Results 151 to 160 of about 1,945 (206)
Some of the next articles are maybe not open access.
Dysfibrinogenemia and Thrombosis
Seminars in Thrombosis and Hemostasis, 1999Congenital abnormal fibrinogen molecules (dysfibrinogenemias) are due to structural defects in the molecule. The molecular structure of the fibrinogen molecule is to a great extent known and this has allowed identification of the abnormalities at a molecular level.
exaly +3 more sources
Current Opinion in Hematology, 1997
Fibrinogen abnormalities can be classified as congenital or acquired. Each class manifests quantitative or qualitative alterations; the latter are known as dysfibrinogenemias. In dysfibrinogenemias, structural defects cause alterations in the conversion of fibrinogen to fibrin.
openaire +2 more sources
Fibrinogen abnormalities can be classified as congenital or acquired. Each class manifests quantitative or qualitative alterations; the latter are known as dysfibrinogenemias. In dysfibrinogenemias, structural defects cause alterations in the conversion of fibrinogen to fibrin.
openaire +2 more sources
Congenital dysfibrinogenemias. A review
La Ricerca in Clinica e in Laboratorio, 1985Inherited qualitative abnormalities of fibrinogen have been documented in 144 families. These dysfibrinogenemias have been inherited as autosomal dominant traits and usually are clinically silent, but in some cases are associated with bleeding, thrombosis, or defective wound healing. Dysfibrinogenemias may be associated with defects in any of the three
E, Rocha +4 more
openaire +2 more sources
Sneddon Syndrome revealing dysfibrinogenemia
International Journal of Dermatology, 2003Sneddon syndrome (SS) is the association of cerebral ischemic events and livedo and is caused by vascular thrombosis. It is often associated with a primitive antiphospholipid syndrome (PAPS). In other cases, several thrombophilic conditions have been implicated. Dysfibrinogenemia is a qualitative defect of fibrinogen.
Khosrotehrani, Kiarash +4 more
openaire +3 more sources
Congenital dysfibrinogenemia : Fibrinogen lille
Thrombosis Research, 1978A dysfibrinogenemia (fibrinogen Lille) was detected in a 6 year old girl with no history of unusual bleeding. Thrombin and batroxobin (“reptilase”) times were markedly prolonged. The plasma fibrinogen level was unmeasurable by a kinetic method (Clauss), whereas normal values were obtained by immunochemical (Laurell) and gravimetric (Ingram) assays ...
M H, Denninger +5 more
openaire +2 more sources
Dysfibrinogenemia in Obstructive Liver Disease
Journal of Pediatric Gastroenterology and Nutrition, 1987SummaryAcquired dysfibrinogenemia was documented in a 4‐year‐old child with obstructive jaundice of 1‐month duration, secondary to a choledochal cyst involving the distal common bile duct. It was characterized by decreased thrombin coagulable protein with elevated immunoassayable fibrinogen resulting in abnormal thrombin and reptilase times.
J, Levy, M J, Pettei, J I, Weitz
openaire +2 more sources
A Hereditary Dysfibrinogenemia: Fibrinogen Awaji
Pathophysiology of Haemostasis and Thrombosis, 1987Abnormal function of fibrinogen was observed in a 2 5-year-old woman with no symptoms attributable to dysfibrinogenemia. Disturbed polymerization of fibrin monomer was identified, but the release of fibrinopeptide from the purified fibrinogen and the cross-linking by factor XIII were normal.
T, Matsuo +5 more
openaire +2 more sources
A New Dysfibrinogenemia: Fibrinogen Oslo IV
Thrombosis and Haemostasis, 1983SummaryA family with dysfibrinogenemia is described. The abnormal fibrinogen occurred in three successive generations indicating a dominant hereditary pattern. Thrombin and reptilase times were about twice the normal value. This was shown to be caused by a polymerization defect, fibrinopeptide release being normal. Platelet aggregation was undisturbed,
H, Stormorken, F, Brosstad, H, Seim
openaire +2 more sources
Acquired Dysfibrinogenemia Secondary to Multiple Myeloma
Acta Haematologica, 2008Abnormal coagulation properties indicative of a dysfibrinogen were found in the plasma of a 72-year-old male with multiple myeloma (IgGĸ, stage IIIA). The patient had high paraprotein concentration (85.75 g/l) and prolonged thrombin time (76.8 s), activated partial thromboplastin time (39.5 s), prothrombin time (23.5 s) and reptilase time (72.0 s). The
Roman, Kotlín +8 more
openaire +2 more sources
Fibrinogen Aarhus — a new case of dysfibrinogenemia
Thrombosis Research, 1986Fibrinogen Aarhus was found in a woman with slightly prolonged whole blood clotting time. The thrombin induced clotting of plasma and purified fibrinogen was much prolonged. Kinetic analysis of FPA and FPB release revealed larger apparent Km and Vmax values for fibrinogen Aarhus than for normal fibrinogen.
B, Hessel +5 more
openaire +2 more sources