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- W2895509600 abstract "Inherited fibrinogen disorders causing quantitative or qualitative alterations in this molecule have been classified phenotypically as hypofibrinogenemia, afibrinogenemia, dysfibrinogenemia, and hypodysfibrinogenemia. As many as 400 cases of inherited fibrinogen disorders have been listed on the GEHT homepage [ [1] Groupe d'Etude sur 1'Hémostase et al. Thrombose. “Base de Données des Variants du Fibrinogène”. http://site.geht.org/base-de-donnees-fibrinogene/Date: 2017 Google Scholar ]. The clinical manifestations of inherited fibrinogen disorders are very heterogeneous: the absence of symptoms, bleeding, thrombosis, and recurrent miscarriages in women as well as rare cases of fibrinogen storage disease and renal amyloidosis. Approximately 14% of reported dysfibrinogens are associated with thrombosis [ [2] Casini A. Blondon M. Lebreton A. Koegel J. Tintillier V. de Maistre E. Gautier P. Biron C. Neerman-Arbez M. de Moerloose P. Natural history of patients with congenital dysfibrinogenemia. Blood. 2015; 125: 553-561 Crossref PubMed Scopus (109) Google Scholar ]; however, difficulties are associated with demonstrating that fibrinogen mutations directly cause thrombosis. The homozygous BβAla68Thr mutation, known as Naples I or Milano II [ [3] Haverkate F. Koopman J. Kluft C. D'Angelo A. Cattaneo M. Mannucci P.M. Fibrinogen Milano II: a congenital dysfibrinogenemia associated with juvenile arterial and venous thrombosis. Thromb. Haemost. 1986; 55: 131-135 PubMed Google Scholar ], which is one of the most common mutations associated with thrombosis, causes markedly defective thrombin binding to its fibrin in vitro and an increase in free active thrombin in the circulation [ [4] Koopman J. Haverkate F. Lord S.T. Grimbergeb J. Mannucci P.M. Molecular basis of fibrinogen Naples associated with defective thrombin binding and thrombophilia. J. Clin. Invest. 1992; 90: 238-244 Crossref PubMed Scopus (63) Google Scholar ]. Zhou J et al. reported the same mutation in five Chinese patients, two of whom had thrombosis [ [5] Zhou J. Ding Q. Chen Y. Ouyang Q. Jiang L. Dai J. Lu Y. Wu X. Liang Q. Wang H. Wang X. Clinical features and molecular basis of 102 Chinese patients with congenital dysfibrinogenemia. Blood Cell Mol. Dis. 2015; 55: 308-315 Crossref PubMed Scopus (34) Google Scholar ]." @default.
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- W2895509600 date "2018-12-01" @default.
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- W2895509600 title "Fibrin monomers derived from thrombogenic dysfibrinogenemia, Naples-type variant (BβAla68Thr), showed almost entirely normal polymerization" @default.
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- W2895509600 doi "https://doi.org/10.1016/j.thromres.2018.10.004" @default.
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