Impact of direct-acting antiviral on subclinical atherosclerosis in chronic hepatitis C infected patients

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Published Mar 10, 2024
https://doi.org/10.62438/tunismed.v102i3.4601
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Vol. 102 No. 3 (2024): Tunis med mar 2024

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Sarra Laabidi
Department of Gastroenterology , Mohamed Taher Maamouri Hospital, Nabeul, Tunisia
Mouna Medhioub
Department of Gastroenterology , Mohamed Taher Maamouri Hospital, Nabeul, Tunisia
Amal Khsiba
Department of Gastroenterology , Mohamed Taher Maamouri Hospital, Nabeul, Tunisia
Asma Bach Ali
Department of Biology ,Mohamed Taher Maamouri Hospital, Nabeul, Tunisia
Asma Ben Mohamed
Department of Gastroenterology , Mohamed Taher Maamouri Hospital, Nabeul, Tunisia
Lamine Hamzaoui
Department of Gastroenterology , Mohamed Taher Maamouri Hospital, Nabeul, Tunisia

Abstract

Introduction: The impact of direct antiviral drugs (DAAs) on extrahepatic manifestations in chronic hepatitis C (CHC) has been poorly studied.


Aim: To assess the prevalence of subclinical atherosclerosis in patients with CHC and the impact of DAAs on atherosclerotic lesions.


Methods A 5-year prospective evaluative study, including patients followed for CHC at hepato-gastroenterology department. The subclinical atherosclerosis was assessed by ultrasound measurement of carotid intima-media thickness (IMTc) and the highest IMTc measurements from the left and right side defined the IMTc maximum (IMTc max). IMTc>75th percentile (IMTc75) define subclinical atherosclerosis with high cardiovascular risk. Patients were evaluated before (T0) and one year after DAAs therapy achievement (T1).


Results: At time T0, forty patients (median age: 55 y.; sex ratio M / F = 0.48), were included. Average value of IMTc max was 0.68 ± 0.16 mm. Subclinical atherosclerosis was noted in 82.5 %. At time T1, 28 patients were evaluated, all of whom completed sustained virological response (SVR). Compared to time T0, there was a significant increase in cholesterol (p = 0.001) and triglyceride (p = 0.009) levels. IMTc max was significantly higher at time T1 compared to T0 (0.75 Vs 0.67 mm, p = 0.04). Prevalence of IMTc75 was 82.1% at time T0 and 75% at time T1 (p=0.5).


Conclusions: SVR, in CHC patients treated with DAA, was associated with worsening of carotid atherosclerotic lesions.

Keywords:

Hepatitis C virus , Chronic viral hepatitis , atherosclerosis, Antiviral therapy

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References

  1. Petruzziello A, Marigliano S, Loquercio G, Cozzolino A, Cacciapuoti C. Global epidemiology of hepatitis C virus infection: an up-date of the distribution and circulation of hepatitis C virus genotypes. World J Gastroenterol. 2016;22(34):7824 40.
  2. Negro F, Forton D, Craxì A, Sulkowski MS, Feld JJ, Manns MP. Extrahepatic Morbidity and Mortality of Chronic Hepatitis C. Gastroenterology. 2015;149(6):1345 60.
  3. Kukla M, Piotrowski D, Waluga M, Hartleb M. Review article Insulin resistance and its consequences in chronic hepatitis C. Clin Exp Hepatol. 2015;1:17 29.
  4. Adinolfi LE, Restivo L, Zampino R, Guerrera B, Lonardo A, Ruggiero L, et al. Chronic HCV infection is a risk of atherosclerosis. Role of HCV and HCV-related steatosis. Atherosclerosis. 2012;221(2):496 502.
  5. Boddi M, Abbate R, Chellini B, Giusti B, Solazzo V, Sofi F, et al. HCV infection facilitates asymptomatic carotid atherosclerosis: preliminary report of HCV RNA localization in human carotid plaques. Dig Liver Dis. 2007;39:S55 60.
  6. Nahon P, Bourcier V, Layese R, Audureau E, Cagnot C, Marcellin P, et al. Eradication of Hepatitis C Virus Infection in Patients With Cirrhosis Reduces Risk of Liver and Non-Liver Complications. Gastroenterology. 2017;152(1):142-56.
  7. Salama II, Raslan HM, Abdel-Latif GA, Salama SI, Sami SM, Shaaban FA, et al. Impact of direct-acting antiviral regimens on hepatic and extrahepatic manifestations of hepatitis C virus infection. World J Hepatol. 2022;27;14(6):1053-73.
  8. Roguljic H, Nincevic V, Bojanic K, Kuna L, Smolic R, Vcev A, et al. Impact of DAA Treatment on Cardiovascular Disease Risk in Chronic HCV Infection: An Update. Front Pharmacol. 2021;11;12:67.
  9. EASL Recommendations on Treatment of Hepatitis C 2016. J Hepatol. 2017;66(1):153 94.
  10. Société tunisienne de gastro-entérologie. Le nouveau consensus tunisien sur le VHC. Tunis:
  11. STGE; 2022.
  12. Alberti KG, Zimmet P, Shaw J. Metabolic syndrome-a new world-wide definition. A Consensus Statement from the International Diabetes Federation. Diabet Med. 2006;23(5):469 80.
  13. Boursier J, de Ledinghen V, Zarski J-P, Fouchard-Hubert I, Gallois Y, Oberti F, et al. Comparison of eight diagnostic algorithms for liver fibrosis in hepatitis C: new algorithms are more precise and entirely noninvasive. Hepatology. 2012;55(1):58 67.
  14. Stein JH, Korcarz CE, Hurst RT, Lonn E, Kendall CB, Mohler ER, et al. Use of carotid ultrasound to identify subclinical vascular disease and evaluate cardiovascular disease risk: a consensus statement from the American Society of Echocardiography Carotid Intima-Media Thickness Task Force. J Am Soc Echocardiogr. 2008;21(2):93 111.
  15. Herinirina NF, Ny LH, Herijoelison AR, Ahmad A. Epaisseur de l’intima-média carotidienne et facteurs de risque cardio-vasculaires. PAMJ. 2015;21.
  16. Butt AA, Xiaoqiang W, Budoff M, Leaf D, Kuller LH, Justice AC. Hepatitis C virus infection and the risk of coronary disease. Clin Infect Dis. 2009;49(2):225 32.
  17. Bailey AL, Al-Adwan S, Sneij E, Campbell N, Wiisanen ME. Atherosclerotic Cardiovascular Disease in Individuals with Hepatitis C Viral Infection. Curr Cardiol Rep. 2021;23(5):52.
  18. Medhioub M, Bouzaidi K, Bachali A, Khsiba A, Hamzaoui L, Azouz MM. The risk of subclinical carotidatherosclerosis in patients with chronic hepatitis C. Tunis Med. 2021;99(4):449 55.
  19. Ishizaka N, Ishizaka Y, Takahashi E, Tooda E, Hashimoto H, Nagai R, et al. Association between hepatitis C virus seropositivity, carotid-artery plaque, and intima-media thickening. Lancet. 2002;359(9301):133 5.
  20. Adinolfi LE. Chronic hepatitis C virus infection and atherosclerosis: Clinical impact and mechanisms. World J Gastroenterol. 2014;20(13):3410.
  21. Petta S, Maida M, Macaluso FS, Barbara M, Licata A, Craxì A, et al. Hepatitis C Virus Infection Is Associated With Increased Cardiovascular Mortality: A Meta-Analysis of Observational Studies. Gastroenterology. 2016;150(1):145-55
  22. Petta S, Torres D, Fazio G, Cammà C, Cabibi D, Di Marco V, et al. Carotid atherosclerosis and chronic hepatitis C: a prospective study of risk associations. Hepatol Baltim Md. 2012;55(5):1317 23.
  23. Revuelto Artigas T, Zaragoza Velasco N, Gómez Arbones X, Vidal Ballester T, Piñol Felis C, Reñe Espinet JM, et al. Infección crónica por el virus de la hepatitis C: un factor de riesgo independiente para la ateromatosis subclínica. Rev Clínica Esp. 2019;219(6):293 302.
  24. Bilora F, Campagnolo E, Rinaldi R, Rossato A, Arzenton M, Petrobelli F. Carotid and femoral atherosclerosis in chronic hepatitis C: a 5-year follow-up. Angiology. 2008;59(6):717 20.
  25. Zaki MS. The effect of Hepatitis C Virus infection on cardiovascular complications in end stage kidney disease patients on regular hemodialysis. Electron Physician. 2017;9(2):3857 61.
  26. Fletcher NF, Wilson GK, Murray J, Hu K, Lewis A, Reynolds GM, et al. Hepatitis C virus infects the endothelial cells of the blood-brain barrier. Gastroenterology. 2012;142(3):634-43.
  27. Owusu DO, Phillips R, Owusu M, Sarfo FS, Frempong M. Increased levels of circulating IL-10 in persons recovered from hepatitis C virus (HCV) infection compared with persons with active HCV infection. BMC. 2020;13(1):472.
  28. Al-Jiffri OH. Adhesive molecules and inflammatory markers among hepatitis C virus Saudi patients. Electron J Gen Med. 2017;14(4).
  29. Nakhjavani M, Mashayekh A, Khalilzadeh O, Asgarani F, Morteza A, Omidi M, et al. Oxidized low-density lipoprotein is associated with viral load and disease activity in patients with chronic hepatitis C. Clin Res Hepatol Gastroenterol. 2011;35(2):111 6.
  30. Simon TG, Butt AA. Lipid dysregulation in hepatitis C virus, and impact of statin therapy upon clinical outcomes. World J Gastroenterol. 2015;21(27):8293 303.
  31. Petta S, Adinolfi LE, Fracanzani AL, Rini F, Caldarella R, Calvaruso V, et al. Hepatitis C virus eradication by direct-acting antiviral agents improves carotid atherosclerosis in patients with severe liver fibrosis. J Hepatol. 2018;69(1):18 24.
  32. Salomone F, Petta S, Micek A, Pipitone RM, Distefano A, Castruccio Castracani C, et al. Hepatitis C virus eradication by direct antiviral agents abates oxidative stress in patients with advanced liver fibrosis. Liver Int. 2020;40(11):2820 7.
  33. Carrero A, Berenguer J, Hontañón V, Navarro J, Hernández-Quero J, Galindo MJ, et al. Effects of Eradication of HCV on Cardiovascular Risk and Preclinical Atherosclerosis in HIV/HCV-Coinfected Patients. J Acquir Immune Defic Syndr. 2020;83(3):292 300.
  34. Ichikawa T, Miyaaki H, Miuma S, Motoyoshi Y, Narita S, Toda S, et al. Carotid Intima-media Thickness and Small Dense Low-density Lipoprotein Cholesterol Increase after One Year of Treatment with Direct-acting Antivirals in Patients with Hepatitis C Virus Infection. Intern Med. 2019;58(9):1209 15.