Journals / Turkish Journal of Gastroenterology / 2015 / Cilt: 26 - Sayı: 6

Evaluation of fluvastatin in combination with the standard of care therapy (PEG-IFN/Ribavirin) in Egyptian patients with hepatitis C virus

Pages
511–516
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Fluvastatin yielded a borderline, significantly higher complete early virological response than SOC; therefore, it is a safe adjuvant to the SOC therapy

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Background/Aims: Cholesterol biosynthesis suppresses the replication of HCV-1b replicons, thus influencing hepatitis C virus (HCV) natural history.
📊
Key Findings & Data:Materials and Methods: Sixty HCV patients were enrolled and allocated to either group I, who received the triple therapy (fluvastatin + SOC), or group II, who received SOC; the duration for both treatments was 48 weeks.
💡
Conclusion & Impact:Conclusion: Fluvastatin yielded a borderline, significantly higher complete early virological response than SOC; therefore, it is a safe adjuvant to the SOC therapy
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Background/Aims: Cholesterol biosynthesis suppresses the replication of HCV-1b replicons, thus influencing hepatitis C virus (HCV) natural history. This study aimed at comparing the efficacy and safety of fluvastatin (FLV) as an adjuvant therapy to the standard of care (SOC) therapy, i.e., pegylated interferon (PEG-IFN) and ribavirin, for the treatment of HCV patients. Materials and Methods: Sixty HCV patients were enrolled and allocated to either group I, who received the triple therapy (fluvastatin + SOC), or group II, who received SOC; the duration for both treatments was 48 weeks. All patients were subjected to pretreatment liver biopsy and monthly biochemical tests (liver profile, CBC), and quantitative HCV-RNA test was performed at weeks 0, 4, 12, 48, and 72. Results: All virological responses were higher in group I than in group II, with no statistical difference. Group I showed no manifestations of hepatotoxicity. Conclusion: Fluvastatin yielded a borderline, significantly higher complete early virological response than SOC; therefore, it is a safe adjuvant to the SOC therapy

🔖

Cite This Article

SEYAM, M. S., GABR, H. A., SALAMA, Z. A., MOKHLES, M. A., MARZABAN, R. N., SOLİMAN, A. F. (2015). Evaluation of fluvastatin in combination with the standard of care therapy (PEG-IFN/Ribavirin) in Egyptian patients with hepatitis C virus. Turkish Journal of Gastroenterology, Cilt: 26 - Sayı: 6, 511–516. https://ajindex.com/articles/410748

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (15)

  1. Esmat G, El Raziky M, El Kassas M, et al. The future for the treatment of genotype 4 chronic hepatitis C Liver Int 2012
  2. 32(Suppl 1): 146-50. [CrossRef] 2. Ye J, Wang C, Sumpter R Jr, et al. Disruption of hepatitis C virus RNA replication through inhibition of host protein geranylgeranylation. Proc Natl Acad Sci USA 2003
  3. 15865-70. [CrossRef] 3. Aizaki H, Lee KJ, Sung VM, et al. Characterization of the hepatitis C virus RNA replication complex associated with lipid rafts. Virology 2004
  4. [CrossRef] 4. Kapadia SB, Chisari FV. Hepatitis C virus RNA replication is regulated by host geranylgeranylation and fatty acids. Proc Natl Acad Sci USA 2005
  5. [CrossRef] 5. Ikeda M, Abe K, Yamada M, et al. Different anti-HCV profiles of statins and their potential for combination therapy with interferon. Hepatol 2006
  6. [CrossRef] 6. Bader T, Fazili J, Madhoun M, et al. Fluvastatin inhibits hepatitis C replication in humans. Am J Gastroenterol 2008
  7. [CrossRef] 7. O’Leary JG, Chan JL, McMahon CM, Chung RT. Atorvastatin does not exhibit antiviral activity against HCV at conventional doses: a pilot clinical trial. Hepatol 2007
  8. [CrossRef] 8. The French METAVIR Cooperative Study Group. Intraobserver and interobserver variations in liver biopsy interpretation in patients with chronic hepatitis C Hepatol 1994
  9. Asselah T, Benhamou Y, Marcellin P. Protease and polymerase inhibitors for the treatment of hepatitis C. Liver international: official journal of the International Association for the Study of the Liver. 2009
  10. 29 (Suppl 1): 57-67. 10. Goldstein J, Brown M. Regulation of the mevalonate pathway. Nature 1990
  11. [CrossRef] 11. Andre P, Komurian-Pradel F, Deforges S, et al. Characterization of low- and very-low-density hepatitis C virus RNA-containing particles. J Virol 2002
  12. [CrossRef] 12. Angello V, Abel G, Elfahal M, et al. Hepatitis C virus and other Flaviviridae viruses enter cells via low-density lipoprotein receptor. Proc Natl Acad Sci USA 1999
  13. 12766-71. [CrossRef] 13. Molina S, Castet V, Fournier-wirth C, et al. The low-density lipoprotein receptor plays a role in the infection of primary human hepatocytes by hepatitis C virus. J Hepatol 2007
  14. [CrossRef] 14. Miyanari Y, Atsuzawa K, Usuda N, et al. The lipid droplet is an important organelle for hepatitis C virus production. Nat Cell Biol 2007
  15. [CrossRef] 15. Akuta N, Suzuki F, Kawamura Y,