Severe Liver Injury Associated With High-Dose Atorvastatin Therapy

Saha, Amit; Garg, Abhimanyu

doi:10.1177/23247096211014050

Cited by 8 publications

(3 citation statements)

References 23 publications

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“…Using the Scopus, PubMed, and Google Scholar databases, we identified 531 manuscripts using the key words "statin" and "liver injury". Of the 15 manuscripts evaluated, there were nine case reports, [10][11][12][13][14][15][16][17][18] two of which discussed two patients. 11,17 The case reports are summarized in Table 1.…”

Section: Reported Casesmentioning

confidence: 99%

“…The other seven patients were followed by serial aminotransferase and imaging studies. [10][11][12][13][14][15][16][17][18] Eight of the patients had reported normal baseline aminotransferases prior to initiation of statin therapy, and nine had resolution of aminotransferase elevations following discontinuation of statin therapy, although three had also received steroid maintenance therapy. [10][11][12][13][14][15][16][17][18] None of the case reports took into consideration the possible presence of nonalcoholic fatty liver disease or elevated body mass index.…”

Section: Reported Casesmentioning

confidence: 99%

“…Changes in aminotransferases suggestive of hepatocellular pattern liver injury have been observed as early as a few hours after initial statin exposure to as late as 8 months after initiation. [10][11][12][13][14][15][16][17][18] While statin-induced hepatocellular liver injury is predominantly selflimiting and generally resolves within 6 months of offending agent cessation, some cases had autoimmune features and were treated with a brief steroid course to accelerate resolution. 10,11 A few reports described attempts at statin rechallenge, although with alternate formulations that did not induce liver injury.…”

Section: Treatment and Conclusionmentioning

confidence: 99%

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Statin-induced Liver Injury Patterns: A Clinical Review

Averbukh¹,

Turshudzhyan²,

Wu³

et al. 2022

J Clin Transl Hepatol

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Since their introduction in 1987, hydroxymethyl glutaryl coenzyme A reductase (HMG-CoA) inhibitors, more commonly known as statins, have become some of the most widely prescribed medications in the world. Though generally considered to be safe and well tolerated, statins have been associated with several side effects including mild liver dysfunction manifested by increases in aminotransferases. Rarely, statins have been noted to induce more serious hepatic injury, including liver injury with autoimmune features. Current literature supports statin induced liver injury presenting in either hepatocellular or cholestatic patterns, though with the former being the prevailing pattern of injury. Fortunately, severe liver injury is uncommon with statin use and is generally reversible without any intervention other than offending statin cessation. When evaluating cases of suspected statin-induced liver injury, a complete medical history, laboratory tests including a complete metabolic panel, autoimmune markers, and viral panel, as well as hepatic imaging, are crucial for a complete causality analysis with validated tools such as Roussel Uclaf Causality Assessment Method. The aim of this review is to review the current evidence for statin-induced liver injury and cholestasis.

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Section: Reported Casesmentioning

confidence: 99%

Section: Reported Casesmentioning

confidence: 99%

Section: Treatment and Conclusionmentioning

confidence: 99%

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Statin-induced Liver Injury Patterns: A Clinical Review

Averbukh¹,

Turshudzhyan²,

Wu³

et al. 2022

J Clin Transl Hepatol

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Attenuation of high-fat high-sucrose diet and CCl4-induced non-alcoholic steatohepatitis in rats by activating autophagy and SIGMAR1/GRP78/ITPR1 signaling using berberine-loaded albumin nanoparticles: in vivo prediction and in-silico molecular modeling

Saleh,

Younis,

Abdelrahman

et al. 2024

J. Pharm. Investig.

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Purpose Non-alcoholic fatty liver disease is the most prevalent metabolic disorder that can lead to the development of non-alcoholic steatohepatitis (NASH) and, eventually, result in hepatocellular carcinoma. This study evaluated the therapeutic potential of berberine-loaded bovine serum albumin nanoparticles (BBR-BSA NPs) toward the induced NASH physical, biochemical, and ultrastructural changes. Methods NASH was induced in male rats by an high-fat high-sucrose diet (HFHSD) and repeated carbon tetrachloride (CCl4) injections. The treated groups received HFHSD/CCl4 and were then administered BBR, BBR-BSA NPs, BSA NPs, and Atorvastatin for four weeks. Finally, physical, liver function, lipid profile, hepatic oxidative stress, and inflammatory biomarkers were determined. Furthermore, hepatic sigma 1 receptor (SIGMAR1) and autophagy signaling proteins were evaluated. The hepatic transmission electron microscopic and histopathological examinations were also assessed. Finally, the chemical- and protein–protein interaction networks were presented using the visualization tools STITCH 5.0 and STRING databases. In addition, molecular docking analyses were conducted to illustrate the binding of BBR and Atorvastatin toward SREBP-2 and mTOR targets. Results The long-term administration of HFHSD/CCl4 had the potential to develop a NASH model. This model is characterized by hepatic steatosis, necro-inflammation, and impaired endoplasmic reticulum-mitochondrial signaling. The results revealed an impaired SIGMAR1 and autophagy flux signaling pathways. In contrast, the administration of BBR-BSA NP improved the therapeutic properties of entrapped BBR on the alterations associated with NASH. The BBR-BSA NPs enhanced the autophagic flux and SIGMAR1 signaling modulators compared to BBR and Atorvastatin. The in-silico bioinformatics analysis demonstrated that BBR exhibited a more robust interaction with SREBP-2 and mTOR compared to Atorvastatin, which supports the in vivo results. Conclusion BBR-BSA NPs restored hepatic homeostasis and enhanced the free BBR’s hepatoprotection against the induced NASH via the upregulation of SIGMAR1 and autophagy flux signaling.

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Atorvastatin/pioglitazone

2021

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Severe Liver Injury Associated With High-Dose Atorvastatin Therapy

Cited by 8 publications

References 23 publications

Statin-induced Liver Injury Patterns: A Clinical Review

Statin-induced Liver Injury Patterns: A Clinical Review

Attenuation of high-fat high-sucrose diet and CCl4-induced non-alcoholic steatohepatitis in rats by activating autophagy and SIGMAR1/GRP78/ITPR1 signaling using berberine-loaded albumin nanoparticles: in vivo prediction and in-silico molecular modeling

Atorvastatin/pioglitazone

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