Prothrombin fragment 1+2: Difference between revisions

Revision as of 22:34, 29 January 2023

Latest revision as of 12:22, 19 January 2024

(One intermediate revision by one other user not shown)

Line 1:

{{cs1 config|name-list-style=vanc}}

'''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]]'' [[bond cleavage|cleavage]] of prothrombin into [[thrombin]] (factor IIa) by the [[enzyme]] [[prothrombinase]] (a complex of [[factor Xa]] and [[factor Va]]).<ref name="pmid20857616">{{cite journal | vauthors = Páramo JA | title = Prothrombin fragments in cardiovascular disease | journal = Adv Clin Chem | series = Advances in Clinical Chemistry | volume = 51 | issue = | pages = 1–23 | date = 2010 | pmid = 20857616 | doi = 10.1016/s0065-2423(10)51001-1 | isbn = 9780123809810 | url = }}</ref><ref name="pmid23809130">{{cite journal | vauthors = Krishnaswamy S | title = The transition of prothrombin to thrombin | journal = J Thromb Haemost | volume = 11 Suppl 1 | issue = 1| pages = 265–76 | date = June 2013 | pmid = 23809130 | pmc = 3713535 | doi = 10.1111/jth.12217 | url = }}</ref><ref name="pmid10608009" /> It is released from the [[N-terminus]] of prothrombin.<ref name="pmid10608009" /> F1+2 is a marker of [[thrombin generation]] and hence of [[coagulation]] activation.<ref name="pmid9834011">{{cite journal | vauthors = Dati F, Pelzer H, Wagner C | title = Relevance of markers of hemostasis activation in obstetrics/gynecology and pediatrics | journal = Semin Thromb Hemost | volume = 24 | issue = 5 | pages = 443–8 | date = 1998 | pmid = 9834011 | doi = 10.1055/s-2007-996037 | s2cid = 27803157 | url = }}</ref><ref name="pmid10608009" /><ref name="pmid20857616" /> It is considered the best marker of ''in vivo'' thrombin generation.<ref name="pmid20857616" />

F1+2 levels can be quantified with [[blood test]]s and is used in the diagnosis of [[hypercoagulability|hyper-]] and [[hypocoagulable]] states and in the monitoring of [[anticoagulant]] therapy.<ref name="pmid9834011" /><ref name="pmid20857616" /> It was initially determined with a [[radioimmunoassay]], but is now measured with several [[enzyme-linked immunosorbent assay]]s.<ref name="pmid20857616" />

The [[molecular weight]] of F1+2 is around 41 to 43&nbsp;kDa.<ref name="pmid9834011" /><ref name="pmid20857616" /> Its [[biological half-life]] is 90&nbsp;minutes and it persists in blood for a few hours after formation.<ref name="pmid9834011" /><ref name="pmid10608009">{{cite journal | vauthors = Merlini PA, Ardissino D | title = Laboratory Measurement of Thrombin Activity--What Every Clinician Scientist Needs to Know | journal = J Thromb Thrombolysis | volume = 2 | issue = 2 | pages = 85–92 | date = 1995 | pmid = 10608009 | doi = 10.1007/BF01064374 | s2cid = 28203940 | url = }}</ref><ref name="pmid20857616" /> The half-life of F1+2 is relatively long, which makes it more reliable for measuring ongoing coagulation than other markers like [[thrombin–antithrombin complex]]es and [[fibrinopeptide A]].<ref name="pmid20857616" /><ref name="pmid10608009" /> Concentrations of F1+2 in healthy individuals range from 0.44 to 1.11&nbsp;nM.<ref name="pmid9834011" />

F1+2 levels increase with [[aging|age]].<ref name="pmid10608009" /> 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 [[smoking|smoker]]s.<ref name="pmid10608009" /><ref name="pmid20857616" /> Anticoagulants have been found to reduce F1+2 levels.<ref name="pmid20857616" /> F1+2 levels are increased with [[pregnancy]]<ref name="pmid12709915">{{cite journal | vauthors = Hellgren M | title = Hemostasis during normal pregnancy and puerperium | journal = Semin Thromb Hemost | volume = 29 | issue = 2 | pages = 125–30 | date = April 2003 | pmid = 12709915 | doi = 10.1055/s-2003-38897 | s2cid = 22082884 | url = }}</ref> and by [[ethinylestradiol]]-containing [[birth control pill]]s.<ref name="pmid33080636">{{cite journal | vauthors = Douxfils J, Morimont L, Bouvy C | title = Oral Contraceptives and Venous Thromboembolism: Focus on Testing that May Enable Prediction and Assessment of the Risk | journal = Semin Thromb Hemost | volume = 46 | issue = 8 | pages = 872–886 | date = November 2020 | pmid = 33080636 | doi = 10.1055/s-0040-1714140 | s2cid = 224821517 | url = }}</ref> Conversely, they do not appear to be increased with [[estetrol (medication)|estetrol]]- or [[estradiol-containing birth control pill]]s.<ref name="pmid33080636"/> However, F1+2 levels have been reported to be increased with oral [[estrogen (medication)|estrogen]]-based [[menopausal hormone therapy]], whereas [[transdermal]] estradiol-based menpausal hormone therapy appears to result in less or no consistent increase.<ref name="pmid17923128">{{cite journal | vauthors = Hemelaar M, van der Mooren MJ, Rad M, Kluft C, Kenemans P | title = Effects of non-oral postmenopausal hormone therapy on markers of cardiovascular risk: a systematic review | journal = Fertil Steril | volume = 90 | issue = 3 | pages = 642–72 | date = September 2008 | pmid = 17923128 | doi = 10.1016/j.fertnstert.2007.07.1298 | url = | doi-access = free }}</ref>

==References==