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Fibrinogen, also known as factor I, is a plasma protein that can be transformed by thrombin into a fibrin gel ("the clot"). Fibrinogen is synthesized in the liver and circulates in the plasma as a disulfide-bonded dimer of 3 subunit chains. The biological half-life of plasma fibrinogen is 3 to 5 days.
An isolated deficiency of fibrinogen may be inherited as an autosomal recessive trait (afibrinogenemia or hypofibrinogenemia) and is 1 of the rarest of the inherited coagulation factor deficiencies.
Acquired causes of decreased fibrinogen levels include: acute or decompensated intravascular coagulation and fibrinolysis (disseminated intravascular coagulation [DIC]), advanced liver disease, L-asparaginase therapy, and therapy with fibrinolytic agents (eg, streptokinase, urokinase, tissue plasminogen activator).
Fibrinogen function abnormalities, dysfibrinogenemias, may be inherited (congenital) or acquired. Patients with dysfibrinogenemia are generally asymptomatic. However, the congenital dysfibrinogenemias are more likely than the acquired to be associated with bleeding or thrombotic disorders. While the dysfibrinogenemias are generally not associated with clinically significant hemostasis problems, they characteristically produce a prolonged thrombin time clotting test. Congenital dysfibrinogenemias usually are inherited as autosomal codominant traits.
Acquired dysfibrinogenemias mainly occur in association with liver disease (eg, chronic hepatitis, hepatoma) or renal diseases (eg, chronic glomerulonephritis, hypernephroma) and usually are associated with elevated fibrinogen levels.
Fibrinogen is an acute phase reactant, so a number of acquired conditions can result in an increase in its plasma level:
-Acute or chronic inflammatory illnesses
-Liver disease and cirrhosis
-Pregnancy or estrogen therapy
-Compensated intravascular coagulation
The finding of an increased level of fibrinogen in a patient with obscure symptoms suggests an organic rather than a functional condition. Chronically increased fibrinogen has been recognized as a risk factor for development of arterial thromboembolism.
Detecting increased or decreased fibrinogen (factor I) concentration of acquired or congenital origin
Monitoring severity and treatment of disseminated intravascular coagulation and fibrinolysis
This kinetic assay assesses levels of functional (clottable) fibrinogen (see Cautions).
In patients with dysfibrinogenemias, kinetic fibrinogen assays may give spuriously-low values.
In patients with markedly elevated plasma levels of fibrin degradation products (eg, thrombolytic therapy or disseminated intravascular coagulation and fibrinolysis), clottable fibrinogen determined by kinetic (rate) technique may be lower than when measured by an end-point method (eg, nephelometric assay).
Patients with antibodies to bovine thrombin (which can arise in association with surgical application of topical bovine thrombin) may have spuriously-decreased fibrinogen when assayed by kinetic technique.
In each of the above cases, end-point determinations of clottable fibrinogen (eg, nephelometric assay) may be helpful or diagnostic. The nephelometric assay is available as part of a Coagulation Consultation.
The presence of large amounts of heparin (>5-10 U/mL) may cause erroneously-low kinetic estimates of fibrinogen or make it impossible to measure fibrinogen by the nephelometric end-point technique.
In these cases, end-point determinations of clottable fibrinogen by a gravimetric/spectrophotometric (biuret) technique or fibrinogen immunoassay may be helpful.
Males: 200-375 mg/dL
Females: 200-430 mg/dL
In normal, full-term newborns and in healthy, premature infants (30-36 week gestation), fibrinogen is near adult levels and reaches adult levels by < or =21 days postnatal.
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2. Bowie EJW, Owen CA Jr: Clinical and laboratory diagnosis of hemorrhagic disorders. In Disorders of Hemostasis. Edited by OD Ratnoff, CD Forbes. Philadelphia, WB Saunders Company, 1991, pp 68-69
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