated with double heterozygosity for factor v R506Q and prothrombin G20210A mutations.

    Double heterozygosity for factor v R506Q and prothrombin G20210A mutations was identified in a 24-year-old man with beta-thalassemia major. The patient experienced a first thrombotic event at the age of 19 years and three recurrent thromboses in a short time interval, the third occurring while the patient was receiving long-term anticoagulant treatment. This case suggests that patients with major thalassemia and congenital thrombophilic mutations need intensive and long-lasting anticoagulant treatment. Thus, even if thrombotic events could be explained by a hypercoagulable state observed in patients with major thalassemia, after a first thrombotic event has occurred these patients should be screened for acquired and congenital thrombophilia.
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ranking = 0.8
keywords = thromboembolism
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5/6. Resistance to activated protein C and digital thrombosis.

    Resistance to activated protein C is a newly described genetic coagulation disorder previously only reported in patients with venous thromboembolism or central arterial embolism (cerebral or coronary). We report this defect in association with digital artery thrombosis and describe the pathophysiology of this disorder.
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ranking = 0.2
keywords = thromboembolism
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6/6. Fetal stroke and congenital parvovirus B19 infection complicated by activated protein c resistance.

    parvovirus B19 infection in gestation has been associated with severe fetal complications such as anaemia, hydrops and fetal demise. Fetal infection in the first trimester poses the greatest risk for these complications, but infection during the third trimester is more common than previously appreciated and can be associated with severe complications, i.e. fetal death, in the absence of hydrops or classical clinical symptoms. parvovirus B19 infection has been associated with vasculitis and pathological changes in the central nervous system, which may cause stroke. We report a newborn infant with a rare combination of a recent central nervous system infection with parvovirus B19 and a factor v Leiden mutation, who developed fetal stroke. Conclusion: factor v Leiden mutation leads to activated protein c resistance and increases the risk of thromboembolism. Thromboembolism occurs rarely in newborns with activated protein c resistance, but can be precipitated by dehydration, asphyxia and infection. Although parvovirus B19 infection of the central nervous system may be a precipitant in neonatal and/or fetal stroke, it can also cause stroke independent of a thrombophilic mutation. In this case, both causative factors may have coincided.
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ranking = 0.2
keywords = thromboembolism
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