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Results for “AFIBRINOGENEMIA”

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PubMed1981

Disseminated intravascular coagulation: a clinical/laboratory study of 48 patients.

In summary, this series of 48 patients with acute and chronic DIC demonstrates the reliability of laboratory tests in both aiding a diagnosis of DIC and in offering reasonable predictability of efficacy of therapy, as noted by the correction of abnormalities after delivery of antiprocoagulant therapy for this syndrome. It appears that the diagnostic tests most likely to aid in diagnosis and to reliably inform the clinician when the intravascular clotting process has been stopped are those that determine the antithrombin-III level, the presence of soluble fibrin monomer, and the finding of elevated fibrin(ogen) degradation products, thrombocytopenia and a prolonged thrombin time in the face of the appropriate type of bleeding in the appropriate clinical setting. In addition, it would appear that mini-dose heparin therapy is highly effective in controlling the intravascular clotting process in acute DIC, whereas antiplatelet therapy utilizing two agents is effective in chronic DIC. In addition, in this population, patients with acute disease demonstrated a 74 percent survival rate and those with chronic disease had a 100 percent survival rate from the disseminated intravascular clotting process.

Acute Disease↗
PubMed2001

Antifibrinogen IgG, fibrinogen, and Clq complexes circulating in a hypodysfibrinogenemic proband. Isolation, stoichiometry, and partial characterization.

Circulating antifibrinogen antibodies have been reported in rare afibrinogenemic propositi, apparently occurring following fibrinogen replacement therapy, but immune complexes have not been described. In this report we describe circulating immune complexes formed by a monoclonal antifibrinogen IgG in a heterozygous hypodysfibrinogenemic (A alpha 16 Arg-->Cys) proband. Estimated by partial protein sequence and by other analyses, each immune complex consisted of one fibrin(ogen), one C1q, and 3-4 IgG molecules. The complexes were cryoprecipitable, a property also displayed by mixtures of proband IgG and normal fibrinogen. Indicating that both D and E domains were necessary for this behavior, cryoprecipitability was abolished by preincubation of the isolated IgG with either isolated normal fibrinogen fragment D100 or E. Consistent with the crossreactivity of the IgG with normal and mutant fibrinogen, the results suggest that the primary epitope resides on a D-E locus on the fibrin polymer formed by normal and abnormal molecules containing the uncleaved (or mutant) peptide A.

Afibrinogenemia↗
PubMed1984

Coagulation defect of congenital tyrosinaemia.

Three infants with hereditary tyrosinaemia had a severe coagulation defect due to a combination of deficient hepatic synthesis of clotting factors and a consumption coagulopathy. In all three plasma failed to clot normally with the venom of Bothrops atrox (Reptilase) and we attribute this to a defect of fibrinogen (dysfibrinogenaemia). Treatment was unsuccessful, and all died.

Afibrinogenemia↗
PubMed1971

Permeability of membranes of dead fetus.

Membranes of dead fetuses showed a three-fold increase in permeability to the haemoglobin molecule when compared with normal and stored membranes. The friability of some of these membranes was markedly increased and their strength and elasticity diminished. These findings may be significant in the aetiology of the hypofibrinogenaemia and the increased incidence of amniotic fluid embolism with intrauterine death of the fetus.

Afibrinogenemia↗