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The [[molecular weight]] of F1+2 is around 41 to 43 kDa.<ref name="pmid9834011" /><ref name="pmid20857616" /> Its [[biological half-life]] is 90 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 | 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 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 | 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 | url = }}</ref> Conversely, they do not appear to be increased with [[estetrol (medication)|estetrol]]- or [[estradiol-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 | url = }}</ref> 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 = }}</ref>
==References==
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