Ator vastatin-induced acute hepatitis with absence of cross-toxicity with simvastatin

Nakad, A.; Bataille, Laurent; Hamoir, V.; Sempoux, Christine; Horsmans, Yves

doi:10.1016/s0140-6736(99)00569-3

Cited by 66 publications

(32 citation statements)

References 2 publications

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“…Furthermore, raloxifene use has not been associated with myopathy/ rhabdomyolysis in any large, randomized clinical trials [13,[26][27][28]. In theory, for older postmenopausal women who may have a higher risk of statin-induced rhabdomyolysis, the possible risk of this adverse event may be decreased by using low-dose simvastatin with raloxifene, as compared with higher doses of simvastatin alone or combined with other lipid-altering drugs, which have been shown to increase the risk of rhabdomyolysis [29][30][31][32]. Further data specifically evaluating the safety of raloxifene coadministration with multiple doses of statins are needed.…”

Section: Discussionmentioning

confidence: 99%

Effects of raloxifene and low-dose simvastatin coadministration on plasma lipids in postmenopausal women with primary hypercholesterolemia

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Effects of raloxifene and low-dose simvastatin coadministration on plasma lipids in postmenopausal women with primary hypercholesterolemia

et al. 2005

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“…Modified from Gazzerro et al [11]. Atorvastatin use was also associated with hepatocellular and cholestatic injury [23][24][25][26].…”

Section: Liver Toxicity Of Statinsmentioning

confidence: 99%

The efficacy and safety of statins for the treatment of non-alcoholic fatty liver disease

Pastori¹,

Polimeni²,

Baratta³

et al. 2015

Digestive and Liver Disease

140

105

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Non-alcoholic fatty liver disease is an emerging liver disease in Western countries and the most frequent cause of incidental elevation of serum liver enzymes. Dyslipidaemia is frequently observed in patients with non-alcoholic fatty liver disease, and treatment of dyslipidaemia plays a critical role in the overall management of these patients. Moreover, coronary artery disease remains the most common cause of death. Statins are effective lipid-lowering agents, associated with a lowering the risk of cardiovascular events in several interventional randomized clinical trials. However, statins are often underused in patients with non-alcoholic fatty liver disease and many physicians are concerned about the prescription of statins to patients with unexplained persistent elevation of liver enzymes or active liver disease. Based on currently available data, statin therapy, at low-to-moderate doses, seems to be safe and has low liver toxicity. Treatment of dyslipidaemia in patients with non-alcoholic fatty liver disease is recommended and may also improve liver function tests. In these patients, the risks of not taking statins could outweigh the risks of taking the drug. Conversely, the usefulness of statins for the treatment of non-alcoholic fatty liver disease/non-alcoholic steatohepatitis is still a matter of debate and randomized clinical trials of adequate size and duration are required.

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“…Nakad et al (12) reported a case of atorvastatin-induced acute hepatitis, and Ridruejo and Mandó (13) reported acute cholestatic hepatitis after reinitiating treatment with atorvastatin. Cholestasis and hepatitis induced by statin therapy seem to be rare idiosyncratic reactions (14).…”

Section: Discussionmentioning

confidence: 99%

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone

Ito

Molina

Andriolo

et al. 2007

Braz J Med Biol Res

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Animal studies and premarketing clinical trials have revealed hepatotoxicity of statins, primarily minor elevations in serum alanine aminotransferase levels. The combined chronic use of medicines and eventual ethanol abuse are common and may present a synergistic action regarding liver injury. Our objective was to study the effect of the chronic use of atorvastatin associated with acute ethanol administration on the liver in a rat model. One group of rats was treated daily for 5 days a week for 2 months with 0.8 mg/kg atorvastatin by gavage. At the end of the treatment the livers were perfused with 72 mM ethanol for 60 min. Control groups (at least 4 animals in each group) consisted of a group of 2-month-old male Wistar EPM-1 rats exposed to 10% ethanol (v/v) ad libitum replacing water for 2 months, followed by perfusion of the liver with 61 nM atorvastatin for 60 min, and a group of animals without chronic ethanol treatment whose livers were perfused with atorvastatin and/or ethanol. The combination of atorvastatin with ethanol did not increase the release of injury marker enzymes (alanine aminotransferase, aspartate aminotransferase, and lactic dehydrogenase) from the liver and no change in liver function markers (bromosulfophthalein clearance, and oxygen consumption) was observed. Our results suggest that the combination of atorvastatin with ethanol is not more hepatotoxic than the separate use of each substance.

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Ator vastatin-induced acute hepatitis with absence of cross-toxicity with simvastatin

Cited by 66 publications

References 2 publications

Effects of raloxifene and low-dose simvastatin coadministration on plasma lipids in postmenopausal women with primary hypercholesterolemia

Effects of raloxifene and low-dose simvastatin coadministration on plasma lipids in postmenopausal women with primary hypercholesterolemia

The efficacy and safety of statins for the treatment of non-alcoholic fatty liver disease

The combination of atorvastatin and ethanol is not more hepatotoxic to rats than the administration of each drug alone

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