Letters to the Editor: Fatal fulminant hepatic failure associated with benzbromarone
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Cited by (57)
Comparison of benzbromarone and allopurinol on the risk of chronic kidney disease in people with asymptomatic hyperuricemia
2023, European Journal of Internal MedicineDiscovery of novel benzbromarone analogs with improved pharmacokinetics and benign toxicity profiles as antihyperuricemic agents
2022, European Journal of Medicinal ChemistryCitation Excerpt :In 2003, BM was withdrawn from the European market due to hepatotoxicity [30]. It's worth noting that only several cases showed clear causation between BM and hepatotoxicity [31,32]. Nevertheless, many studies have been carried out to investigate the mechanisms (e.g. involvement of toxic metabolites, mitochondrial toxicity) of BM-induced hepatotoxicity.
Benzbromarone aggravates hepatic steatosis in obese individuals
2018, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :Benzbromarone (BBR) is a uricosuric drug that has been widely used for the treatment of hyperuricemia and chronic gout for approximately 40 years [1]. However, as several cases reported that BBR could cause hepatic toxicity [2–4], the drug was disapproved in the United States and was withdrawn from European markets in 2003. Nonetheless, in some hyperuricemic patients, for example, patients with impaired renal function or allopurinol-intolerance, BBR is greatly effective in lowering uric acid levels [5,6].
Comparative study on the interaction between 3 CYP2C9 allelic isoforms and benzbromarone by using LC–MS/MS method
2017, Journal of Chromatography B: Analytical Technologies in the Biomedical and Life SciencesCitation Excerpt :For many years, BBR was considered to be effective and well tolerated. However, after several reports of severe hepatotoxicity [8–10], this drug had to be withdrawn from the market in several countries. Currently, the drug remains available in some countries in Europe, as well as Brazil, China, Japan, and several other Asian countries [7].
Identification of novel glutathione adducts of benzbromarone in human liver microsomes
2017, Drug Metabolism and PharmacokineticsCitation Excerpt :Therefore, GSH depletion is also thought to be one of the risk factors for BBR-induced liver injury. This contention is supported by the results of studies showing that most patients with BBR-induced liver injury are 50 years of age or older [1–4] and that GSH levels are lower in elderly subjects than in young subjects [26,27]. In a clinical study, two of 11 subjects showed six-times higher Cmax and AUC values of 1′-hydroxy BBR than those in the other nine subjects after oral administration of a single 100 mg dose of BBR [10].
Hepatocellular toxicity of benzbromarone: Effects on mitochondrial function and structure
2014, ToxicologyCitation Excerpt :For many years, benzbromarone was considered to be both effective and well tolerated. However, after several reports of severe hepatotoxicity (Arai et al., 2002; van der Klauw et al., 1994; Wagayama et al., 2000), the drug had to be withdrawn from the market in several countries, e.g. the USA, France and Switzerland. Histological findings in affected patients included microvesicular steatosis of liver (Arai et al., 2002), a finding compatible with inhibition of mitochondrial β-oxidation (Fromenty and Pessayre, 1995; Spaniol et al., 2001, 2003).