ArticleBritish journal of clinical pharmacology2026
Concentration dependency of an acyl glucuronide metabolite in eltrombopag-induced hepatotoxicity: Role of UGT1A1 genotype.
Article in British journal of clinical pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Concentration dependency of an acyl glucuronide metabolite in eltrombopag-induced hepatotoxicity: Role of UGT1A1 genotype.British journal of clinical pharmacology · 2026Article
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6 authors.
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Abstract
aimEltrombopag, a thrombopoietin receptor agonist for aplastic anaemia, can cause hepatotoxicity. It is metabolized by uridine diphosphate-glucuronosyltransferase (UGT) 1A1 to form an acyl glucuronide metabolite; however, the relationships among serum concentrations of the acyl glucuronide metabolite, UGT1A1 genotypes and hepatotoxicity remain unclear.
methodWe examined the serum concentrations of eltrombopag and its acyl glucuronide metabolite, UGT1A1 genotypes and occurrence of hepatotoxicity (abnormal liver function tests or drug-induced liver injury [DILI]) in 104 samples from 42 patients with aplastic anaemia receiving eltrombopag.
resultsThe concentrations of eltrombopag and its acyl glucuronide metabolite were significantly higher in samples with abnormal liver function than in those with normal liver function (23.0 ± 18.5 vs. 10.6 ± 9.3 μg/mL and 6.9 ± 4.5 vs. 2.1 ± 1.2 μg/mL, respectively). Receiver operating characteristic (ROC) analysis demonstrated that the concentration of the acyl glucuronide metabolite provided superior predictive accuracy for hepatotoxicity, with a threshold of 4.0 μg/mL, compared with eltrombopag (area under the ROC curve, 0.83 vs. 0.68). All patients with DILI had higher concentrations of the acyl glucuronide metabolite than the cutoff value. The incidence of hepatotoxicity differed across UGT1A1 genotype: 43% in extensive metabolizers (EMs), 11% in intermediate metabolizers (IMs) and none in poor metabolizers (PMs). The formation of the acyl glucuronide metabolite was 1.5-fold greater in EMs than in IMs/PMs.
conclusionThese findings suggest that eltrombopag-induced hepatotoxicity is dependent on the concentration of eltrombopag acyl glucuronide and influenced by UGT1A1 genotype, highlighting the potential utility of serum acyl glucuronide monitoring and UGT1A1 genotyping for preventing and managing the hepatotoxicity.
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