Prothrombin fragment 1+2 (F1+2), also written as prothrombin fragment 1.2 (F1.2), is a polypeptide fragment of prothrombin (factor II) generated by the in vivo cleavage of prothrombin into thrombin (factor IIa) by the enzyme prothrombinase (a complex of factor Xa and factor Va).[1][2][3] It is released from the N-terminus of prothrombin.[3] F1+2 is a marker of thrombin generation and hence of coagulation activation.[4][3][1] It is considered the best marker of in vivo thrombin generation.[1]
F1+2 levels can be quantified with blood tests and is used in the diagnosis of hyper- and hypocoagulable states and in the monitoring of anticoagulant therapy.[4][1] It was initially determined with a radioimmunoassay, but is now measured with several enzyme-linked immunosorbent assays.[1]
The molecular weight of F1+2 is around 41 to 43 kDa.[4][1] Its biological half-life is 90 minutes and it persists in blood for a few hours after formation.[4][3][1] The half-life of F1+2 is relatively long, which makes it more reliable for measuring ongoing coagulation than other markers like thrombin–antithrombin complexes and fibrinopeptide A.[1][3] Concentrations of F1+2 in healthy individuals range from 0.44 to 1.11 nM.[4]
F1+2 levels increase with age.[3] Levels of F1+2 have been reported to be elevated in venous thromboembolism, protein C deficiency, protein S deficiency, atrial fibrillation, unstable angina, acute myocardial infarction, acute stroke, atherosclerosis, peripheral arterial disease, and in smokers.[3][1] Anticoagulants have been found to reduce F1+2 levels.[1] F1+2 levels are increased with pregnancy[5] and by ethinylestradiol-containing birth control pills.[6] Conversely, they do not appear to be increased with estetrol- or estradiol-containing birth control pills.[6] However, F1+2 levels have been reported to be increased with oral estrogen-based menopausal hormone therapy, whereas transdermal estradiol-based menpausal hormone therapy appears to result in less or no consistent increase.[7]
References
edit- ^ a b c d e f g h i j Páramo JA (2010). "Prothrombin fragments in cardiovascular disease". Adv Clin Chem. Advances in Clinical Chemistry. 51: 1–23. doi:10.1016/s0065-2423(10)51001-1. ISBN 9780123809810. PMID 20857616.
- ^ Krishnaswamy S (June 2013). "The transition of prothrombin to thrombin". J Thromb Haemost. 11 Suppl 1 (1): 265–76. doi:10.1111/jth.12217. PMC 3713535. PMID 23809130.
- ^ a b c d e f g Merlini PA, Ardissino D (1995). "Laboratory Measurement of Thrombin Activity--What Every Clinician Scientist Needs to Know". J Thromb Thrombolysis. 2 (2): 85–92. doi:10.1007/BF01064374. PMID 10608009. S2CID 28203940.
- ^ a b c d e Dati F, Pelzer H, Wagner C (1998). "Relevance of markers of hemostasis activation in obstetrics/gynecology and pediatrics". Semin Thromb Hemost. 24 (5): 443–8. doi:10.1055/s-2007-996037. PMID 9834011. S2CID 27803157.
- ^ Hellgren M (April 2003). "Hemostasis during normal pregnancy and puerperium". Semin Thromb Hemost. 29 (2): 125–30. doi:10.1055/s-2003-38897. PMID 12709915. S2CID 22082884.
- ^ a b Douxfils J, Morimont L, Bouvy C (November 2020). "Oral Contraceptives and Venous Thromboembolism: Focus on Testing that May Enable Prediction and Assessment of the Risk". Semin Thromb Hemost. 46 (8): 872–886. doi:10.1055/s-0040-1714140. PMID 33080636. S2CID 224821517.
- ^ Hemelaar M, van der Mooren MJ, Rad M, Kluft C, Kenemans P (September 2008). "Effects of non-oral postmenopausal hormone therapy on markers of cardiovascular risk: a systematic review". Fertil Steril. 90 (3): 642–72. doi:10.1016/j.fertnstert.2007.07.1298. PMID 17923128.
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