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Thrombin–antithrombin complex

From Wikipedia, the free encyclopedia

Thrombin–antithrombin complex (TAT) is a protein complex of thrombin and antithrombin.[1][2] It is a marker of net activation of coagulation.[3]

Formation and elimination

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TAT is formed in response to the high thrombin level caused by coagulation following a ruptured vessel. Since thrombin is rapidly bound by antithrombin, TAT is a useful measure for thrombin level in the blood. Thrombin can pass the blood–brain barrier, destroying neurons and potentially causing cerebral edemas.[4]

The half-life of TAT is approximately 15 minutes.[5]

Disease

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Cerebral hemorrhage

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TAT levels were studied in patients with intracranial blood clot removal within 24 hours after intracerebral hemorrhage (ICH) in Fujian from 2006 to 2008. This study revealed that TAT levels in the plasma and hematoma fluid of these patients are higher than that those of healthy people, and that TAT levels decreased in the patients after surgery and increased in the patients that had a hemorrhage again. The TAT levels correlate with the severity of ICH according to GCS and NIHSS, and so, the study concluded that TAT complex may be useful in the prognosis for post-operative ICH-patients.[4]

Influences

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TAT levels are increased with pregnancy[6] and by ethinylestradiol-containing birth control pills.[7] They have also been reported to be increased by menopausal hormone therapy, although findings are mixed,[3][8] and with high-dose parenteral estradiol therapy for prostate cancer.[9][10][11]

References

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  1. ^ Lippi G, Cervellin G, Franchini M, Favaloro EJ (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.
  2. ^ Zwicker JI, Furie BC, Furie B (2007). "Cancer-associated thrombosis". Crit. Rev. Oncol. Hematol. 62 (2): 126–36. doi:10.1016/j.critrevonc.2007.01.001. PMID 17293122.
  3. ^ 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.
  4. ^ a b Wu, C. -H.; Yang, R. -L.; Huang, S. -Y.; Li, H. -Z.; Wang, K. -Y.; Yang, D. -H.; Yan, X. -H.; Xue, X. -H.; Wu, S. -Y. (August 2011). "Analysis of thrombin-antithrombin complex contents in plasma and hematoma fluid of hypertensive intracerebral hemorrhage patients after clot removal: TAT in ICH patients". European Journal of Neurology. 18 (8): 1060–1066. doi:10.1111/j.1468-1331.2010.03336.x. PMID 21244583.
  5. ^ 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.
  6. ^ 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.
  7. ^ 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.
  8. ^ Skouby, Sven O.; Sidelmann, Johannes J. (2 July 2020). "Menopausal Hormone Therapy (MHT) and Venous Thrombosis". Managing the Menopause. Cambridge University Press. pp. 223–233. doi:10.1017/9781108869102.023.
  9. ^ 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.
  10. ^ 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): 4726–4726. doi:10.1200/jco.2004.22.90140.4726. eISSN 1527-7755. ISSN 0732-183X.
  11. ^ 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.