Switch from indinavir to ritonavir–indinavir regimen in patients treated with highly active antiretroviral therapy co-infected with hepatitis C is not associated with alteration of liver function tests

Vora, Samir; Michon, C.; Junet, Christian; Balavoine, Jean-François; Renold-Moynier, Catherine; Yerly, Sabine; Perrin, Luc

doi:10.1097/00002030-200012010-00024

Cited by 9 publications

(7 citation statements)

References 7 publications

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“…Furthermore, in a randomized controlled trial that compared lopinavir therapy boosted with low-dose ritonavir and nelfinavir, only 4.5% of lopinavir/ ritonavir recipients developed an AST or ALT level 15 times the ULN, which was similar to the incidence observed in nelfinavir recipients (5.2%) [26]. Similarly, Vora et al [27] reported that the addition of low-dose ritonavir to indinavir therapy for 19 patients coinfected with HBV or HCV was not associated with significant increases in serum ALT or AST levels.…”

Section: Hepatotoxicity Associated With Pismentioning

confidence: 61%

Drug-Induced Liver Injury Associated with Antiretroviral Therapy that Includes HIV-1 Protease Inhibitors

Sulkowski

2004

Clinical Infectious Diseases

177

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Since their introduction, hepatotoxicity has been associated with the use of human immunodeficiency virus (HIV)-1 protease inhibitors (PIs). However, the complexity of the HIV-infected patient and the combinations of medications used to treat HIV complicate the understanding of the independent effects of PIs in the development of drug-induced liver injury (DILI). I discuss the current understanding of PI-associated hepatotoxicity. Of the PI regimens studied, the greatest risk of DILI has been observed among patients receiving full-dose ritonavir. Similarly, hepatitis B and/or C virus coinfection has been associated with a greater risk of DILI, compared with those with no hepatitis. Although the specific mechanism by which viral hepatitis increases this risk is not known, patients with cirrhosis may have decreased cytochrome P450 activity, leading to increased PI exposure. Clearly, further research is needed to define the interaction of PIs and chronic viral hepatitis in the development of DILI.

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Section: Hepatotoxicity Associated With Pismentioning

confidence: 61%

Drug-Induced Liver Injury Associated with Antiretroviral Therapy that Includes HIV-1 Protease Inhibitors

Sulkowski

2004

Clinical Infectious Diseases

177

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“…5.9% incidence for Nelfinavir (NFV) and Saquinavir (SQV) receiving patients, 6.8% for IDV and 5.7% incidence for NRTI-based therapy [37]. Nevertheless, many other studies have not demonstrated that there is an increased liver toxicity associated with RTV when compared with other PIs [23,41,100] and this was observed both when RTV was administered as sole PI and when it was combined with other PIs [33,38].…”

Section: Risk Factorsmentioning

confidence: 99%

“…were not associated with the development of severe hepatotoxicity and no liver events have been observed in patients receiving a PI boosted with baby-dose RTV [33,100,105]. In fact, in a randomized controlled trial comparing lopinavir (LPV) and RTV co-formulated as Kaletra® versus NFV, only 4.5% of LPV/RTV recipients developed a transaminase level higher than five times the ULN, similarly to the incidence observed in NFV recipients (5.2%) [95].…”

Section: Mechanisms Of Pi-toxicitymentioning

confidence: 99%

“…Patients with underlying C or B hepatitis or marked elevations in transaminases prior to ARV treatment may be at increased risk for developing further liver enzyme elevations or hepatic decompensation when receiving HAART containing LPV/RTV [23,33,105]. To date, in clinical practice, other PIs, such as Amprenavir (APV) and IDV, are frequently combined with RTV to boost their plasma levels without significantly higher incidence of severe liver toxicity [33,89,100].…”

Section: Mechanisms Of Pi-toxicitymentioning

confidence: 99%

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Hepatotoxicity of Antiretroviral Drugs

Abrescia

D’Abbraccio

Figoni

et al. 2005

CPD

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The use of highly active antiretroviral therapy (HAART) has significantly slowed the HIV disease progression. However, adverse effects are now a limiting cause of HAART benefit in a substantial proportion of patients. Particularly hepatotoxicity which is a common complication occurring during every HAART regimen. All antiretroviral (ARV) drugs classes, Nucleoside/Nucleotide reverse transcriptase inhibitors (NRTI), non-Nucleoside reverse transcriptase inhibitors (nNRTI) and Protease Inhibitors (PI) may cause hepatotoxicity but in different pathways. Many risk factors have been identified for developing antiretroviral-related hepatotoxicity, however severe hepatitis remains very uncommon in patients receiving HAART, also if the incidence of hepatotoxicity is rather high. That being the case, means that every new available antiretroviral drug strongly necessities studies which can evaluate its hepatotoxicity and drug-drug interactions, to define the potential risk factors and the outcome of any side effects. This report will review the risk factors, the epidemiology and the pathogenic mechanisms of hepatotoxicity caused in every antiretroviral drug.

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“…Although the long-term implications have not been fully defined, coronary artery calcification and increased risk of myocardial infarction have been observed (Parenti et al, 2004). Ritonavir-boosted PIs may also increase the likelihood of grade 3 or 4 elevation of liver enzymes in patients coinfected with hepatitis B or C (Lundgren et al, 2003;Sulkowski, Mehta, Chaisson, Thomas, & Moore, 2004), but this may depend more on the primary PI being boosted rather than on the low dose of ritonavir (Sulkowski et al, 2004;Vora et al, 2000).…”

Section: Background On Ritonavir Boostingmentioning

confidence: 99%

Ritonavir-Boosted Protease Inhibitors: Impact of Ritonavir on Toxicities in Treatment-Experienced Patients

Sension¹,

Piliero²

2007

Journal of the Association of Nurses in AIDS Care

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The purpose of this review is to discuss the basis for ritonavir boosting of protease inhibitors as well as the complications and benefits associated with ritonavir boosting when designing an antiretroviral regimen for treatment-experienced patients. Such patients have fewer viable options because of cross-resistance arising from previous regimen failures. Ritonavir administered at a low dose to boost another protease inhibitor may be a useful strategy for achieving virological efficacy while minimizing the toxicities associated with full-dose ritonavir. There may be an increased risk of adverse events associated with increased plasma concentration of the concurrent protease inhibitor. Still, the incidence of these adverse events is generally low, and clinical trials have suggested that they rarely result in discontinuation or alteration of the regimen. In highly treatment-experienced patients in particular, the potential benefits associated with ritonavir boosting usually outweigh the risks.

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Switch from indinavir to ritonavir–indinavir regimen in patients treated with highly active antiretroviral therapy co-infected with hepatitis C is not associated with alteration of liver function tests

Cited by 9 publications

References 7 publications

Drug-Induced Liver Injury Associated with Antiretroviral Therapy that Includes HIV-1 Protease Inhibitors

Drug-Induced Liver Injury Associated with Antiretroviral Therapy that Includes HIV-1 Protease Inhibitors

Hepatotoxicity of Antiretroviral Drugs

Ritonavir-Boosted Protease Inhibitors: Impact of Ritonavir on Toxicities in Treatment-Experienced Patients

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