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1 omplications in the family members with this dysfibrinogenemia.
2 ologies, diabetes, thrombolytic therapy, and dysfibrinogenemia.
3 itative alterations; the latter are known as dysfibrinogenemias.
4 RP and also in platelets from a patient with dysfibrinogenemia and a fibrinogen polymerization defect
5 with the observation that subjects with this dysfibrinogenemia are asymptomatic.
6 ting that it is a relatively common cause of dysfibrinogenemia-associated thrombosis.
7 center study of 101 patients with congenital dysfibrinogenemia (CD) to characterize the incidence of
8 scular coagulation (DIC), hyperfibrinolysis, dysfibrinogenemia, hemolysis, and a decrease in number o
9                                This acquired dysfibrinogenemia is characterized by fibrin clots that
10                                           In dysfibrinogenemias, structural defects cause alterations
11 h corresponding heterozygous gene mutations (dysfibrinogenemias) were observed in 5 of 33 CTEPH patie
12 erization of fibrinogen Dusart, a congenital dysfibrinogenemia with the amino acid substitution A alp

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