Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AFIBRINOGENEMIA”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed1998

Laboratory investigation of hypercoagulability.

For many years, the laboratory investigation of patients with thrombophilia has lagged behind that of patients with bleeding diathesis. Improved understanding of the mechanisms that control and regulate coagulation, and the resultant recognition of new defects, have greatly stimulated clinical laboratory interest in this area. Assays to detect resistance to activated protein C; deficiencies of antithrombin, protein C, and protein S; and the presence of antiphospholipid antibodies are widely available and should form part of the investigation of patients that present with idiopathic thrombosis. Such a work-up will likely provide an explanation for thrombosis in 40 to 60% of patients. Abnormalities of fibrinogen and fibrinolysis may explain still more, although such defects are currently considered rare. In addition, presently unrecognized defects almost certainly exist, and the identification of such individuals will undoubtedly improve our understanding of the hemostatic mechanism. Laboratory tests to define the hypercoagulable state are continually being developed. They include whole blood coagulation and platelet function tests and novel activation markers. However, acceptance of these approaches by clinical laboratories has been slow.

Afibrinogenemia↗
PubMed1990

[Obstetrical management in dysfibrinogenemia].

Dysfibrinogenaemia is an inherited disorder, characterised by a plasmafibrinogen in normal concentration, but of abnormal quality due to impaired release of fibrinopeptides and/or impaired aggregation of fibrinomonomers. The typical abnormalities of the laboratory findings will be demonstrated by presenting the case reports of 4 patients with 5 pregnancies (1 ectopic pregnancy); the importance of clinical exploration is emphasized. Newborn infants must be subjected to careful clinical and biochemical examination, because of factors of Mendelian dominant inheritance.

Adult↗
PubMed1993

[Kasabach-Merritt syndrome. Intraoperative heparin therapy with follow-up combination therapy of heparin and ticlopidine for the control of intravascular coagulation].

A 39-year-old woman with Kasabach-Merritt syndrome (cavernous vascular malformations with disseminated intravascular coagulation) sustained a displaced fracture of the femoral shaft. Despite pronounced hypofibrinogenemia (< 0.1 g/l) there was no significant bleeding. The concentration of D dimer was raised to > 32 < 64 mg/l and that of prothrombin fragments F1 and F2 to > 10 nmol/l. The platelet count was 102,000/microliters and other coagulation parameters were normal or only slightly abnormal. The consumption coagulopathy was successfully controlled by continuous intravenous infusion of heparin (17,000 I.U./d) without need for clotting factor replacement, and was subsequently stabilized by combined treatment with low molecular weight heparin (5,000 I.U./d s.c.) and ticlopidine (250 mg twice daily by mouth). Oral therapy with acetylsalicylic acid alone or in combination with ticlopidine proved insufficient, being rapidly followed by a renewed fall in fibrinogen level and platelet count. The findings suggest that fibrin formation in the abnormal vascular territories was the principal pathogenetic factor in this case.

Abdominal Neoplasms↗
PubMed1969

Platelet function.

Explore the source record for details and available documents.

Adenine Nucleotides↗
PubMed1971

Use of fibrinogen.

Explore the source record for details and available documents.

Afibrinogenemia↗
PubMed1975

DiC-like syndrome after envenomation by the snake, Crotalus horridus horridus.

After envenomation by the timber rattlesnake (Crotalus horridus horridus) a young man showed massive swelling and ecchymoses of the involved extremity, generalized petechiae and a large hematoma of the left upper eyelid. Two weeks later he was completely well. The first blood sample was incoagulable and showed high titers of fibrin split products by the MISFI and staphylococcal clumping tests. Immounoelectrophoresis showed both D and E fragments, but only D was present at 18 hours. The profound thrombocytopenia and hypofibrinogenemia gradually improved, and split products disappeared. In vitro the venom had thrombin-like activity, clotting fibrinogen or plasma and aggregating platelets. These activities could be inhibited by antivenom but not by heparin. There was no evidence that thrombin formation was actually involved: hence, the syndrome is called DIC-like.

Adult↗
PubMed1984

Molecular defects in interactions of platelets with the vessel wall.

The objectives of this review have been to summarize the recent research on inherited defects involving abnormal platelet function and to illustrate how studies of hemorrhagic syndromes have led to an increased understanding of the molecular events involved in platelet adhesion and aggregation. Emphasis has been placed on the two primary hemostatic reactions: the interaction of platelets with von Willebrand factor to promote adhesion to the subendothelium, and the interaction of platelets with fibrinogen to promote platelet aggregation. Even as these events are more clearly defined, new concepts of molecular structure, function, and heterogeneity are emerging, and the variety of recognized genetic defects is becoming more complex.

Afibrinogenemia↗