Fluvastatin as an adjuvant to pegylated interferon and ribavirin in HIV/hepatitis C virus genotype 1 co-infected patients: an open-label randomized controlled study

Milazzo, Laura; Caramma, Ilaria; Mazzali, Cristina; Cesari, Miriam; Olivetti, M.; Galli, Massimo; Antinori, Spinello

doi:10.1093/jac/dkq002

Cited by 30 publications

(28 citation statements)

References 25 publications

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“…Regarding the laboratory results, only one patient in group I showed a significant rise of ALT by week 24, for which he continued treatment by SOC therapy alone. This was similar to previous studies documenting the safe use of statins in HCVinfected patients without the risk of hepatotoxicity (23,(25)(26)(27)(28). Another patient discontinued treatment at week 28 because of retroperitoneal infection that was drained surgically.…”

Section: Discussionsupporting

confidence: 89%

“…EVR was negatively influenced by smoking (p=0.001) and positively related to low viral load and high ALT. Milazzo et al (23) found none of the patients' demographics or laboratory results to be correlated with SVR. Although Kondo et al (22) found male gender, high Hb, and high TLC to be associated with SVR in FLV-treated patients, Harrison showed that low HDL and high LDL levels influenced SVR (29).…”

Section: Discussionmentioning

confidence: 99%

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

Seyam

Gabr²,

Salama³

et al. 2015

Turk J Gastroenterol

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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.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

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

Seyam

Gabr²,

Salama³

et al. 2015

Turk J Gastroenterol

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“…Gower and Graham (26) reported that statins showed antiviral activity against RSV in vivo. The pharmacological potential of cholesterollowering drugs to curb virus infection has also been proposed and evaluated in hepatitis C virus with promising results in which statins significantly improved the rapid antiviral response caused by pegylated interferon in an open-labeled randomized controlled study (60). …”

Section: Figmentioning

confidence: 99%

Cholesterol-Rich Microdomains as Docking Platforms for Respiratory Syncytial Virus in Normal Human Bronchial Epithelial Cells

San‐Juan‐Vergara

Sampayo-Escobar

Reyes

et al. 2012

J Virol

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Respiratory syncytial virus (RSV) is one of the major causes of respiratory infections in children, and it is the main pathogen causing bronchiolitis in infants. The binding and entry mechanism by which RSV infects respiratory epithelial cells has not yet been determined. In this study, the earliest stages of RSV infection in normal human bronchial epithelial cells were probed by tracking virions with fluorescent lipophilic dyes in their membranes. Virions colocalized with cholesterol-containing plasma membrane microdomains, identified by their ability to bind cholera toxin subunit B. Consistent with an important role for cholesterol in RSV infection, cholesterol depletion profoundly inhibited RSV infection, while cholesterol repletion reversed this inhibition. Merger of the outer leaflets of the viral envelope and the cell membrane appeared to be triggered at these sites. Using small-molecule inhibitors, RSV infection was found to be sensitive to Pak1 inhibition, suggesting the requirement of a subsequent step of cytoskeletal reorganization that could involve plasma membrane rearrangements or endocytosis. It appears that RSV entry depends on its ability to dock to cholesterol-rich microdomains (lipid rafts) in the plasma membrane where hemifusion events begin, assisted by a Pak1-dependent process.

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“…properties such as antiviral (Bader et al, 2008;Bader and Korba, 2010;Jameson et al, 2010;Milazzo et al, 2010) and antitumor activities (Takahashi et al, 2006;Takahashi and Nishibori, 2007;Garwood et al, 2010), however the antitumor molecular mechanisms by which the statin block cancer cell growth are poorly understood (Ghosh-Choudhury et al, 2010), and there are emerging interests to explore the anticancer potentials of HMGCoA reductase inhibitors in the clinical setting, particularly in tumor sites sensitive to these agents in vitro (Chan et al, 2003), some mechanism proposes for anticancer activities are apoptotic inducer, antiangiogenic and antimetastatic. These properties are associates with the inhibition of the synthesis of isoprenoid intermediates of the mevalonate pathway (Slawinska and KandeferSzerszen, 2008 …”

Section: Introductionmentioning

confidence: 99%

Cytotoxic evaluation of fluvastatin and rosuvastatin and effect of fluvastatin in the hela cell cycle

Campos-Lara¹,

Mendoza‐Espinoza²

2011

Afr. J. Pharm. Pharmacol.

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3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, were originally designed to reduce cholesterol biosynthesis and have been extensively used as prevention drugs against hyperlipidemia and cardiovascular conditions. Recently, these compounds have been shown to display chemopreventive activity against cancer. However, the effects of statins on cancer are not completely understood. For this reason, we have studied the cytotoxic effect of rosuvastatin and fluvastatin on three cell tumoral lines: human larynx carcinoma (HEp-2), human nasopharyngeal carcinoma (KB), and human epithelial carcinoma (HeLa). We have found that only fluvastatin has relevant activity against the tumoral cell lines assayed and the capacity to arrest G 1 -phase, whereas a significant decline was observed in the S-phase percentage. Fluvastatin IC 50 were 2.43±0.56 µ µ µ µg/mL (HEp-2), 2.29±0.19 µ µ µ µg/mL (KB), and 5.02±1.52 µ µ µ µg/mL (HeLa), whereas rosuvastatin showed poor activity. These results indicate that the cytotoxic effect of fluvastatin may not depend directly on HMG-CoA reductase inhibition. The antitumor statins effect needs further investigation.

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Fluvastatin as an adjuvant to pegylated interferon and ribavirin in HIV/hepatitis C virus genotype 1 co-infected patients: an open-label randomized controlled study

Cited by 30 publications

References 25 publications

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

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

Cholesterol-Rich Microdomains as Docking Platforms for Respiratory Syncytial Virus in Normal Human Bronchial Epithelial Cells

Cytotoxic evaluation of fluvastatin and rosuvastatin and effect of fluvastatin in the hela cell cycle

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