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PubMed1965

Platelet fibrinogen.

Platelet fibrinogen has been studied in normal, thrombasthenic, and hypofibrinogenaemic subjects. It has been differentiated into adsorbed (plasma) and extractable (intraplatelet) fractions. Isotopic studies suggest that exchange does not occur between intraplatelet and plasma fibrinogen and it appears possible that the intra-platelet fraction may be derived from the megakaryocyte. Six of nine thrombasthenic patients were found to have a severe deficiency of both adsorbed and extractable fibrinogen. Since the remaining three had near-normal platelet fibrinogen and all nine failed to aggregate it is improbable that the failure to adsorb fibrinogen is responsible for the defect in aggregation. Magnesium partially corrects adhesion to fibrin and clot retraction by these platelets, but has not been found to influence their fibrinogen adsorption. It is considered that the basic platelet surface defect, of varying severity, is responsible for the abnormalities of adsorption, aggregation, and adhesion in thrombasthenia. In the case of congenital hypofibrinogenaemia, fibrinogen transfusion corrects the long bleeding time, platelet-adsorbed fibrinogen, and the ability of platelets to spread on glass. It is possible that fibrinogen influences the surface properties of human platelets, although the final mechanism is not determined.

Afibrinogenemia↗
PubMed1967

Hypofibrinogenaemia in metastatic carcinoma of the prostate: suppression of systemic fibrinolysis by haparin.

In a patient with generalized prostatic carcinoma and hypofibrinogenaemia heparin infusion on four occasions abolished systemic fibrinolysis as determined by euglobulin clot lysis time, bovine fibrin plate assay, thromboelastography, and immunoelectrophoretic demonstration of fibrinogen split products. The pathogenesis of hypofibrinogenaemia in cases of prostatic carcinoma and the possibility of a direct heparin effect on fibrinolysis are discussed. Despite the lack of histological evidence for intravascular coagulation, the findings are considered additional evidence for the view that fibrinolysis in this syndrome may be secondary to intravascular coagulation.

Afibrinogenemia↗
PubMed1968

Latex-bound antifibrinogen test for plasma fibrinogen assay.

The semiquantitative latex-bound antifibrinogen test (Fi test) can be modified to quantitate plasma fibrinogen. The test is rapid and simple and does not require complex apparatus. Although the Fi reagent reacts with early fibrinogen and fibrin breakdown products, the degree of interference is not marked and the test is sufficiently accurate to be of clinical value as a fibrinogen assay in patients with increased fibrinolytic activity.

Afibrinogenemia↗
PubMed2005

Hypofibrinogenaemia caused by a novel FGG missense mutation (W253C) in the gamma chain globular domain impairing fibrinogen secretion.

BACKGROUND: Inherited disorders of fibrinogen are rare and affect either the quantity (hypofibrinogenaemia and afibrinogenaemia) or the quality of the circulating fibrinogen (dysfibrinogenaemia). Extensive allelic heterogeneity has been found for all three disorders: in congenital afibrinogenaemia >30 mutations, the majority in FGA, have been identified in homozygosity or in compound heterozygosity. Several mutations have also been identified in patients with hypofibrinogenaemia; many of these are heterozygous carriers of afibrinogenaemia null mutations. OBJECTIVE: To report the case of a patient from Slovakia diagnosed with hypofibrinogenaemia characterised by fibrinogen concentrations of around 0.7 g/l. RESULTS: The patient was found to be heterozygous for a novel missense mutation W253C (W227C in the mature protein) in the C-terminal globular domain of the fibrinogen gamma chain. Co-expression of the W253C FGG mutant cDNA (fibrinogen Bratislava) in combination with wild-type FGA and FGB cDNAs showed that fibrinogen molecules containing the mutant gamma chain can assemble intracellularly but are not secreted into the media, confirming the causative nature of the identified mutation. CONCLUSIONS: Current analysis of fibrinogen Bratislava indicates that the domains important for the processes of hexamer assembly and hexamer secretion should not be considered as strictly restricted to one or other fibrinogen chain.

Adult↗
PubMed1956

Obstetrics.

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Afibrinogenemia↗