Significance of protein C determination in obstetric practice
D.Kh. KHIZROEVA, I.A. MIKHAYLIDI, N.S. STULEVA
I.M. Sechenov First Moscow State Medical University, 8-2 Trubetskaya St. , Moscow, Russian Federation 119991
Khizroeva D.Kh.— Candidate of Medical Science, assistant of the Department of Obstetrics and Gynecology of Public Health Faculty, +7-915-361-90-73, e-mail: gemostasis@mail.ru
Stuleva N.S.—Candidate of Medical Science, assistant of the Department of Obstetrics and Gynecology of Public Health Faculty, +7-915-361-90-73, e-mail: gemostasis@mail.ru1
Mikhaylidi I.A. — postgraduate student of the Department of Obstetrics and Gynecology of Public Health Faculty, +7-915-361-90-73, e-mail: gemostasis@mail.ru1
Activated protein C (APC), interacting with the endothelial protein C receptor (EPCR), receptors, activated by proteases (PAR), apolipoprotina E2 receptor and integrins, has various effects on the hemostatic system (anticoagulant effect) and the immune system (cytoprotective effect).Value of protein C is best demonstrated with prothrombotic and inflammatory complications caused by protein C deficiency or violation of its functions, which in clinical practice appear as ischemic stroke, inflammatory disease, atherosclerosis, vascular complications and obstetric problems.Learning and understanding the biological function of APC provides control over coagulation and inflammation and understanding the use of drugs with protein C as anticoagulant and cytoprotector in clinical practice of a physician.
Key words: activated protein С, endothelial protein C receptor, factor V Leiden mutation, АРС resistance, thromboses.
REFERENCES
1. Weiler H. Multiple receptor-mediated functions of activated protein C. Hamostaseologie, 2011, vol. 31, no. 3, pp. 185-195. DOI:10.5482/ha-1166.
2. Patracchini P., Aiello V., Palazzi P., Calzolari E., Bernardi F. Sublocalization of the human protein C gene on chromosome 2q13-14. Human Genetics, 1989, vol. 81, no. 2, pp. 191-192.
3. Gusina A.A., Gusina N.B. Genetic defects in the pro- and anti-coagulant proteins as risk factors for venous thrombosis. Meditsinskie novosti, 2006, no. 9, pp. 10-14. (in Russ.).
4. Gorbacheva L.R. Neyroprotektivnoe deystvie klyuchevykh proteinaz gemostaza. Dokt. biol. nauk. diss. Avtoref. [Neuroprotective effect of keyhemostasis proteinase. Dr. biol. sci. diss. Synopsis]. Moscow, 2008. 49 p.
5. Spek C.A., Reitsma P.H. Genetic risk factors for venous thrombosis. Molecular Genetics and Metabolism, 2000, vol. 71, no. 1-2, pp. 51-61. DOI: 10.1006/mgme.2000.3051.
6. Larsen T.B., Lassen J.F., Brandslund I., Byriel L., Petersen G.B., Nørgaard-Pedersen B. The Arg506Gln mutation (FV Leiden) among a cohort of 4188 unselected Danish newborns. Thrombosis Research, 1998, vol. 89, no. 5, pp. 211-215. DOI: 10.1016/S0049-3848(98)00010-3.
7. Voetsch B., Loscalzo J. Genetic determinants of arterial thrombosis. Arteriosclerosis, Thrombosis, and Vascular Biology, 2004, vol. 24, no. 2, pp. 216-229. DOI: 10.1161/01.ATV.0000107402.79771.fc.
8. Mosnier L.O., Zlokovic B.V., Griffin J.H. The cytoprotective protein C pathway. Blood, 2007, vol. 109, no. 8, pp.3161-3172. DOI: 10.1182/blood-2006-09-003004.
9. Griffin J.H., Mosnier L.O., Zlokovic B.V. Protein C anticoagulant and cytoprotective pathways. International Journal of Hematology, 2012, vol. 95, no. 4, pp. 333-345. DOI: 10.1007/s12185-012-1059-0.
10. Chen X.D., Tian L., Li M., Jin W., Zhang H.-K., Zheng C.-F. Relationship between endothelial cell protein C receptor gene 6936A/G polymorphisms and deep venous thrombosis. Chinese Medical Journal, 2011, vol. 124, no. 1, pp. 72-75. DOI: 10.3760/cma.j.issn.0366-6999.2011.01.014.
11. Saposnik B., Reny J.-L., Gaussem P., Emmerich J., Aiach M., Gandrille S. A haplotype of the EPCR gene is associated with increased plasma levels of sEPCR and is a candidate risk factor for thrombosis. Blood, 2004, vol. 103, no. 4, pp. 1311-1318. DOI: 10.1182/blood-2003-07-2520.
12. Makatsariya A.D., Bitsadze V.O. Trombofilii i protivotromboticheskaya terapiya v akusherskoy praktike [Thrombophilia and antithrombotic therapy in obstetric practice]. Moscow, Triada-X Publ., 2003. 904 p.
13. Dahlbäck B., Carlsson M., Svensson P.J. Familial thrombophilia due to a previously unrecognized mechanism characterized by poor anticoagulant response to activated protein C: Prediction of a cofactor to activated protein C. Proceedings of the National Academy of Sciences of the United States of America, 1993, vol. 90, no. 3, pp. 1004-1008. DOI: 10.1073/pnas.90.3.1004.
14. Gerhardt A., Scharf R.E., Beckmann M.W., Struve S., Bender H.G., Pillny M., Sandmann W., Zotz R.B. Prothrombin and factor V mutations in women with a history of thrombosis during pregnancy and the puerperium. New England Journal of Medicine, 2000, vol. 342, no. 6, pp. 374-380. DOI: 10.1056/NEJM200002103420602.
15. Meinardi J.R., Middeldorp S., de Kam P.J., Koopman M.M.W., Van Pampus E.C.M., Hamulyák K., Prins M.H., et al. Increased risk for fetal loss in carriers of the factor V Leiden mutation. Annals of Internal Medicine, 1999, vol. 130, no. 9, pp. 736-739.
16. Baré S.N., Póka R., Balogh I., Ajzner E. Factor V Leiden as a risk factor for miscarriage and reduced fertility. Australian and New Zealand Journal of Obstetrics and Gynaecology, 2000, vol. 40, no. 2, pp. 186-190.