Fibrinogen known as factor I, is a plasma protein that is  converted into a fibrin gel ("the clot") by thrombin. Fibrinogen is synthesized in the liver and circulates in the plasma.
An isolated deficiency of fibrinogen may be inherited as an autosomal recessive trait (afibrinogenemia or hypofibrinogenemia) and is one 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 (e.g., 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.
Acquired dysfibrinogenemias mainly occur in association with liver disease (e.g., chronic hepatitis, hepatoma) or renal diseases (e.g., 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 concentration:
-Acute or chronic inflammatory illnesses.
-Nephrotic syndrome.
-Liver disease and cirrhosis.
-Pregnancy or estrogen therapy.
-Compensated intravascular coagulation.
-Diabetes.
-Obesity.
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.