Plasma fibrinogen

Abstract

Fibrinogen is the major plasma protein coagulation factor. Low plasma fibrinogen concentrations are therefore associated with an increased risk of bleeding due to impaired primary and secondary haemostasis. Fibrinogen is a classical positive acute-phase reactant protein and is an independent predictor of coronary heart disease events. This review considers available methods for measurement of fibrinogen and makes recommendations as to their appropriate use.Total clottable fibrinogen assays are the definitive and reference method for plasma fibrinogen measurement. However, they are time-consuming and are rarely required in clinical practice. Clotting rate assays remain the routine method of choice for investigation, monitoring and treatment of bleeding disorders associated with low plasma fibrinogen concentrations. They are appropriately sited in haematology or haemostasis laboratories, with facilities for further relevant investigations, and expert advice from consultant haematologists on appropriate management. They have also been used in the majority of studies investigating increasing fibrinogen concentrations as a cardiovascular risk factor. Prothrombin-time derived assays are widely used, because they are less expensive and come at no extra cost with prothrombin time assays. However, their results vary widely with analysers and reagents, show discrepancies with clotting rate assays for both low and normal plasma fibrinogen samples, and at present they are not recommended by routine clinical use. Immunoassays (radial immunodiffusion, enzyme-linked immunosorbent assay or nephelometric) are useful in (a) differentiating hypofibrinogenaemia from dysfibrinogenaemia, and (b) assessing cardiovascular risk and acute-phase reactions. Unlike clottable fibrinogen assays, immunoassays can be performed in dipotassium edetate anticoagulated samples.

Oxidation of proteins: Basic principles and perspectives for blood proteomics

“…It consists of two sets of three disulphide-bridged chains (Aa, Bb, and g) of 610, 461, and 411 amino acid residues, respectively. Structure, heterogeneity, function and assays were all reviewed else-where [177][178][179][180]. Western blot immunoassay showed that fibrinogen, among other plasma proteins, is highly susceptible to attack by oxidants [181].…”

Interrelation between inflammation, thrombosis, and neuroprotection in cerebral ischemia

“…Thus, not all circulating fi brinogen is functional or clottable. As the tissue repair process takes place, the fi brin plug is digested by fi brinolytic enzymes (Lowe et al , 2004 ). On the one hand, low levels of plasma fi brinogen are associated with an increased risk for bleeding, as platelet aggregation as well as fi brin plug formation is impaired.…”

“…Platelet adhesion and activation are thus regulated by specifi c proteins on the platelet surface, and fi brinogen as well as fi bronectin plays a fundamental role in the coagulation process (Ni et al , 2000 ;Lowe et al , 2004 ). Fibrin assembly (through the coagulation pathway and involvement of the platelets) from fi brinogen proceeds in a highly ordered fashion.…”

“…Sex hormones not only alter procoagulant protein expression (Lowe et al , 2004 ) and the function of blood and vascular cells (Kadir et al , 1999 ;Butenas and Mann , 2002 ;Leng et al , 2004 ), but differences in platelet function (Liao et al , 2001 ;Suzuki et al , 2009 ) and in thrombosis activity (Bailey et al , 2009 ) have also been noted. Estrogen is to a degree neuroprotective (Liao et al , 2001 ;Suzuki et al , 2009 ;Selvamani and Sohrabji , 2010 ) in certain cases of induced cerebral ischemia, as females appear to suffer less severe consequences of stroke, including lesser neural tissue loss, than their male counterparts (McCullough and Hurn , 2003 ;Suzuki et al , 2009 ).…”

“…Activated platelets synthesize/secrete inducers of platelet aggregation and adhere to the injured vessel wall, as well as aggregate to each other in order to form a platelet-rich plug or thrombus, which secures hemostasis; this plug is then stabilized by fi brin formation as fi brinogen is activated by binding to activated platelets. Fibrinogen is the major plasma protein coagulation factor (Lowe et al , 2004 ), and though plasma levels thereof are decreased by estrogen during the menstrual cycle, these levels are known to be higher in females than in males (Bailey et al , 2009 ). Although fi brin forms the core matrix of a thrombus, its structure depends also on the cellular elements embedded in its meshwork and the overall rate of coagulation reactions initiated by platelet aggregation (Wohner , 2008 ).…”