Sorted By Test Name - Mayo Medical Laboratories

FFIBR
91933
FIB
8484
An interpretive report will be provided.
Clinical References: 1. Benson MD: The hereditary amyloidoses. Best Pract Res Clin Rhematol
2003;17:909-927 2. Benson MD: Ostertag revisited: The inherited systemic amyloidoses without
neuropathy. Amyloid 2005;12(2):75-87 3. Asselta R, Duga S, Tenchini ML: The molecular basis of
quantitative fibrinogen disorders. Thromb Haemost 2006 Oct;4(10):2115-2129 4. Shiller SM, Dogan A,
Highsmith WE: Laboratory methods for the diagnosis of hereditary amyloidoses. In
Amyloidosis-Mechanisms and Prospects for Therapy. Edited by S Sarantseva. InTech 2011, pp101-120
Fibrinogen Antigen
Reference Values:
201-454 mg/dL
Interpretive note: Differentiation of congenital from acquired defects
of fibrinogen requires clinical correlation. Fibrinogen antigen data
should be compared with functional fibrinogen activity on the same
sample for evaluation of afibrinogenemia, hypofibrinogenemia and
dysfibrinogenemia.
Test Performed by: BloodCenter of Wisconsin
638 N. 18th Street
Milwaukee, WI 53233-2121
Fibrinogen, Plasma
Clinical Information: 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 -Nephrotic syndrome -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.
Useful For: Detecting increased or decreased fibrinogen (factor I) concentration of acquired or
congenital origin Monitoring severity and treatment of disseminated intravascular coagulation and
fibrinolysis
Interpretation: This kinetic assay assesses levels of functional (clottable) fibrinogen (see Cautions).
Reference Values:
Males: 200-375 mg/dL
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