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  model can potentially serve for research on dysfibrinogenemia and amyloidosis as it provides insight

6 with the observation that subjects with this dysfibrinogenemia are asymptomatic.

7 ting that it is a relatively common cause of dysfibrinogenemia-associated thrombosis.

8                                   Congenital dysfibrinogenemia (CD) is caused by structural changes i

9 center study of 101 patients with congenital dysfibrinogenemia (CD) to characterize the incidence of

10 scular coagulation (DIC), hyperfibrinolysis, dysfibrinogenemia, hemolysis, and a decrease in number o

11                                This acquired dysfibrinogenemia is characterized by fibrin clots that

12                                           In dysfibrinogenemias, structural defects cause alterations

13 h corresponding heterozygous gene mutations (dysfibrinogenemias) were observed in 5 of 33 CTEPH patie

14 erization of fibrinogen Dusart, a congenital dysfibrinogenemia with the amino acid substitution A alp