电邮这篇文章 Role of polymorphic markers for the genes of hemostasis and platelet receptors in liver fibrosis progression in patients with chronic hepatitis C
- 作者: Starostina EE1, Samokhodskaya LM1, Rozina TP1,2, Krasnova TN1,2, Yarovaya EB1, Mukhin NA1,3
-
隶属关系:
- МГУ им. М.В. Ломоносова
- Первый Московский государственный медицинский университет им. И.М. Сеченова Минздрава России
- Первый Московский государственный медицинский университет им. И.М. Сеченова Минздрава России
- 期: 卷 88, 编号 8 (2016)
- 页面: 93-98
- 栏目: Editorial
- URL: https://bakhtiniada.ru/0040-3660/article/view/32097
- DOI: https://doi.org/10.17116/terarkh201688893-98
- ID: 32097
如何引用文章
全文:
详细
Aim. To estimate the clinical and prognostic value of the carriage of different allele variants of the gene polymorphisms of the coagulation system and platelet receptors in the progression of liver fibrosis (LF) in patient with chronic hepatitis C (CHC). Subjects and methods. The investigation enrolled 177 patients with CHC and liver cirrhosis at its outcome who were divided into 2 groups according to the rate of LF progression: 1) 89 patients with rapid (rapid fibrosis) and 2) 88 patients with slow (slow fibrosis) progression. The polymorphism of the study genes was studied using a real-time polymerase chain reaction and a melting curve analysis. Results. In CHC patients, the FV 1691G/A genotype was more often in the rapid progressors than that in the slow progressors (10.11% vs 1.14%; p=0.011). The A allele of the 1691 G/A FV gene was more common in the rapid fibrosis group than that in the slow fibrosis group (1.7% vs 5.56%, odd ratio 9.787; p=0.139). In our investigation, the polymorphic marker GA in the FII 20210 G/A gene, as well as the 4G allele (5G4G + 4G4G genotypes) and the 4G allele of PAI-I -675 5G/4G were more often seen in the rapid fibrosis group than that in the slow fibrosis group; the detection rate was only at the trend level (p=0.118, p=0.112, and p=0.117 respectively). There were no significant differences between the groups in the spread of variant genotypes and alleles of other study genes. Integral model construction by coding «profibrogenic» genotypes (FV 1691 G/A, FII 20210 G/A, PAI-I -675 5G/4G) showed that the fibrosis progression rate expressed as fibrosis units annually also increased with higher total scores (p=0.039), indicating the combined effect of these genes. Conclusion. The carriage of mutant genotypes of FV 1691 G/A, FII 20210 G/A, and PAI-I -675 5G/4G genes is a prognostic factor for rapid CHC progression.
作者简介
E Starostina
МГУ им. М.В. ЛомоносоваМосква, Россия
L Samokhodskaya
МГУ им. М.В. ЛомоносоваМосква, Россия
T Rozina
МГУ им. М.В. Ломоносова; Первый Московский государственный медицинский университет им. И.М. Сеченова Минздрава России
T Krasnova
МГУ им. М.В. Ломоносова; Первый Московский государственный медицинский университет им. И.М. Сеченова Минздрава России
E Yarovaya
МГУ им. М.В. ЛомоносоваМосква, Россия
N Mukhin
МГУ им. М.В. Ломоносова; Первый Московский государственный медицинский университет им. И.М. Сеченова Минздрава России
参考
- Таратина О.В., Краснова Т.Н., Самоходская Л.М., Лопаткина Т.Н., Ткачук В.А., Мухин Н.А. Полиморфизм генов эндотелиальной дисфункции и скорость прогрессирования фиброза печени при хроническом гепатите С. Терапевтический архив. 2014;86(4):45-51.
- Самоходская Л.М., Игнатова Т.М., Абдуллаев С.М., Краснова Т.Н., Некрасова Т.П., Мухин Н.А., Ткачук В.А. Прогностическое значение комбинации аллельных вариантов генов цитокинов и гемохроматоза у больных хроническим гепатитом С. РЖГГК. 2007;17(2):50-56.
- Poujol-Robert A, Boelle PY, Poupon R, Robert A. Factor V Leiden as a risk factor for cirrhosis in chronic hepatitis C. Hepatology. 2004;39(4):1174-1175. doi: 10.1002/hep.20166
- Levi M, Dik K. Fibrophilia: a new disease entity? J Thromb Haemost. 2008;6(8):1334-1335. doi: 10.1111/j.1538-7836.2008.03058.x
- Anstee QM, Goldin RD, Wright M, Martinelli A, Cox R, Thursz MR. Coagulation status modulates murine hepatic fibrogenesis: implications for the development of novel therapies. J Thromb Haemost. 2008;6(8):1336-1343. doi: 10.1111/j.1538-7836.2008.03015.x
- Mannucci PM. Laboratory detection of inherited thrombophilia: a historical perspective. Semin Thromb Hemost. 2005;31(1):5-10. doi: 10.1055/s-2005-863799
- Gabriel A, Kukla M, Wilk M., Liszka L, Petelenz M.,Musialik J. Angiogenesis in chronic hepatitis C is associated with inflammatory activity grade and fibrosis stage. Pathol Res Pract. 2009;205(11):758-764. doi: 10.1016/j.prp.2009.06.007
- Poynard T, Ratziu V, Benmanov Y, Di Martino V, Bedossa P, Opolon P. Fibrosis in patients with chronic hepatitis C: detection and significance. Semin Liver Dis. 2000;20(1):47-55.
- Wright M, Goldin R, Hellier S, Knapp S, Frodsham A, Hennig B, Hill A, Apple R, Cheng S, Thomas H, Thursz M. Factor V Leiden polymorphism and the rate of fibrosis development in chronic hepatitis C virus infection. Gut. 2003;52(8):1206-1210.
- Goulding C, O’brien C, Egan H, Hegarty JE, Mcdonald G, O’farrelly C, White B, Kelleher D, Norris S. The impact of inherited prothrombotic risk factors on individuals chronically infected with hepatitis C virus from a single source. J Viral Hepat. 2007;14(4):255-2559. doi: 10.1111/j.1365-2893.2006.00790.x
- Maharshak N, Halfon P, Deutsch V, Peretz H, Berliner S, Fishman S, Zelber-Sagi S, Rozovski U, Leshno M, Oren R. Increased fibrosis progression rates in hepatitis C patients carrying the prothrombin G20210A mutation. World J Gastroenterol. 2011;17(45):5007-5013. doi: 10.3748/wjg.v17.i45.5007
- Plompen EP, Murad SD, Hansen BE, Loth DW, Schouten JN, Taimr P, Hofman A, Uitterlinden AG, Stricker BH, Janssen HL, Leebeek FW. Prothrombotic Genetic Risk Factors are associated with an Increased Risk of Liver Fibrosis in the General Population: The Rotterdam Study. J Hepatol. 2015. doi: 10.1016/j.jhep.2015.07.026
- Lim BC, Ariens RA, Carter AM, Weisel JW, Grant PJ. Genetic regulation of fibrin structure and function: complex gene-environment interactions may modulate vascular risk. Lancet. 2003;361(9367):1424-1431. doi: 10.1016/s0140-6736(03)13135-2
- Tsantes AE, Nikolopoulos GK, Bagos PG, Bonovas S, Kopterides P, Vaiopoulos G. The effect of the plasminogen activator inhibitor-1 4G/5G polymorphism on the thrombotic risk. Thromb Res. 2008;122(6):736-742. doi: 10.1016/j.thromres.2007.09.005
- Dik K, De Bruijne J, Takkenberg RB, Roelofs JJ, Tempelmans MJ, Dijkgraaf MG, Gelderblom HC, Reesink HW, Meijers JC, Jansen PL, Levi M. Factor XIII Val34Leu mutation accelerates the development of fibrosis in patients with chronic hepatitis B and C. Hepatol Res. 2012;42(7):668-676. doi: 10.1111/j.1872-034X.2011.00963.x
- Adinolfi LE, Ingrosso D, Cesaro G, Cimmino A, D’anto M, Capasso R, Zappia V, Ruggiero G. Hyperhomocysteinemia and the MTHFR C677T polymorphism promote steatosis and fibrosis in chronic hepatitis C patients. Hepatology. 2005;41(5):995-1003. doi: 10.1002/hep.20664
- Toniutto P, Fabris C, Falleti E, Cussigh A, Fontanini E, Bitetto D, Fornasiere E, Minisini R, De Feo T, Marangoni F, Pirisi M. Methylenetetrahydrofolate reductase C677T polymorphism and liver fibrosis progression in patients with recurrent hepatitis C. Liver Int. 2008;28(2):257-263. doi: 10.1111/j.1478-3231.2007.01591.x
- Asselah T, Bieche I, Laurendeau I, Paradis V, Vidaud D, Degott C, Martinot M, Bedossa P, Valla D, Vidaud M, Marcellin P. Liver gene expression signature of mild fibrosis in patients with chronic hepatitis C. Gastroenterology. 2005;129(6):2064-2075. doi: 10.1053/j.gastro.2005.09.010
- Nejjari M, Couvelard A, Mosnier JF, Moreau A, Feldmann G, Degott C, Marcellin P, Scoazec JY. Integrin up-regulation in chronic liver disease: relationship with inflammation and fibrosis in chronic hepatitis C. J Pathol. 2001;195(4):473-481. doi: 10.1002/path.964
补充文件
