Wikipedia

Coagulation activation marker

Coagulation activation markers are biomarkers of net activation of coagulation and fibrinolysis.[1][2] Examples include prothrombin fragment 1+2 (F1+2), thrombin–antithrombin complex (TAT), fibrinopeptide A (FpA), fibrin monomers (FMs), plasmin-α2-antiplasmin complex (PAP), activated protein C–protein C inhibitor (APC-PCI), and D-dimer (DD).[1][2] These compounds are markers of thrombin generation (F1+2, TAT, APC-PCI), fibrin generation (FpA, FMs), and fibrinolysis (DD, PAP).[1][2] Coagulation activation markers, particularly D-dimer, are useful in the diagnosis of acute venous thromboembolism.[1][3] They may also be useful in the assessment of hypercoagulability and venous thromboembolism risk.[4][5][6]

Levels of coagulation activation markers are increased with pregnancy,[7] with estrogen-containing birth control pills,[8] with menopausal hormone therapy,[9][6] and with high-dose parenteral estradiol therapy for prostate cancer.[10][11][12] Transdermal estradiol appears to have less influence on coagulation activation markers than oral estrogens in menopausal hormone therapy.[9] Birth control pills containing estradiol or estetrol also appear to have less influence on coagulation activation markers than ethinylestradiol-containing birth control pills.[8]

Markers of platelet activation (primary hemostasis) include platelet factor 4 (PF4), β-thromboglobulin (β-TG), and P-selectin.[13][14]

References

edit
  1. ^ a b c d Lippi G, Cervellin G, Franchini M, Favaloro EJ (November 2010). "Biochemical markers for the diagnosis of venous thromboembolism: the past, present and future". J Thromb Thrombolysis. 30 (4): 459–71. doi:10.1007/s11239-010-0460-x. PMID 20213258. S2CID 23806848.
  2. ^ a b c 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.
  3. ^ Anghel L, Sascău R, Radu R, Stătescu C (March 2020). "From Classical Laboratory Parameters to Novel Biomarkers for the Diagnosis of Venous Thrombosis". Int J Mol Sci. 21 (6): 1920. doi:10.3390/ijms21061920. PMC 7139541. PMID 32168924.
  4. ^ Baglin T (August 2011). "Using the laboratory to predict recurrent venous thrombosis". Int J Lab Hematol. 33 (4): 333–42. doi:10.1111/j.1751-553X.2011.01345.x. PMID 21692994. S2CID 30451755.
  5. ^ Kyrle PA, Rosendaal FR, Eichinger S (December 2010). "Risk assessment for recurrent venous thrombosis". Lancet. 376 (9757): 2032–9. doi:10.1016/S0140-6736(10)60962-2. PMID 21131039. S2CID 31610364.
  6. ^ a b Cushman M, Larson JC, Rosendaal FR, Heckbert SR, Curb JD, Phillips LS, Baird AE, Eaton CB, Stafford RS (April 2018). "Biomarkers, menopausal hormone therapy and risk of venous thrombosis: The Women's Health Initiative". Res Pract Thromb Haemost. 2 (2): 310–319. doi:10.1002/rth2.12100. PMC 5974918. PMID 30046733.
  7. ^ 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.
  8. ^ 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.
  9. ^ a b 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.
  10. ^ Ockrim JL, Lalani EN, Kakkar AK, Abel PD (August 2005). "Transdermal estradiol therapy for prostate cancer reduces thrombophilic activation and protects against thromboembolism". J Urol. 174 (2): 527–33, discussion 532–3. doi:10.1097/01.ju.0000165567.99142.1f. PMID 16006886.
  11. ^ Kohli, M.; Alikhan, M. A.; Spencer, H. J.; Carter, G. (15 July 2004). "Phase I trial of intramuscular estradiol valerate (I/M-E) in hormone refractory prostate cancer". Journal of Clinical Oncology. 22 (14 suppl): 4726. doi:10.1200/jco.2004.22.90140.4726. eISSN 1527-7755. ISSN 0732-183X.
  12. ^ Kohli M (January 2006). "Phase II study of transdermal estradiol in androgen-independent prostate carcinoma". Cancer. 106 (1): 234–5, author reply 235. doi:10.1002/cncr.21528. PMID 16284988. S2CID 11047031.
  13. ^ Gurney D, Lip GY, Blann AD (June 2002). "A reliable plasma marker of platelet activation: does it exist?". Am J Hematol. 70 (2): 139–44. doi:10.1002/ajh.10097. PMID 12111787. S2CID 39870245.
  14. ^ Schutte MH, Kleemann R, Nota NM, Wiepjes CM, Snabel JM, T'Sjoen G, Thijs A, den Heijer M (2022). "The effect of transdermal gender-affirming hormone therapy on markers of inflammation and hemostasis". PLOS ONE. 17 (3): e0261312. Bibcode:2022PLoSO..1761312S. doi:10.1371/journal.pone.0261312. PMC 8923509. PMID 35290388.



 

This hematology article is a stub. You can help Wikipedia by expanding it.

Retrieved from "https://en.wikipedia.org/w/index.php?title=Coagulation_activation_marker&oldid=1170208627"