Factor I Antigen
Diagnosis of homozygous and heterozygous fibrinogen deficiency as well as dysfibrinogenemia; diagnosis of disseminated intravascular coagulation; fibrinogen levels can be used to assess the effectiveness of thrombolytic therapy.
Fibrinogen, also referred to as factor I, is a 340 kilodalton glycoprotein that is produced by the liver. Fibrinogen has a plasma half-life of about four days. Proteolytic conversion of fibrinogen to fibrin occurs through both the extrinsic and intrinsic pathways. Fibrinogen deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). Fibrinogen activity should be measured when a patient has a history of bleeding and the PT and aPTT are normal, as these assays are generally insensitive to fibrinogen deficiency unless levels drop to <100 mg/dL.
Congenital afibrinogenemia, a condition associated with the complete absence of fibrinogen, is rare with only about 150 cases reported in the literature. Fibrinogen deficiency is inherited as an autosomal recessive trait. Afibrinogenemia occurs in individuals who are homozygous or doubly heterozygous for mutations. These individuals have infinite protime and aPTT results due to the inability to produce fibrin. Approximately 25% of patients with afibrinogenemia have mild thrombocytopenia.
Individuals who are heterozygous for congenital fibrinogen deficiency are usually asymptomatic unless their fibrinogen levels fall to <50 mg/dL. Both functional (activity) and antigenic levels are diminished in these individuals. Fibrinogen deficiency affects both males and females with a prevalence that is equal in all ethnic groups. Acquired deficiencies occur in individuals with significant hepatic dysfunction, renal disease, and after L-asparaginase therapy. Diminished levels can also be seen in patients with disseminated intravascular coagulation (DIC) or who are undergoing thrombolytic therapy. Fibrinogen is one of the major determinants of the erythrocyte sedimentation rate and individuals with afibrinogenemia typically have greatly extended sedimentation rates.
Individuals with dysfibrinogenemia have fibrinogen that is qualitatively defective with low functional fibrinogen levels (activity) and normal or decreased antigenic levels. Congenital dysfibrinogenemia is inherited as an autosomal dominant mutation. A number of disfibrinogenemic defects have been identified with a variety of manifestations including abnormal fibrin polymerization, impaired fibrinopeptide release, abnormal fibrin stabilization, and abnormal fibrin clot lysis. Fibrinogen activity and antigen levels are useful in the diagnosis of dysfibrinogenemia since these individuals often have diminished activity relative to antigen levels. Reptilase time is generally greatly prolonged, to a greater degree than prolongation of the thrombin time
Individuals with afibrinogenemia have bleeding tendencies of varying severity. Symptoms often start in early infancy with umbilical cord bleeding, intracerebral hemorrhage, or bleeding at circumcision. Individuals with afibrinogenemia also suffer from deep muscle and joint bleeding and other mucous membrane bleeding throughout life. Women with afibrinogenemia typically do not experience menorrhagia. Patients with heterozygous hypofibrinogenemia usually have a minimal history of bleeding with symptoms only observed after major surgery or trauma. Approximately 50% of individuals with dysfibrinogenemia are asymptomatic. These individuals are usually detected when prolonged clotting times are discovered as a result of routine laboratory testing; however, about one in four will suffer prolonged bleeding after surgery and approximately 20% will have an increased tendency toward thrombosis.
A number of clinical and epidemiological studies have revealed a consistent association between elevated fibrinogen levels and increased risk for atherosclerotic vascular disease however, it remains to be determined whether increased fibrinogen acts as a mediator of arterial thrombosis or simply reflects the inflammation associated with atherosclerosis.
Separate plasma from cells. Transfer specimen to a plastic transport tube and transport frozen. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Stable frozen (-20°C) for one year if frozen within 24 hours after collection. Repeated freeze/thaw cycles are to be avoided. Alternatively, refrigerate at 2°C to 8°C for no more than eight days.
Microbially contaminated samples; hemolysis; gross lipemia that cannot be cleared by ultracentrifugation; serum sample
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