Relevant bibliographies by topics / Thrombophilia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Thrombophilia'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Thrombophilia"

1

Gogia, Navneet, and Geoffrey A. Machin. "Maternal Thrombophilias Are Associated with Specific Placental Lesions." Pediatric and Developmental Pathology 11, no. 6 (November 2008): 424–29. http://dx.doi.org/10.2350/07-09-0345.1.

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Maternal floor infarction (MFI), massive perivillous fibrin deposition (MPVFD), and fetal thrombotic vasculopathy (FTV) are specific placental lesions with associations to recurrent adverse fetal outcomes and with maternal thrombophilia. We studied the frequency of a range of acquired and genetic maternal thrombophilias in MFI (40 cases), MPVFD (87 cases), FTV (7 cases), and FTV+MPVFD (4 cases). Thrombophilias were identified in 16 (40%), 20 (23%), 5 (71%), and 2 (50%) of these lesions, respectively. Seventy-seven percent of the identified thrombophilias were genetic, and 23% were acquired. The most common genetic thrombophilia was protein S deficiency, which constituted 14 of the 36 genetic thrombophilias (39%). We advocate full maternal thrombophilia testing when the diagnosis of MFI, MPVFD, and FTV is made by placental pathology examination. Because of the possible contribution of paternal thrombophilic mutations to the fetal genotype, it would be desirable to test the whole family as well.
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Salehi Omran, Setareh, Adam Hartman, Neil A. Zakai, and Babak B. Navi. "Thrombophilia Testing After Ischemic Stroke." Stroke 52, no. 5 (May 2021): 1874–84. http://dx.doi.org/10.1161/strokeaha.120.032360.

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Thrombophilia testing is frequently performed after an ischemic stroke, particularly when cryptogenic. However, there is minimal evidence supporting a significant association between most conditions assessed through thrombophilia testing and ischemic stroke, and the rationale for thrombophilia testing in many clinical situations remains uncertain. In this topical review, we review and contextualize the existing data on the risks, predictors, and outcomes of thrombophilic conditions in patients with ischemic stroke. We report that inherited thrombophilias have an uncertain relationship with ischemic stroke. Conversely, antiphospholipid syndrome, an acquired immune-mediated thrombophilia, seems to be a strong risk factor for arterial thromboembolic events, including ischemic stroke, and especially among young patients. Our findings suggest that certain circumstances may warrant targeted thrombophilia testing, such as stroke in the young, cryptogenic stroke, and high estrogen states. Future prospective studies should investigate the utility and cost effectiveness of thrombophilia testing in various stroke settings, including among patients with patent foramen ovale; as well as the optimal secondary stroke prevention regimen in patients with confirmed thrombophilia, particularly if no other potential stroke mechanism is identified.
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Lindhoff-Last and Luxembourg. "Evidence-based indications for thrombophilia screening." Vasa 37, no. 1 (February 1, 2008): 19–30. http://dx.doi.org/10.1024/0301-1526.37.1.19.

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Thrombophilic defects have been shown to be associated with an increased risk of venous thrombosis, fetal loss, and gestational complications. The knowledge about the clinical relevance of thrombophilic defects is increasing, and evidence-based indications for thrombophilia screening are therefore discussed in this review. Selective thrombophilia screening based on previous personal and/or family history of venous thromboembolism is more cost-effective than universal screening in all patient groups evaluated. In the majority of patients with acute venous thrombosis, the results of thrombophilia screening do not influence the duration of oral anticoagulation. The only patient population who clearly profits from thrombophilia screening in this situation are patients with a newly diagnosed antiphospholipid syndrome, because prolonged anticoagulation can avoid the high incidence of recurrence in this patient population. Because of the increased risk of venous thrombosis during pregnancy and the puerperium, thrombophilia screening is indicated in selected patients with a previous history of venous thrombosis or a positive family history. Significant associations with early and late pregnancy loss are observed for carriers of the heterozygous factor V Leiden mutation, the heterozygous prothrombin-mutation G20210A and anticardiolipin antibodies, while protein S deficiency is significantly associated with late pregnancy loss. Antithrombotic drugs like UFH, LMWH or low-dose aspirin may have a potential therapeutic benefit in patients with recurrent pregnancy loss and thrombophilia, but placebo-controlled, multicenter trials are urgently needed to clarify this issue. Although a supra-additive effect for the risk of venous thrombosis is observed between oral contraceptives and some thrombophilias, the absolute incidence of venous thromboembolism is low in premenopausal women and mass screening strategies are therefore unlikely to be effective. While antiphospholipid antibodies are known to be associated with arterial thrombosis, screening for heritable thrombophilias is not useful in arterial thrombosis, although subgroup analysis indicates that they may play a role particularly in young patients and children.
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Glueck, C. J., Naila Goldenberg, Howard Bell, Karl Golnik, and Ping Wang. "Amaurosis Fugax: Associations with Heritable Thrombophilia." Clinical and Applied Thrombosis/Hemostasis 11, no. 3 (July 2005): 235–41. http://dx.doi.org/10.1177/107602960501100301.

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The aim of this study was to prospectively assess associations between amaurosis fugax, inherited thrombophilia, and acquired thrombophilia. Thrombophilia and hypofibrinolysis were studied in 11 cases (eight women, three men; all white) with amaurosis fugax, 57 ± 17 years old, selected by the absence of abnormal brain magnetic resonance imaging (MRI), magnetic resonance angiography (MRA), magnetic resonance venography (MRV), ipsilateral internal carotid artery plaque, atrial fibrillation, or cardiac thrombus. Cases were compared to 78 healthy adult white controls (53 ± 18 years old) for serologic measures, and by polymerase chain reaction to 248 healthy white controls (78 adults, 170 children) for gene mutations. All 11 cases had one or more familial thrombophilic coagulation disorder including one heterozygous for the G1691A factor V Leiden mutation, two with low free protein S, four with high factor VIII, three with resistance to activated protein C, three homozygous for the C677T methylenetetrahydrofolate reductase (MTHFR) mutation, two compound C677T-A1298C MTHFR heterozygotes, and three with hypofibrinolytic 4G4G homozygosity for the PAI-1 gene. The case with factor VIII of 160% had two other thrombophilias (compound MTHFR C677T-A1298C heterozygosity, resistance to activated protein C), and hypofibrinolytic high Lp(a). Thrombophilic C677T MTHFR homozygosity or compound C677T-A1298C heterozygosity was present in five of 10 (50%) cases vs. 30 of 248 (12%) controls, Fisher’s p (pf) = .005. Thrombophilic factor VIII was high in four of 10 (40%) cases vs. 0 of 38 controls, pf = .001. Thrombophilic hyperestrogenemia in five of the eight women (four exogenous estrogen, one pregnant) may have interacted with inherited thrombophilia-hypofibrinolysis, promoting thrombus formation. In cases selected by the absence of abnormal brain magnetic resonance imaging, significant ipsilateral internal carotid artery plaque, atrial fibrillation, or cardiac thrombus, we speculate that amaurosis fugax can be caused by reversible (by anticoagulation) retinal artery thrombi associated with heritable thrombophilia and/or hypofibrinolysis, often augmented by estrogen-driven acquired thrombophilia.
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Fontaine, Robert, Ping Wang, and Charles Glueck. "Interaction of Heritable and Estrogen-induced Thrombophilia: Possible Etiologies for Ischemic Optic Neuropathy and Ischemic Stroke." Thrombosis and Haemostasis 85, no. 02 (2001): 256–59. http://dx.doi.org/10.1055/s-0037-1615698.

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SummaryOur specific aim was to assess how thrombophilic exogenous estrogens interacted with heritable thrombophilias leading to nonarteritic ischemic optic neuropathy (NAION) and ischemic stroke. Coagulation measures were performed in a 74 year old patient and her immediate family. The proband had a 47 year history of 9 previous thrombotic episodes, and developed unilateral NAION 4 years after starting estrogen replacement therapy (ERT). The proband was heterozygous for two thrombophilic gene mutations (G20210A prothrombin gene, platelet glycoprotein IIIa PlA1/A2 polymorphism), and homozygous for the C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene. Of 238 normal controls, none had these 3 gene mutations together. The proband’s mother and brother had deep venous thrombosis (DVT). The proband’s brother, sister, nephew, daughter, and two granddaughters were homozygous for the C677T MTHFR mutation. The proband’s brother was heterozygous for the G20210A prothrombin gene mutation. The proband’s niece was heterozygous for the G20210A prothrombin gene mutation, homozygous for the C677T MTHFR mutation, homozygous for the hypofibrinolytic 4G polymorphism of the plasminogen activator inhibitor-1 (PAI-1) gene, and heterozygous for the platelet glycoprotein IIIa PlA1/A2 polymorphism. Of 238 normal controls, none had the niece’s combination of 4 gene mutations. When ERT-mediated thrombophilia was superimposed on the proband’s heritable thrombophilias, unilateral ischemic optic neuropathy developed, her tenth thrombotic event over a 5 decade period. When estrogenprogestin oral contraceptives were given to the proband’s niece, she had an ischemic stroke at age 22. Exogenous estrogen-mediated thrombophilia superimposed on heritable thrombophilia and hypofibrinolysis is associated with arterial and venous thrombi, and appears to be a preventable, and potentially reversible etiology for ischemic optic neuropathy and ischemic stroke.
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Moran, Jason, and Kenneth A. Bauer. "Managing thromboembolic risk in patients with hereditary and acquired thrombophilias." Blood 135, no. 5 (January 30, 2020): 344–50. http://dx.doi.org/10.1182/blood.2019000917.

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Abstract While we are now able to diagnose inherited thrombophilias in a substantial number of patients with venous thromboembolism (VTE), the initial hope that their presence would inform recurrence risk and thus decisions on anticoagulation duration has largely been disappointing. Indeed, the presence or absence of transient provoking risk factors has proven to be the most important determinant of VTE recurrence risk. Thus, particular attention to transient acquired risk factors for VTE remains paramount, as they have generally been shown to carry more prognostic weight than inherited thrombophilias. The presence of other acquired risk factors may require additional management considerations, whether pertaining to anticoagulant choice, as in antiphospholipid antibody syndrome, or to addressing a new predisposing medical condition, as in malignancy. Antithrombin deficiency or the presence of ≥1 thrombophilic defect may be exceptions that can have a role in prognostication; however, as illustrated in this review through several case vignettes, interpretation and clinical application of the results of inherited thrombophilia testing is nuanced. We have chosen to focus on cases in which patients have been identified as having thrombophilic defects rather than the indications for undertaking testing in the first place or the extent of investigation. Management decisions in such cases ultimately hinge on individualized consideration of the benefits and risks of anticoagulation along with patient preference rather than on an algorithmic pathway based on thrombophilia status.
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LaHue, Sara C., Helen Kim, Ludmila Pawlikowska, Jeffrey Nelson, Daniel L. Cooke, Steven W. Hetts, and Vineeta Singh. "Frequency and characteristics associated with inherited thrombophilia in patients with intracranial dural arteriovenous fistula." Journal of Neurosurgery 130, no. 4 (April 2019): 1346–50. http://dx.doi.org/10.3171/2017.10.jns171987.

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OBJECTIVEThe pathogenesis of dural arteriovenous fistulas (DAVFs) remains poorly defined. Prior studies on thrombophilia as a risk factor for DAVF development are limited by small sample sizes and poor generalizability.METHODSIn this longitudinal observational study, all patients with intracranial DAVFs evaluated at the University of California, San Francisco from December 1994 through April 2014 were identified. After obtaining patient consent, 3 thrombophilic mutations, factor V Leiden (rs6025), MTHFR (rs1801133), and prothrombin G20210A, were genotyped. The authors evaluated the association of thrombophilia status (presence of any thrombophilic mutation) and clinical and angiographic characteristics using either a 2-sample t-test or Fisher’s exact test.RESULTSA total of 116 patients with diagnosed intracranial DAVFs were included in the study. Twenty-five (22%) patients met criteria for thrombophilia. Focal neurological deficits tended to occur more frequently in the thrombophilia group (78% vs 57%, p = 0.09). Angiographic characteristics of DAVFs, including high-risk venous flow pattern, multiplicity of DAVF, and the presence of venous sinus thrombosis, did not differ significantly between the 2 groups but tended to be more common in the thrombophilic than in the nonthrombophilic group.CONCLUSIONSThis study is one of the largest of thrombophilia and DAVF to date. The frequency of mutations associated with thrombophilia in this study was higher than that in the general population.
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Waldman, Dalia, Aharon Lubetsky, Nurit Kornbrut, Abdalla Khalil, Ariel Koren, Baruch Wolach, Aviva Fattal, et al. "Paediatric cerebral sinus vein thrombosis." Thrombosis and Haemostasis 92, no. 10 (2004): 713–18. http://dx.doi.org/10.1160/th04-03-0182.

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SummaryThe etiology and pathophysiology of cerebral sinus venous thrombosis (CSVT) in the paediatric population is still poorly understood, and the role of thrombophilic risk factors remains to be elucidated. In our multi-center case-controlled study we studied 46 patients with CSVT diagnosed from April 1996 to December 2003, consecutively referred for thrombophilia work-up. The results of thrombophilia screen were compared to 112 healthy paediatric controls. Anticoagulant therapy was applied according to treating physicians’ decisions, and all cases were prospectively followed for a median of 4.1 years. Of 46 children, 8 had CSVT diagnosed in the neonatal period and therefore were analyzed separately. The prevalence of single thrombophilia markers and combinations of thrombophilic risk factors were similar among cases and controls. Among children with CSVT co-morbid systemic illness was present in most patients at diagnosis. Seven out of 8 children with idiopathic CSVT had thrombophilic risk factors as compared to 31/38 patients with co-morbid conditions. Anticoagulation was initiated in most patients, 11/46 patients continued therapy for a total of one year or more post event. Neither clinical presentation nor initial treatment decisions were affected by presence of thrombophilic risk factors in our study group. Thrombophilia prevalence was not increased in children with CSVT as compared to controls, however thrombophilia was more frequent among children with idiopathic CSVT. Thus, those selected patients would benefit most from thrombophilia work-up, required for long-term therapy considerations.
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Stefanski, Ana-Luisa, Christoph Specker, Rebecca Fischer-Betz, Wolfgang Henrich, Ekkehard Schleussner, and Thomas Dörner. "Maternal Thrombophilia and Recurrent Miscarriage – Is There Evidence That Heparin is Indicated as Prophylaxis against Recurrence?" Geburtshilfe und Frauenheilkunde 78, no. 03 (March 2018): 274–82. http://dx.doi.org/10.1055/s-0044-100919.

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Abstract Background Recurrent miscarriage, also referred to as recurrent spontaneous abortion (RSA), affects 1 – 5% of couples and has a multifactorial genesis. Acquired and congenital thrombophilia have been discussed as hemostatic risk factors in the pathogenesis of RSA. Method This review article was based on a selective search of the literature in PubMed. There was a special focus on the current body of evidence studying the association between RSA and antiphospholipid syndrome and hereditary thrombophilia disorders. Results Antiphospholipid syndrome (APS) is an acquired autoimmune thrombophilia and recurrent miscarriage is one of its clinical classification criteria. The presence of lupus anticoagulant has been shown to be the most important serologic risk factor for developing complications of pregnancy. A combination of low-dose acetylsalicylic acid and heparin has shown significant benefits with regard to pregnancy outcomes and APS-related miscarriage. Some congenital thrombophilic disorders also have an increased associated risk of developing RSA, although the risk is lower than for APS. The current analysis does not sufficiently support the analogous administration of heparin as prophylaxis against miscarriage in women with congenital thrombophilia in the same way as it is used in antiphospholipid syndrome. The data on rare, combined or homozygous thrombophilias and their impact on RSA are still insufficient. Conclusion In contrast to antiphospholipid syndrome, the current data from studies on recurrent spontaneous abortion do not support the prophylactic administration of heparin to treat women with maternal hereditary thrombophilia in subsequent pregnancies. Nevertheless, the maternal risk of thromboembolic events must determine the indication for thrombosis prophylaxis in pregnancy.
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Paidas, Michael, Edmund Funai, Edward Kuczynski, Charles Lockwood, and Henry Roqué. "Maternal thrombophilias are not associated with early pregnancy loss." Thrombosis and Haemostasis 91, no. 02 (2004): 290–95. http://dx.doi.org/10.1160/th03-09-0596.

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SummaryWe investigated the association between inherited and acquired maternal thrombophilias and adverse pregnancy events. A cohort of 491 patients with a history of adverse pregnancy outcomes was evaluated for activated protein C resistance, factor V Leiden and prothrombin G20210A mutations, hyperhomocysteinemia, deficiencies of antithrombin, protein C and S and both anticardiolipin antibodies and lupus anticoagulants. The study had an 80% power to detect a 15% difference in the prevalence of thrombophilia for 1st trimester loss. In our high-risk cohort the presence of 1 maternal thrombophilia or more than one thrombophilia were found to be protective of recurrent losses at < 10 weeks (1 thrombophilia: OR: 0.55, 95% CI: 0.33–0.92; >1 thrombophilia: OR: 0.48, 95%CI:0.29–0.78). In contrast, the presence of maternal thrombophilia(s) was modestly associated with an increased risk of losses ≥ 10 weeks (1 thrombophilia: OR:1.76, 95%CI: 1.05–2.94, >1 thrombophilia: OR:1.66, 95%CI:1.03–2.68). Women who experienced only euploid losses were not more likely to have an identified thrombophilia than women who experienced only aneuploid losses (OR 1.03; 0.38–2.75). The presence of maternal thrombophilia was associated with an increased risk of fetal loss after 14 weeks, fetal growth restriction, abruption and preeclampsia. There was a significant “dose-dependent” increase in the risk of abruption (OR:3.60, 95%CI: 1.43–9.09) and preeclampsia (OR:3.21, 95%CI:1.20–8.58). In conclusion, these data indicate maternal thrombophilias are not associated with pregnancy wastage prior to 10 weeks of gestation.
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Dissertations / Theses on the topic "Thrombophilia"

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Simmonds, Rachel Elizabeth. "Protein S deficiency and familial thrombophilia." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267993.

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Beauchamp, Nicholas James. "Molecular genetic basis of inherited thrombophilia." Thesis, University of Sheffield, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287349.

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Sanson, Bernd-Jan. "Risks of thrombophilia and diagnostics of pulmonary embolism." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/83894.

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Lijfering, Willem Marten. "Thrombophilia issue or non-issue in clinical practice? /." [S.l. : [Groningen : s.n.] ; University of Groningen] [Host], 2008. http://irs.ub.rug.nl/ppn/.

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Ibrahim, Ayman Hussein. "The thrombomodulin gene and its contribution to adverse pregnancy outcome." Thesis, University of Liverpool, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288113.

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Jennings, I. "An investigation of diagnostic errors in laboratory screening for thrombophilia." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419385.

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Folkeringa, Nienke. "Pregnancy-related thrombosis and fetal loss in women with thrombophilia." [S.l. : [Groningen : s.n.] ; University of Groningen] [Host], 2009. http://irs.ub.rug.nl/ppn/.

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Pecheniuk, Natalie Maria. "DNA analysis of common genetic variations which predispose to thrombophilia." Thesis, Queensland University of Technology, 2000.

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Wakeman, Lisa Jayne. "Whole blood platelet function testing as an adjunct to thrombophilia screening." Thesis, University of the West of England, Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.601348.

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Platelet hyperaggregability, including Sticky Platelet Syndrome has been identified as a cause of thrombotic conditions including venous thrombosis and foetal loss. The laboratory diagnosis of classical Sticky Platelet Syndrome is based on enhanced platelet aggregation responses to submaximallevels of adenosine diphosphate and epinephrine by optical aggregometry techniques. This study sought to evaluate platelet hyperaggregability by Multiple Electrode Aggregometry, PFA-100 analysis and quantitative analysis of associated platelet parameters as an adjunct to thrombophilia screening. Forty nine patients and 50 control subjects (nonna! volunteers) were investigated in this study. Multiple Electrode Aggregometry was performed on all participants at standard and submaxima! concentrations of adenosine diphosphate, collagen, thrombin receptor agonist protein-6, arachidonic acid and epinephrine together with PFA-100 closure times, immature platelet fraction, mean platelet volume, plateletcrit, platelet distribution width and platelet-large cell ratio measurement. Statistically significant differences in PFA-100 (collagen/adenosine diphosphate cartridges) were observed between the test and control cohort. Observations of study results and clinical presentation in the test cohort identified results outside of reference ranges in symptomatic and asymptomatic test individuals in whom no abnormalities were recorded by conventional thrombophilia testing. Binary logistic regression models identified that mean platelet volume levels were found to contribute significantly to the prediction of whether an individual presented as a member of the test or control cohort. Mean platelet volume was also shown to contribute significantly to predicting whether a participant feU into test and control subgroups. Study results suggest that evaluation of platelet reactivity by whole blood platelet analysis may play a role as an adjunct to conventional laboratory investigation of patients who present for thrombophilia screening.
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Gomer, Kerry Gretchen. "Women, birth control pills, and thrombophilia an analysis of current risk communication /." Connect to this title online, 2009. http://etd.lib.clemson.edu/documents/1247509090/.

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Books on the topic "Thrombophilia"

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K, MacCallum P., and Meade T. W, eds. Thrombophilia. London: Baillière Tindall, 1999.

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W, Meade T., ed. Thrombophilia. London: Baillière Tindall, 1994.

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Benjamin, Brenner, ed. Thrombophilia in pregnancy. London: Baillière Tindall, 2003.

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Benjamin, Brenner, ed. Thrombophilia in pregnancy. London: Baillière Tindall, 2003.

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Lockwood, Charles J. Thrombosis, thrombophilia and thromboembolism. Washington, DC: American College of Obstetricians and Gynecologists, 2007.

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Z, Goldhaber Samuel, and Ridker Paul M. 1959-, eds. Thrombosis and thromboembolism. New York: M. Dekker, 2002.

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J, Seghatchian M., Samama Meyer M, and Hecker S. P, eds. Hypercoagulable states: Fundamental aspects, acquired disorders, and congenital thrombophilia. Boca Raton: CRC Press, 1996.

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R, Higgins J., and Brennecke S. P, eds. Inherited thrombophilias. London: Baillière Tindall, 2003.

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Benjamin, Brenner, Marder Victor J, and Conard Jacqueline, eds. Women's issues in thrombosis and hemostasis. London: Martin Dunitz, 2002.

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E, Preston F., Kitchen Steve Dr, and Olson John David 1944-, eds. Quality in laboratory hemostasis and thrombosis. Chichester, West Sussex: Wiley-Blackwell, 2009.

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Book chapters on the topic "Thrombophilia"

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DeLoughery, Thomas G. "Thrombophilia." In Hemostasis and Thrombosis, 87–90. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-09312-3_17.

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Heit, John A. "Thrombophilia." In Vascular Medicine and Endovascular Interventions, 59–74. Oxford, UK: Society for Vascular Medicine and Biology, 2008. http://dx.doi.org/10.1002/9780470692356.ch5.

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Neumann, Kay, and Georg Griesinger. "Thrombophilia." In Recurrent Implantation Failure, 72–78. Boca Raton : CRC Press, [2019]: CRC Press, 2019. http://dx.doi.org/10.1201/9781315165707-8.

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Mantha, Simon, and Gerald A. Soff. "Unidentifiable Thrombophilia." In Nonmalignant Hematology, 495–502. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30352-9_43.

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Franchini, Massimo. "Thrombophilia Testing." In Handbook of Venous Thromboembolism, 49–54. Chichester, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119095606.ch6.

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Carman, Teresa L. "Thrombophilia Testing." In Anticoagulation Therapy, 345–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-73709-6_16.

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Baglin, Trevor, and David Keeling. "Heritable Thrombophilia." In Postgraduate Haematology, 795–808. Oxford, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118853771.ch44.

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Baglin, Trevor. "Heritable Thrombophilia." In Postgraduate Haematology, 872–87. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444323160.ch45.

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de Jesús, Guilherme Ramires, Flavia Cunha dos Santos, Marcela Ignacchiti Lacerda, Roger Abramino Levy, and Nilson Ramires de Jesús. "Hereditary Thrombophilia." In Perinatology, 437–48. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-83434-0_24.

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Gurza, Guillermo. "Inherited Thrombophilia." In Maternal-Fetal Evidence Based Guidelines, 315–23. 4th ed. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003099062-29.

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Conference papers on the topic "Thrombophilia"

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Thabet, Afef Ben, Rim Zaaghdoud, Manel Charfi, Chiraz Regaieg, Amel Ben Hmed, Nedia Hmida, Amira Bouraoui, and Abdellatif Gargouri. "P443 Hereditary Thrombophilia in newborn." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.779.

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Vilhena, João, M. Rosário Martins, Henrique Vicente, Luís Nelas, José Machado, and José Neves. "Thrombophilia Screening - An Artificial Neural Network Approach." In International Conference on Health Informatics. SCITEPRESS - Science and and Technology Publications, 2015. http://dx.doi.org/10.5220/0005197500510059.

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Briët, E., L. Engesser, E. J. P. Brommer, A. W. Broekmans, and R. M. Bertina. "THROMBOPHILIA:ITS CAUSES AND A ROUGH ESTIMATE OF ITS PREVALENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642945.

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Idiopathic venous thrombosis and embolism have gained widespread interest since the discovery that, deficiencies of antithrombin III, protein C, and protein S are associated with familial venous thrombophilia. The purpose of our study was to obtain an estimate of the prevalence of this syndrome and to establish the etiology in as many cases as possible.We collaborated with specialists from 37 Dutch hospitals, covering about 10% of the Dutch population. A history as well as blood samples were obtained from 113 unrelated cases with familial thrombophilia and from 90 isolated cases. Assuming that each proband in a family with thrombophilia has an average of four affected relatives, a rough estimate of the prevalence of familial thrombophilia in The Netherlands is 40 cases per 100.000. The prevalence of non-familial thrombophilia is probably lower.In 35 out of the 113 familial cases we established a diagnosis of hereditary antithrombin III deficiency (n=5), protein C deficiency (type I: n=9; type II: n=4), protein S deficiency (n=15) and dysfibrinogenemia (n=2). In 36 cases we found no abnormality at all and in the remaining 42 cases abnormalities were found in one or more of the following: heparin cofactor II, factor V, factor VII, factor VIII, von Willebrand factor, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, alpha 2 antiplasmin and histidine rich glycoprotein. In most of these cases, however, the hereditary nature of the abnormalities could not be demonstrated and the causal relationships remain to be established.In the 90 isolated cases, we diagnosed hereditary deficiencies of anti thrombin III, protein C and protein S each in one case and a lupus anticoagulant in two cases. In 54 cases no abnormality was found and in the remaining 31 cases various abnormalities were found in one or more of the proteins mentioned above.We conclude that the syndrome of thrombophilia is not rare but its true prevalence needs to be established by more rigorous means. An etiological diagnosis can be made with confidence in only one third of the familial cases and in less than 10 percent of the isolated cases.
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Abduganieva, E. "Thrombophilia as a factor in increasing inflammation in COPD." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.1910.

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Hassan, H. J., L. Cianetti, P. M. Mannucci, V. Vicente, R. Cortese, and C. Peschle. "HEREDITARY THROMBOPHILIA CAUSED BY MISSENSE MUTATION IN PROTEIN C GENE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642944.

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The structure of the gene for protein C was analyzed in 13 protein C deficient unrelated patients (11 heterozygous, 2 homozygous), who showed an equivalent reduction of this serine protease at both enzymatic and antigen level. No deletion(s) or rearrangement(s) was demonstrated by Southern blot after hybridization to a cDNA probe. One patient showed a variant restriction pattern after Bam HI digestion, characterized by an abnormal 9.6 kb band in addition to the 8.3 and 1.3 normal ones. Extensive family studies, including 7 heterozygotes with the same clinical phenotype, showed the same abnormal pattern in all and only these heterozygotes. Protein C gene from the propositus was cloned in EMBL3 lambda vector. A 411 bp PstI - SacI fragment from exon 9 encompassing the mutation in the Bam HI site was subcloned in M13mpl8. Its sequence showed a single transversion in the Bam HI palyndrome (GGATCC -> GCATCC) : this causes a substitution of the 402 thryptophan residue with a cystein. The 402 thryptophan residue is constantly conserved in a biochemical domain present in all eukaryotic serine proteases: substitution of the large thryptophan aromatic ring with the small cysteine hydrophilic side-chain conceivably leads to destabilization of the tertiary structure of protein C in these heterozygotes. Thus, the point mutation reported here is sufficient to explain the protein C deficiency in these subjects, and is apparently responsible for their clinical phenotype.
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Miyahira, Clara Kimie, Beatriz Medeiros Correa, Raphael Palomo Barreira, Thomas Zurga Markus Torres, Natália Figueiredo Miranda, Natasha Soares Cutolo, Thiago da Cruz Marques, Vanessa Moraes Rossette, and Eduardo de Almeida Guimarães Nogueira. "Artery of Percheron territory infarct in a young patient with thrombophilia." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.026.

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Context: Stroke, when affecting territories dependent on posterior circulation, affects the thalamus and mesencephalic structures, regions irrigated by the paramedian arteries and perforating arteries of the posterior communicating artery and posterior cerebral artery. However, there is an anatomical variant of the paramedian arteries, the Percheron artery, when occluded causes bilateral thalamic infarction. Case report: a 53-year-old woman who presented blurred vision, holocranial headache, hypertensive peak, decreased level of consciousness, anisocoria, conjugate eye deviation. Tomography was normal and after 48 hours there was periventricular hypodensity of white matter, corona radiate and bilateral thalamic. Cerebral angiography confirmed moderate stenosis in the cavernous segments of the internal carotid arteries. In the investigation, a heterozygous mutation for factor V of Leiden was found. The patient evolved well, after blood pressure control and secondary prophylaxis. Clinical picture brings the classic triad of Percheron Artery infarction: decreased level of consciousness, vertical changes in the look and cognitive changes in memory and learning. Other symptoms could be found hypersomnia, oculomotor paralysis and ataxia. The diagnosis is clinical and radiological by visualizing bilateral thalamic involvement. Predisposing factors should be investigated, such as the Leiden factor V mutation, which increases thromboembolic events. Conclusion: It is important to research risk factors and execute an early diagnosis for acute intervention and prophylaxis of stroke.
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Abduganieva, Elnorahon, Irina Liverko, Kadirjon T. Boboev, and Shahboshon Ahmedov. "Inherited thrombophilia in the development of thrombotic conditions in patients with COPD." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2387.

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Mannuccl, P. M., and A. Tripodl. "DIAGNOSTIC SCREENING OF CONGENITAL THROMBOTIC SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643717.

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The prevalence of inherited thrombotic syndromes in the general population (1 in 2,500/5,000) appears to be higher than that of inherited bleeding disorders. We have reviewed the problems of their diagnosis and propose a simple screening procedure. The most important candidates far. screening are patients with unexplained venous thromboembolism at ages ofless than 40 years, particularly when thrombotic episodes are recurrent.Screening must start from collectionof the clinical and family history of the propositus and from the exclusion of common acquired forms of thrombophilia. A negative family historydoes not exclude inherited thrombophilia, because the defects have oftena low penetrance and fresh mutationsmay have occurred in the propositi. The test chosen for laboratoryscreening of inherited thrombotic syndromes must be limited in number, easy todo and, more importantly, their results should be clinically relevent Which defects should be screened and what type of methodology should be used? The table is intended to answerthese questions by proposing a two-step screening procedure.The tests included in the .first step of the screening are aimed at evaluating Laboratory screening of inherited thrombotic syndromes the most frequent and well established causes of inherited thrombophilia, —-antithrombin III, protein C. protein S.plasminogen and fibrinogen.FIRST STEP Antithrombin III (heparin cofactorI chromogenic assay)Protein C (Francis' clotting assay)Protein S(electroimmunoassay of total proteinSantigen)Plasminogen (chromogenic assay)Fibrinogen (clotting assay)SECONSTEP(Tran's functional assay) Plasminogen activator (fibrin plate assay before and after venous stasisor DDAVP)Plasminogen activator inhibitor(chromogenic assay)The tests offirst choice that we propose (see table) are in general functional assaysdetecting both type I and type IIdeficiencies and are simple enough tobecarried out even in non specialized laboratories.For protein S, however,this goal has not been achieved yet and only type I protein S deficiencycan be currently identified with immunoassays measuring total protein S antigen. Since a number of laboratories may still not have the facilities to perform protein C functional assays, they are advised to set up at least an immunoassay, since type I deficiencies are much more frequent than type II deficiencies. The tests included in the second step of the screening are aimed at detectingthe less common or less well established causes of thrombophilia, and should be carried out when the clinical history suggests the existence of inherited thrombophilia and yet the first step has failed to reveal any laboratory abnormality. Defective plasminogen activation can be evaluated by measuring plasminogen activator activity with the simple fibrin plate assay carried out before and after stimuli such as venous occlusion and/or DDAVP infusion. The parallel measurement of plasminogen activator inhibitor allows to distinguish cases of detective plasminogen activation due to high inhibitor levels. The measurement of heparin cofactor II should also be included in this battery of second-step screening tests.Using this screening procedure in95 propositi with juvenile venous thromboembolism, we have identified 7 kindreds with antithrombin III deficiency (5 type I and 2 type II) (7.5%),7 kindreds with protein C deficiency (1 type II) (7.5%), 5 kindredswith protein S deficiency (5%), 1 withhypoplasminogenemia (1%) and 1 with dysfibrinogenemia Milano II (1). Theremaining undiagnosed cases might bedue to as yet unidentified deficiencies or abnormalities of other antithrombotic mechanisms such as,for instance, endothelial thrombomodulin or the fibrinolysis enhancing property of the protein C-protein S system.
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deVeber, G., F. Kirkham, L. R. Brandao, R. Sträter, G. Kenet, M. Kausch, M. Stoll, et al. "Recurrent Pediatric Stroke: The Role of Thrombophilia in a Large International Pediatric Stroke Population." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680137.

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deVeber, G., F. Kirkham, L. R. Brandao, R. Sträter, G. Kenet, M. Kausch, M. Stoll, et al. "Recurrent Pediatric Stroke: The Role of Thrombophilia in a Large International Pediatric Stroke Population." In 63rd Annual Meeting of the Society of Thrombosis and Haemostasis Research. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1680209.

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