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Evaluation Of the Etiological Factors of Atypically Located Thrombosis and Typical Thrombosis İn Adults Under 40 Years of Age

Year 2021, Volume: 10 Issue: 2, 231 - 240, 31.08.2021
https://doi.org/10.47493/abantmedj.860822

Abstract

References

  • Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet. 1999 Apr 3;353(9159):1167-73.
  • Lichtman M.A. BE, Kipps T.J., Seligsohn U., Kaushansky K., Prchal J.T. . 7th ed, ed: McGraw-Hill Co. ; 2005.
  • Malone PC, Agutter PS. The aetiology of deep venous thrombosis. QJM. 2006 Sep;99(9):581-93.
  • Van der Hagen PB, Folsom AR, Jenny NS, Heckbert SR, O'Meara ES, Reich LM, et al. Subclinical atherosclerosis and the risk of future venous thrombosis in the Cardiovascular Health Study. J Thromb Haemost. 2006 Sep;4(9):1903-8.
  • Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ, 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study. Arch Intern Med. 1998 Mar 23;158(6):585- 93.
  • Biggs R. Human Blood Coagulation 2nd Ed. ed: Blackwell Scientific Publications 1976. Besa E.C. CPM, Kant J.A., Jefferies L.C. . Harwal Publishing Co. ; 1992.
  • Cushman M, Glynn RJ, Goldhaber SZ, Moll S, Bauer KA, Deitcher S, et al. Hormonal factors and risk of recurrent venous thrombosis: the prevention of recurrent venous thromboembolism trial. J Thromb Haemost. 2006 Oct;4(10):2199-203.
  • De Stefano V, Finazzi G, Mannucci PM. Inherited thrombophilia: pathogenesis, clinical syndromes, and management. Blood. 1996 May 1;87(9):3531-44.
  • Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, et al. Inherited thrombophilia: Part 1. Thromb Haemost. 1996 Nov;76(5):651-62.
  • Dahlback B, Carlsson M, Svensson PJ. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc Natl Acad Sci U S A. 1993 Feb 1;90(3):1004-8.
  • Poort SR, Rosendaal FR, Reitsma PH, Bertina RM. A common genetic variation in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood. 1996 Nov 15;88(10):3698-703.
  • Makris M, Rosendaal FR, Preston FE. Familial thrombophilia: genetic risk factors and management. J Intern Med Suppl. 1997;740:9-15.
  • Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, et al. Inherited thrombophilia: Part 2. Thromb Haemost. 1996 Dec;76(6):824-34.
  • Wu O, Robertson L, Twaddle S, Lowe G, Clark P, Walker I, et al. Screening for thrombophilia in high-risk situations: a meta-analysis and cost-effectiveness analysis. Br J Haematol. 2005 Oct;131(1):80-90.
  • Svensson PJ, Dahlback B. Resistance to activated protein C as a basis for venous thrombosis. N Engl J Med. 1994 Feb 24;330(8):517-22.
  • Braun A, Muller B, Rosche AA. Population study of the G1691A mutation (R506Q, FV Leiden) in the human factor V gene that is associated with resistance to activated protein C. Hum Genet. 1996 Feb;97(2):263-4.
  • Gerhardt A, Scharf RE, Beckmann MW, Struve S, Bender HG, Pillny M, et al. Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium. N Engl J Med. 2000 Feb 10;342(6):374- 80.
  • Decousus, H., Quere, I., Presles, E., Becker, F.,Barrellier, M.T., Chanut, M., Gillet, J.L., Guenneguez,H., Leandri, C., Mismetti, P., Pichot,O. & Leizorovicz, A. (2010a) Superficial venou thrombosis and venous thromboembolism: alarge, prospective epidemiologic study. Annals ofInternal Medicine, 152, 218–224.
  • Martinelli I: Risk factors for venous thromboembolism.Thromb Haemost 2001;86:395-403
  • Akar N, Akar E, Akçay R, Avcu F, Yalcin A, Cin S. Effect of methylenetetrahydrofolate reductase 677 C-T, 1298 A-C, and 1317 T-C on factor V 1691 mutation in Turkish deep vein thrombosis patients. Thromb Res 2000; 97: 163-7
  • Dodinger M, Horl WH, Sunder-Plassman G. Molecular biology of 5,10- methylenetetrahydrofolate reductase. J Nephrol, 2000;13(1):20-33.
  • Alkanlı. N Iskemik inmeli hastalrda calca, MTHFR gen polimorfizmleri ile plazma total homosistein düzeylerinin araştırılması 2014.
  • Kaya H, Karkucak M, Salifoǧlu H, Torun D, Kozan S, Tunca Y. Venöz tromboembolili hastalarda anjiotensin dönüş- türücü enzim I/D ve plazminojen aktivatör-1 4G/5G gen polimorfizmlerinin araştırılması. Tuberk Toraks 2013; 61: 88-95.
  • Rallidis LS, Megalou AA, Papageorgakis NH, Trikas AG, Chatzidimitriou GI, Tsitouris GK. Plasminogen activator inhibitor 1 is elevated in the children of men with premature myocardial infarction. Thromb Haemost 1996; 76: 417- 21.
  • Huber K. Plasminogen activator inhibitor type-1: basic mechanisms, regulation, and role for thromboembolic disease. J Thromb Thrombolysis 2001; 11: 183-93.
  • Seguí R, Estellés A, Mira Y, España F, Villa P, Falcó C, et al. PAI-1 promoter 4G/5G genotype as an additional risk factor for venous thrombosis in subjects with genetic thrombophilic defects. Br J Haematol 2000; 111: 122-8.
  • Tsantes AE, Nikolopoulos GK, Bagos PG, Rapti E, Mantzios G, Kapsimali V, et al. Association between the plasminogen activator inhibitor-1 4G/5G polymorphism and venous thrombosis. A meta-analysis. Thromb Haemost 2007; 97: 907-13.
  • Martinelli I, Sacchi E, Landi G, Taioli E, DucaF, Mannucci PM: High risk of cerebral-veinthrombosis in carriers of a prothrombin genemutation and in users of oral contraceptives. NEngl J Med 1998;338:1793-7
  • De Stefano, V., Za, T., Rossi, E., Vannucchi, A.M.,Ruggeri, M., Elli, E., Mico, C., Tieghi, A., Cacciola,R.R., Santoro, C., Gerli, G., Vianelli, N.,Guglielmelli, P., Pieri, L., Scognamiglio, F.,Rodeghiero, F., Pogliani, E.M., Finazzi, G., Gugliotta,L., Marchioli, R., Leone, G. & Barbui, T.(2008) Recurrent thrombosis in patients with polycythemia vera and essential thrombocythemia:incidence, risk factors, and effect of treatments.Haematologica, 93, 372–380.
  • De Stefano, V., Teofili, L., Leone, G. & Michiels, J.J. (1997) Spontaneous erythroid colony formationas the clue to an underlying myeloproliferative disorder in patients with Budd-Chiarisyndrome or portal vein thrombosis. Seminars in Thrombosis and Hemostasis, 23, 411–418.
  • de Bruijn, S.F., Stam, J., Koopman, M.M. & Vandenbroucke,J.P. (1998a) Case-control study ofrisk of cerebral sinus thrombosis in oral contraceptiveusers and in[correction of who are] carriersof hereditary prothrombotic conditions.The Cerebral Venous Sinus Thrombosis

Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler.

Year 2021, Volume: 10 Issue: 2, 231 - 240, 31.08.2021
https://doi.org/10.47493/abantmedj.860822

Abstract

GİRİŞ VE AMAÇ: Yerleşim yerine göre semptomlar oluşturan, antikoagülan ve prokoagülan dengenin kalıtsal veya edinsel nedenlerle bozulması ile ortaya çıkan trombozlar, önemli morbidite ve mortalite nedenidir. Bu çalışmada atipik yerleşimli ve genç (40 yaş ve altı) tromboz tanılı hastalarda etyolojik risk faktörlerini belirlemeyi amaçladık.
MATERYAL–METOD: Retrospektif yapılan çalışmamızda; 40 yaşın altındaki hastalarda görülen tipik yerleşimli trombozlar ve herhangi bir yaşta atipik lokalizasyonlu trombozu bulunan hastalar seçildi. Atipik trombozlu hastalarda öne çıkan etiyolojik risk faktörleri kalıtsal ve edinsel nedenler açısından tarandı. Trombozların lokalizasyonlarına göre öne çıkan risk faktörleri araştırıldı.
BULGULAR: Çalışmamıza 32’si kadın (yaş ort:34.78±14.34) 18'i erkek (yaş ort:36±12.41) olmak üzere 50 hasta (yaş ort:35.22±13.56) dahil edildi. Hastaların 12’si (%24) 40 yaş üstü, 38’i (%76) 40 yaş altı idi. Hastaların 7’sinde (%14) oral kontraseptif (OKS) kullanımına bağlı, 6’sında (%12) cerrahi sonrası, 1’inde (%2) gebelik esnasında, 1’inde (%2) immobilzasyon nedeniyle, 2’sinde (%4) hipertansiyona sekonder tromboz saptandı. MTHFR C677T, 8 (%16) hastada homozigot, 4 (%8) hastada heterozigot saptandı. MTHFR A1298C, 8 (%16) hastada homozigot, 12 (%24) hastada heterozigot ve MTHFR A1298C/C677T heterozigot birlikteliği 6 (%12) hastada saptandı. Hastalardan 7’sinde (%14) esansiyel trombositoz ve bu hastaların 4’ünde (%8) JAK2 mutasyonu saptandı. Malignite öyküsü 1 (%2), talasemi majör 1 (%2) ve SLE 1 (%2) hastada saptandı. Fak-V leiden mutasyonu 3 (%6), Protein–S eksikliği 1 (%2), Antitrombin III eksikliği 2 (%4) hastada saptandı. Protrombin gen mutasyonu 2 (%4) hastada heterozigot olarak tespit edildi. Lupus antikoagülanı 2 (%4) hastada, fibrinojen düzeyi 1 (%2) hastada yüksek saptandı. PAI-1 (4G/5G) gen polimorfizmi 5 (%10) hastada saptandı. Tanı alan hastaların 31’inde (%62) kalıtsal ve edinsel risk faktörleri bir arada saptandı. Hastaların 6’sında (%12) herhangi bir kalıtsal veya edinsel risk faktörü saptanmadı.
SONUÇ: Atipik yerleşimli trombozlar ve 40 yaş altı erişkin hastalarda görülen tipik trombozlar kalıtsal ve edinsel etyolojik risk faktörlerinin bir arada saptanabildiǧi kompleks patolojik bir hastalıktır. Abdominal bölge trombozlarında etyolojik faktör olarak myeloproliferatif hastalıkların değerlendirilmesi gerektiği ve kadınlarda OKS kullanımının altta yatan kalıtsal risk faktörlerinin varlığında tromboz riskini arttırdıǧı görüldü. Gebelik, lohusalık, OKS kullanımı gibi nedenlerden ötürü kadın cinsiyette daha fazla tromboz görüldüǧü saptandı.

References

  • Rosendaal FR. Venous thrombosis: a multicausal disease. Lancet. 1999 Apr 3;353(9159):1167-73.
  • Lichtman M.A. BE, Kipps T.J., Seligsohn U., Kaushansky K., Prchal J.T. . 7th ed, ed: McGraw-Hill Co. ; 2005.
  • Malone PC, Agutter PS. The aetiology of deep venous thrombosis. QJM. 2006 Sep;99(9):581-93.
  • Van der Hagen PB, Folsom AR, Jenny NS, Heckbert SR, O'Meara ES, Reich LM, et al. Subclinical atherosclerosis and the risk of future venous thrombosis in the Cardiovascular Health Study. J Thromb Haemost. 2006 Sep;4(9):1903-8.
  • Silverstein MD, Heit JA, Mohr DN, Petterson TM, O'Fallon WM, Melton LJ, 3rd. Trends in the incidence of deep vein thrombosis and pulmonary embolism: a 25-year population-based study. Arch Intern Med. 1998 Mar 23;158(6):585- 93.
  • Biggs R. Human Blood Coagulation 2nd Ed. ed: Blackwell Scientific Publications 1976. Besa E.C. CPM, Kant J.A., Jefferies L.C. . Harwal Publishing Co. ; 1992.
  • Cushman M, Glynn RJ, Goldhaber SZ, Moll S, Bauer KA, Deitcher S, et al. Hormonal factors and risk of recurrent venous thrombosis: the prevention of recurrent venous thromboembolism trial. J Thromb Haemost. 2006 Oct;4(10):2199-203.
  • De Stefano V, Finazzi G, Mannucci PM. Inherited thrombophilia: pathogenesis, clinical syndromes, and management. Blood. 1996 May 1;87(9):3531-44.
  • Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, et al. Inherited thrombophilia: Part 1. Thromb Haemost. 1996 Nov;76(5):651-62.
  • Dahlback B, Carlsson M, Svensson PJ. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C. Proc Natl Acad Sci U S A. 1993 Feb 1;90(3):1004-8.
  • Poort SR, Rosendaal FR, Reitsma PH, Bertina RM. A common genetic variation in the 3'-untranslated region of the prothrombin gene is associated with elevated plasma prothrombin levels and an increase in venous thrombosis. Blood. 1996 Nov 15;88(10):3698-703.
  • Makris M, Rosendaal FR, Preston FE. Familial thrombophilia: genetic risk factors and management. J Intern Med Suppl. 1997;740:9-15.
  • Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, et al. Inherited thrombophilia: Part 2. Thromb Haemost. 1996 Dec;76(6):824-34.
  • Wu O, Robertson L, Twaddle S, Lowe G, Clark P, Walker I, et al. Screening for thrombophilia in high-risk situations: a meta-analysis and cost-effectiveness analysis. Br J Haematol. 2005 Oct;131(1):80-90.
  • Svensson PJ, Dahlback B. Resistance to activated protein C as a basis for venous thrombosis. N Engl J Med. 1994 Feb 24;330(8):517-22.
  • Braun A, Muller B, Rosche AA. Population study of the G1691A mutation (R506Q, FV Leiden) in the human factor V gene that is associated with resistance to activated protein C. Hum Genet. 1996 Feb;97(2):263-4.
  • Gerhardt A, Scharf RE, Beckmann MW, Struve S, Bender HG, Pillny M, et al. Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium. N Engl J Med. 2000 Feb 10;342(6):374- 80.
  • Decousus, H., Quere, I., Presles, E., Becker, F.,Barrellier, M.T., Chanut, M., Gillet, J.L., Guenneguez,H., Leandri, C., Mismetti, P., Pichot,O. & Leizorovicz, A. (2010a) Superficial venou thrombosis and venous thromboembolism: alarge, prospective epidemiologic study. Annals ofInternal Medicine, 152, 218–224.
  • Martinelli I: Risk factors for venous thromboembolism.Thromb Haemost 2001;86:395-403
  • Akar N, Akar E, Akçay R, Avcu F, Yalcin A, Cin S. Effect of methylenetetrahydrofolate reductase 677 C-T, 1298 A-C, and 1317 T-C on factor V 1691 mutation in Turkish deep vein thrombosis patients. Thromb Res 2000; 97: 163-7
  • Dodinger M, Horl WH, Sunder-Plassman G. Molecular biology of 5,10- methylenetetrahydrofolate reductase. J Nephrol, 2000;13(1):20-33.
  • Alkanlı. N Iskemik inmeli hastalrda calca, MTHFR gen polimorfizmleri ile plazma total homosistein düzeylerinin araştırılması 2014.
  • Kaya H, Karkucak M, Salifoǧlu H, Torun D, Kozan S, Tunca Y. Venöz tromboembolili hastalarda anjiotensin dönüş- türücü enzim I/D ve plazminojen aktivatör-1 4G/5G gen polimorfizmlerinin araştırılması. Tuberk Toraks 2013; 61: 88-95.
  • Rallidis LS, Megalou AA, Papageorgakis NH, Trikas AG, Chatzidimitriou GI, Tsitouris GK. Plasminogen activator inhibitor 1 is elevated in the children of men with premature myocardial infarction. Thromb Haemost 1996; 76: 417- 21.
  • Huber K. Plasminogen activator inhibitor type-1: basic mechanisms, regulation, and role for thromboembolic disease. J Thromb Thrombolysis 2001; 11: 183-93.
  • Seguí R, Estellés A, Mira Y, España F, Villa P, Falcó C, et al. PAI-1 promoter 4G/5G genotype as an additional risk factor for venous thrombosis in subjects with genetic thrombophilic defects. Br J Haematol 2000; 111: 122-8.
  • Tsantes AE, Nikolopoulos GK, Bagos PG, Rapti E, Mantzios G, Kapsimali V, et al. Association between the plasminogen activator inhibitor-1 4G/5G polymorphism and venous thrombosis. A meta-analysis. Thromb Haemost 2007; 97: 907-13.
  • Martinelli I, Sacchi E, Landi G, Taioli E, DucaF, Mannucci PM: High risk of cerebral-veinthrombosis in carriers of a prothrombin genemutation and in users of oral contraceptives. NEngl J Med 1998;338:1793-7
  • De Stefano, V., Za, T., Rossi, E., Vannucchi, A.M.,Ruggeri, M., Elli, E., Mico, C., Tieghi, A., Cacciola,R.R., Santoro, C., Gerli, G., Vianelli, N.,Guglielmelli, P., Pieri, L., Scognamiglio, F.,Rodeghiero, F., Pogliani, E.M., Finazzi, G., Gugliotta,L., Marchioli, R., Leone, G. & Barbui, T.(2008) Recurrent thrombosis in patients with polycythemia vera and essential thrombocythemia:incidence, risk factors, and effect of treatments.Haematologica, 93, 372–380.
  • De Stefano, V., Teofili, L., Leone, G. & Michiels, J.J. (1997) Spontaneous erythroid colony formationas the clue to an underlying myeloproliferative disorder in patients with Budd-Chiarisyndrome or portal vein thrombosis. Seminars in Thrombosis and Hemostasis, 23, 411–418.
  • de Bruijn, S.F., Stam, J., Koopman, M.M. & Vandenbroucke,J.P. (1998a) Case-control study ofrisk of cerebral sinus thrombosis in oral contraceptiveusers and in[correction of who are] carriersof hereditary prothrombotic conditions.The Cerebral Venous Sinus Thrombosis
There are 31 citations in total.

Details

Primary Language Turkish
Subjects Clinical Sciences
Journal Section Research Articles
Authors

Ferhat Bingöl 0000-0001-6219-673X

İhsan Solmaz 0000-0002-6624-8063

Orhan Ayyıldız 0000-0001-5673-8408

Publication Date August 31, 2021
Submission Date January 14, 2021
Published in Issue Year 2021 Volume: 10 Issue: 2

Cite

APA Bingöl, F., Solmaz, İ., & Ayyıldız, O. (2021). Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler. Abant Medical Journal, 10(2), 231-240. https://doi.org/10.47493/abantmedj.860822
AMA Bingöl F, Solmaz İ, Ayyıldız O. Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler. Abant Med J. August 2021;10(2):231-240. doi:10.47493/abantmedj.860822
Chicago Bingöl, Ferhat, İhsan Solmaz, and Orhan Ayyıldız. “Atipik Yerleşimli Trombozlar Ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler”. Abant Medical Journal 10, no. 2 (August 2021): 231-40. https://doi.org/10.47493/abantmedj.860822.
EndNote Bingöl F, Solmaz İ, Ayyıldız O (August 1, 2021) Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler. Abant Medical Journal 10 2 231–240.
IEEE F. Bingöl, İ. Solmaz, and O. Ayyıldız, “Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler”., Abant Med J, vol. 10, no. 2, pp. 231–240, 2021, doi: 10.47493/abantmedj.860822.
ISNAD Bingöl, Ferhat et al. “Atipik Yerleşimli Trombozlar Ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler”. Abant Medical Journal 10/2 (August 2021), 231-240. https://doi.org/10.47493/abantmedj.860822.
JAMA Bingöl F, Solmaz İ, Ayyıldız O. Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler. Abant Med J. 2021;10:231–240.
MLA Bingöl, Ferhat et al. “Atipik Yerleşimli Trombozlar Ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler”. Abant Medical Journal, vol. 10, no. 2, 2021, pp. 231-40, doi:10.47493/abantmedj.860822.
Vancouver Bingöl F, Solmaz İ, Ayyıldız O. Atipik Yerleşimli Trombozlar ile 40 Yaş Altı Erişkin Hastalardaki Tipik Yerleşimli Trombozlarda Etyolojik Faktörler. Abant Med J. 2021;10(2):231-40.