Detecting increased or decreased fibrinogen (factor 1) concentration of acquired or congenital origin
Differentiating hypofibrinogenemia from dysfibrinogenemia
Only orderable as part of a coagulation reflex. For more information see:
ALUPP / Lupus Anticoagulant Profile, Plasma
ALBLD / Bleeding Diathesis Profile, Limited, Plasma
AATHR / Thrombophilia Profile, Plasma and Whole Blood
APROL / Prolonged Clot Time Profile, Plasma
ADIC / Disseminated Intravascular Coagulation/Intravascular Coagulation and Fibrinolysis (DIC/ICF) Profile, Plasma
Optical Clot-Based
Plasma Na Cit
Only orderable as part of a coagulation reflex. For more information see:
ALUPP / Lupus Anticoagulant Profile, Plasma
ALBLD / Bleeding Diathesis Profile, Limited, Plasma
AATHR / Thrombophilia Profile, Plasma and Whole Blood
APROL / Prolonged Clot Time Profile, Plasma
ADIC / Disseminated Intravascular Coagulation/Intravascular Coagulation and Fibrinolysis (DIC/ICF) Profile, Plasma
Gross hemolysis | Reject |
Gross lipemia | Reject |
Gross icterus | Reject |
Specimen Type | Temperature | Time | Special Container |
---|---|---|---|
Plasma Na Cit | Frozen | 14 days |
Detecting increased or decreased fibrinogen (factor 1) concentration of acquired or congenital origin
Differentiating hypofibrinogenemia from dysfibrinogenemia
Fibrinogen, also known as factor 1, 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 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), 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 kidney diseases 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 and venous thromboembolism.
Only orderable as part of a coagulation reflex. For more information see:
ALUPP / Lupus Anticoagulant Profile, Plasma
ALBLD / Bleeding Diathesis Profile, Limited, Plasma
AATHR / Thrombophilia Profile, Plasma and Whole Blood
APROL / Prolonged Clot Time Profile, Plasma
ADIC / Disseminated Intravascular Coagulation/Intravascular Coagulation and Fibrinolysis (DIC/ICF) Profile, Plasma
261-595 mg/dL
In normal full-term newborns and in healthy pre-mature infants (30-36 weeks gestation) fibrinogen is near adult levels (>150) and remains at adult levels throughout childhood.
This test assesses the level of total clottable fibrinogen (see Cautions).
Fibrinogen assay results may be affected by excess heparin (>1 U/mL), hemoglobin (>100 mg/dL), triglycerides (>700 mg/dL), bilirubin (>15 mg/dL), and by degradation products (fibrin or fibrinogen) in the plasma assayed.
Favaloro EJ, Lippi G. eds. Hemostasis and Thrombosis, Methods and Protocols. Humana Press 2017.
The PT Fibrinogen assay is performed using the HemosIL PT-Fibrinogen kit on the Instrumentation Laboratory ACL TOP. Prothrombin Time (PT) thromboplastin reagent is added to patient plasma; endogenous thrombin from the patient’s plasma is generated during the reaction and converts fibrinogen to fibrin. This change from fibrinogen to fibrin is monitored by the instrument through reading the light absorbance over a set amount of time. At the end of the allotted time, the instrument uses a set algorithm to determine the delta and plot it against the calibration curve. The delta value is directly proportional to the amount of fibrinogen in the sample.(Package insert: HemosIL PT Fibrinogen. Instrumentation Laboratory Company; 01/2016)
Monday through Friday
This test has been cleared, approved, or is exempt by the US Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.
85385
Test Id | Test Order Name | Order LOINC Value |
---|---|---|
PTFIB | PT-Fibrinogen, P | 3255-7 |
Result Id | Test Result Name |
Result LOINC Value
Applies only to results expressed in units of measure originally reported by the performing laboratory. These values do not apply to results that are converted to other units of measure.
|
---|---|---|
PTFIB | PT-Fibrinogen, P | 3255-7 |