Povezanost faktora rizika, bazalnog nivoa virusa, genotipa virusa i stepena fibroze jetre sa odgovorom na terapiju kod bolesnika sa hroničnom hepatitis C virusnom infekcijom

  • Vuk R. Vuković Garrison Clinic, Kragujevac, Serbia
  • Dejan Baskić Center for Molecular Medicine and Stem Cell Research,Faculty of Medicinal Sciences, University of Kragujevac, Kragujevac, Serbia; Public Health Institute of Kragujevac, Kragujevac, Serbia
  • Željko Mijailović Department of Infectious Diseases, Clinical Center of Kragujevac, Kragujevac, Serbia
  • Predrag Djurdjević Department of Hematology, Clinical Center of Kragujevac, Kragujevac, Serbia
  • Danijela Jovanović Department of Hematology, Clinical Center of Kragujevac, Kragujevac, Serbia
  • Slobodanka Mitrović Center for Pathological Anatomy, Faculty of Medicinal Sciences, University of Kragujevac, Kragujevac, Serbia
  • Suzana Popović Center for Molecular Medicine and Stem Cell Research, Faculty of Medicinal Sciences, University of Kragujevac, Kragujevac, Serbia
DOI: https://doi.org/10.2298/5755
Ključne reči: hepatitis c||, ||hepatitis c, hepatitis, chronic||, ||hepatitis, hronični, treatment outcome||, ||lečenje, ishod, risk factors||, ||faktori rizika, genotype||, ||genotip, histological techniques||, ||histološke tehnike, disease transmission, infections||, ||bolest, prenošenje,

Sažetak


Uvod/Cilj. Hepatitis C virusna (HCV) infekcija predstavlja veliki medicinski, ekonomski i socijalni problem u svetu. Standardna terapija pegilovanim interferonom alfa 2a i ribavirinom dovodi do rezolucije bolesti kod samo oko 50% bolesnika. Cilj ovog rada bio je da se utvrdi povezanost faktora rizika od nastanka infekcije, genotipske zastupljenosti virusa i stepena patohistoloških promena jetre sa odgovorom na terapiju kod bolesnika sa hroničnom HCV infekcijom. Metode. Ispitivanjem je obuhvaćena grupa od 121 bolesnika sa hroničnom HCV infekcijom. Lečenje je sprovedeno tokom 24 nedelje za genotip virusa 2 i 3, i tokom 48 nedelja za genotip 1 i 4. Za određivanje genotipa virusa korišćena je metodologija lančane reakcije polimeraze. Stepen patohistoloških promena jetre određivan je standardnom hematoksilin-eozin metodom. Rezultati. U ispitivanoj grupi bolesnika najzastupljeniji HCV genotip bio je genotip 1. U grupi bolesnika bez odgovora na terapiju genotip 1 bio je zastupljen sa 100%, dok je u ostalim grupama, iako dominantno prisutan, njegov procenat bio znatno niži. Najveći broj virusnih čestica registrovan je u grupi bolesnika sa nepovoljnim odgovorom na terapiju. Najviši procenat bolesnika bez fibroze (F0) ili sa niskim stepenom fibroze (F1) nalazio se u grupi bolesnika sa povoljnim odgovorom na terapiju, dok se najveći broj bolesnika sa izraženom fibrozom (F3 i F4) nalazio među bolesnicima sa nepovoljnim odgovorom  na terapiju. Intravenska upotreba psihoaktivnih supstanci kao faktor rizika bila je prisutna u visokom procentu kod bolesnika sa povoljnim odgovorom, dok su transfuzija krvi i dijaliza bili vodeći faktor rizika za bolesnike kod kojih je došlo do relapsa HCV i kod onih bolesnika koji nisu odgovorili na terapiju. Zaključak. Rezultati ove studije pokazuju da je ishod lečenja hronične HCV infekcije povezan sa bazalnim nivoom HCV ribonukleinske kiseline u momentu postavljanja dijagnoze, genotipom HCV virusa, načinom infekcije i stepenom oštećenja parenhima jetre.

Reference

Lavanchy D. The global burden of hepatitis C. Liver Int 2009; 29( Suppl 1): 74−81.

Shepard CW, Finelli L, Alter MJ. Global epidemiology of hepatitis C virus infection. Lancet Infect Dis 2005; 5(9): 558−67.

Esteban JI, Sauleda S, Quer J. The changing epidemiology of hepatitis C virus infection in Europe. J Hepatol 2008; 48(1): 148−62.

Afdhal NH. The Natural History of Hepatitis C. Semin Liver Dis 2004; 24 Suppl 2: 3−8.

Poynard T, Bedossa P, Opolon P. Natural history of liver fibrosis progression in patients with chronic hepatitis C. The OBSVIRC, METAVIR, CLINIVIR, and DOSVIRC groups. Lancet 1997; 349(9055): 825−32.

Zein CO, Levy C, Basu A, Zein NN. Chronic hepatitis C and type II diabetes mellitus: a prospective cross-sectional study. Am J Gastroenterol 2005; 100(1): 48−55.

Fried MW, Shiffman ML, Reddy RK, Smith C, Marinos G, Gonçales FL, et al. Peginterferon alfa-2a plus ribavirin for chronic hepatitis C virus infection. N Engl J Med 2002; 347(13): 975−82.

Operskalski EA, Kovacs A. HIV/HCV co-infection: pathogenesis, clinical complications, treatment, and new therapeutic technologies. Curr HIV/AIDS Rep 2011; 8(1): 12−22.

Thompson C, Rogers G, Hewson P, Wright D, Anderson R, Cramp M, et al. Surveillance of cirrhosis for hepatocellular carcinoma: systematic review and economic analysis. Health Technol Assess 2007; 11(34): 1−206.

Knodell RG, Ishak KG, Black WC, Chen TS, Craig R, Kaplowitz N, et al. Formulation and application of a numerical scoring system for assessing histological activity in asymptomatic chronic active hepatitis. Hepatology 1981; 1(5): 431−5.

Berg T, Sarrazin C, Herrmann E, Hinrichsen H, Gerlach T, Zachoval R, et al. Prediction of treatment outcome in patients with chronic hepatitis C: significance of baseline parameters and viral dynamics during therapy. Hepatology 2003; 37(3): 600−9.

Pozzato G, Moretti M, Crocé LS, Sasso F, Kaneko S, Unoura M, et al. Interferon therapy in chronic hepatitis C virus: evidence of different outcome with respect to different viral strains. J Med Virol 1995; 45(4): 445−50.

Sarin SK, Kumar CK. Treatment of patients with genotype 3 chronic hepatitis C- current and future therapies. Liver Int 2012; 32(1 Suppl): 141−5.

Zein NN, Rakela J, Krawitt EL, Reddy KR, Tominaga T, Persing DH. Hepatitis C virus genotypes in the United States: epidemiology, pathogenicity, and response to interferon therapy. Collaborative Study Group. Ann Intern Med 1996; 125(8): 634−9.

Attaullah S, Khan S, Ali I. Hepatitis C virus genotypes in Pakistan: a systemic review. Virol J 2011; 8: 433.

Kamal SM, Nasser IA. Hepatitis C genotype 4: What we know and what we don't yet know. Hepatology 2008; 47(4): 1371−83.

Antonucci G, Angeletti C, Vairo F, Longo MA, Girardi E. Age and prediction of sustained virological response to hepatitis C virus (HCV) infection treatment based on 28-day decrease in HCV RNA levels. J Infect Dis 2009; 200(9): 1484−5.

Manns MP, McHutchison JG, Gordon SC, Rustgi VK, Shiffman M, Reindollar R, et al. Peginterferon alfa-2b plus ribavirin compared with interferon alfa-2b plus ribavirin for initial treatment of chronic hepatitis C: a randomised trial. Lancet 2001; 358(9286): 958−65.

Shiratori Y, Imazeki F, Moriyama M, Yano M, Arakawa Y, Yokosuka O, et al. Histologic improvement of fibrosis in patients with hepatitis C who have sustained response to interferon therapy. Ann Intern Med 2000; 132(7): 517−24.

Karino Y, Toyota J, Sugawara M, Miyazaki K, Kuwata Y, Yamazaki K, et al. Hepatitis C virus genotypes and hepatic fibrosis regulate 24-h decline of serum hepatitis C virus RNA during interferon therapy in patients with chronic hepatitis C. J Gastroenterol Hepatol 2003; 18(4): 404−10.

Objavljeno
2015/07/08
Broj časopisa
Vol. 72 Br. 6 (2015)
Rubrika
Originalni članak