Fibrinogen

Fibrinogen (mg/dl) an acute-phase plasma protein, and its level rises in all inflammatory and destructive processes. It is specifically a clotting factor (factor I), that is essential for proper blood clot formation. Fibrinogen is produced by the liver and released into the blood along with several other clotting factors (also called coagulation factors). Normally, when a body tissue or blood vessel wall is injured, a process called hemostasis begins to help stop the bleeding by forming a plug at the injury site. Platelets clump and stick to the injury site and clotting factors are activated one after the other (the coagulation cascade). As the cascade nears completion, soluble fibrinogen is converted into insoluble fibrin threads. These threads then crosslink together to form a fibrin net that stabilizes at the injury site. The fibrin net adheres to the site of injury along with the platelets to form a stable blood clot. This barrier prevents additional blood loss and remains in place until the injured area is healed.

Abnormalities. Disorders or diseases caused or related.

Low fibrinogen levels that persist over time (chronic) may be related to the body's inability to produce fibrinogen due to:

An acquired condition such as end-stage liver disease or severe malnutrition

A rare inherited condition such as dysfibrinogenemia, afibrinogenemia or hypofibrinogenemia (For details, see below.)

Acutely low levels are often related to conditions in which fibrinogen is used up more quickly than the body can produce it. This can occur with disseminated intravascular coagulation (DIC) and abnormal fibrinolysis, which occurs when the body is overactive in breaking down and clearing blood clots.

Reduced fibrinogen levels may also occur following rapid, large-volume blood transfusions.

Rare inherited coagulation disorders caused by changes (mutations) in the genes controlling the production of fibrinogen in the liver exist.

Congenital dysfibrinogenemia causes the liver to make abnormal, dysfunctional fibrinogen, one that resists degradation when converted to fibrin or cannot function normally in the coagulation cascade. Dysfibrinogenemia may increase a person's risk of a blood clot or, rarely, cause a mild bleeding tendency. People with fibrinogen deficiency or dysfibrinogenemia may experience poor wound healing.

Congenital hypofibrinogenemia results in decreased fibrinogen. People with this condition can experience mild bleeding episodes, such as a bloody nose or bleeding gums.

Congenital afibrinogenemia is a severe lack of fibrinogen. People with this condition may be at risk of severe bleeding (hemorrhaging) episodes, especially as babies or as young children. They may experience excessive bleeding from the umbilical cord, frequent, easy bruising, nose bleeds that are difficult to stop, excessive bleeding after surgical procedures, and bleeding in the digestive tract.

Genetic testing is occasionally performed for people with these inherited disorders to identify the responsible genetic mutation. Testing for this mutation may also be performed for other family members.

Fibrinogen is an acute-phase reactant, meaning that fibrinogen levels may rise sharply in any condition that causes inflammation or tissue damage. High levels of fibrinogen are not specific. They do not tell the healthcare practitioner the cause or location of the inflammation or damage. Usually these increased levels are temporary, returning to normal after the underlying condition has resolved.

Increased fibrinogen levels may be seen with:

Infections

Cancer

Coronary heart disease, heart attack

Stroke

Inflammatory disorders (like rheumatoid arthritis and glomerulonephritis, a form of kidney disease)

Trauma

Peripheral artery disease

Heavy smoking

When fibrinogen levels are elevated, a person's risk of developing a blood clot may be increased and, over time, they could contribute to an increased risk for cardiovascular disease.

1.        Fibrinogen. Available online Review. https://labtestsonline.org/tests/fibrinogen

2.        Gersten, T. et. al. (2017 February 7, Updated). Fibrinogen blood test. MedlinePlus Medical Encyclopedia. Available online at https://medlineplus.gov/ency/article/003650.htm. Accessed February 2019

3.        de Moerloose P, Casini A, Neerman-Arbez M (2013). "Congenital fibrinogen disorders: an update". Seminars in Thrombosis and Hemostasis. 39 (6): 585–95. doi:10.1055/s-0033-1349222. PMID 23852822.

4.        Yong J, Doolittle RF (2003). "The evolution of vertebrate blood coagulation as viewed from a comparison of puffer fish and sea squirt genomes". Proceedings of the National Academy of Sciences of the United States of America. 100 (13): 7527–7532. doi:10.1073/pnas.0932632100. ISSN 0027-8424. PMC 164620. PMID 12808152.

5.        Mosesson MW (2005). "Fibrinogen and fibrin structure and functions". Journal of Thrombosis and Haemostasis. 3 (8): 1894–904. doi:10.1111/j.1538-7836.2005.01365.x. PMID 16102057. S2CID 22077267.

6.        Casini A, de Moerloose P, Neerman-Arbez M (2016). "Clinical Features and Management of Congenital Fibrinogen Deficiencies". Seminars in Thrombosis and Hemostasis. 42 (4): 366–74. doi:10.1055/s-0036-1571339. PMID 27019462.

7.        Undas A (2011). "Acquired dysfibrinogenemia in atherosclerotic vascular disease". Polskie Archiwum Medycyny Wewnetrznej. 121 (9): 310–9. PMID 21952526.

8.        Davalos D, Akassoglou K (2012). "Fibrinogen as a key regulator of inflammation in disease". Seminars in Immunopathology. 34 (1): 43–62. doi:10.1007/s00281-011-0290-8. PMID 22037947. S2CID 14997530.

9.        Repetto O, De Re V (2017). "Coagulation and fibrinolysis in gastric cancer". Annals of the New York Academy of Sciences. 1404 (1): 27–48. doi:10.1111/nyas.13454. PMID 28833193. S2CID 10878584.