Severe and Late Acute Liver Injury Induced by Capecitabine

Habib, Mhd Baraa; Hanafi, Ibrahem; Zoubi, Maya Al; Bdeir, Zeina Nizar; Yassin, Mohamed A

doi:10.7759/cureus.12477

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…While liver enzymes play a central role in the three-step enzymatic cascade of capecitabine activation to its active metabolite, hepatotoxicity is considered a relatively rare side effect of capecitabine due to its selective activation within the tumor tissue [29,30]. There are however reports of capecitabine-induced liver injury, including cases of acute liver injury and hepatic steatosis [31,32]. In our study, the adjusted risk of steatosis development was 1.56 when compared with intravenous regimens of 5-FU administration, but this point estimate was not statistically significant.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Adjuvant Chemotherapy-Associated Steatosis (CAS) in Colorectal Cancer

et al. 2021

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Chemotherapy-associated steatosis is poorly understood in the context of colorectal cancer. In this study, Stage II–III colorectal cancer patients were retrospectively selected to evaluate the frequency of chemotherapy-associated steatosis and to determine whether patients on statins throughout adjuvant chemotherapy develop chemotherapy-associated steatosis at a lower frequency. Baseline and incident steatosis for up to one year from chemotherapy start date was assessed based on radiology. Of 269 patients, 76 (28.3%) had steatosis at baseline. Of the remaining 193 cases, patients receiving adjuvant chemotherapy (n = 135) had 1.57 (95% confidence interval [CI], 0.89 to 2.79) times the adjusted risk of developing steatosis compared to patients not receiving chemotherapy (n = 58). Among patients who underwent chemotherapy, those using statins for pre-existing hyperlipidemia (n = 37) had 0.71 (95% CI, 0.10 to 2.75) times the risk of developing steatosis compared to patients who were not prevalent users of statins (n = 98). Chemotherapeutic treatment of Stage II–III colorectal cancer appears to be consistent with a moderately increased risk of steatosis, although larger studies are necessary to assess the significance of this observation. Prospective trials should be considered to further explore the potential for protective use of statins in this curative patient population.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Adjuvant Chemotherapy-Associated Steatosis (CAS) in Colorectal Cancer

et al. 2021

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“…Notably, discontinuing capecitabine was enough to rectify the liver damage. These cases highlight the need for increased vigilance in monitoring for severe liver toxicity during capecitabine treatment, despite the drug's generally favorable safety profile, and the significance of discontinuing the drug promptly when necessary (71,72).…”

Section: Antimetabolitesmentioning

confidence: 99%

Chemotherapy-Induced Liver Injury: Unveiling Emerging Mechanisms and Exploring Mitigation Strategies

Alkabbani,

Shatat,

Ghazy

et al. 2024

ERU Research Journal

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In this comprehensive overview of chemotherapy-induced liver injury, various classes of chemotherapeutic agents were reviewed to elucidate the complex cellular events contributing to hepatotoxicity and potential mitigation strategies. Alkylating agents, such as cyclophosphamide and busulfan, exhibited diverse mechanisms, with compounds like fucoidan and pyrroloquinoline quinone demonstrating protective effects through modulation of Nrf2/HO-1 and NF-κB pathways.Methotrexate-induced hepatotoxicity, characterized by oxidative stress and inflammation, highlighted the importance of addressing disruptions in lipid metabolism and the gut-liver axis.The multifaceted nature of cisplatin-induced liver damage emphasized the role of gastrointestinal microbiota and therapeutic interventions like curcumin. Anthracyclines, including doxorubicin and epirubicin, posed challenges in mitigating severe hepatotoxicity, with potential protective agents identified. Topoisomerase inhibitors, plant alkaloids, and antitumor antibodies showcased diverse impacts on liver function, emphasizing the need for tailored interventions. Targeted therapies, immune checkpoint inhibitors, and miscellaneous agents like L-asparaginase revealed distinct patterns of hepatotoxicity, prompting a nuanced understanding of patient safety. This comprehensive exploration offers a foundation for future research and therapeutic developments to enhance patient outcomes during chemotherapy.

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Drug-Induced Liver Injury: Highlights and Controversies in the Recent Literature

et al. 2021

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Drug-induced liver injury (DILI) remains an important, yet challenging diagnosis for physicians. Each year, additional drugs are implicated in DILI and this year was no different, with more than 1400 articles published on the subject. This review examines some of the most significant highlights and controversies in DILI-related research over the past year and their implications for clinical practice. Several new drugs were approved by the US Food and Drug Administration including a number of drugs implicated in causing DILI, particularly among the chemotherapeutic classes. The COVID-19 pandemic was also a major focus of attention in 2020 and we discuss some of the notable aspects of COVID-19-related liver injury and its implications for diagnosing DILI. Updates in diagnostic and causality assessments related to DILI such as the Roussel Uclaf Causality Assessment Method are included, mindful that there is still no single biomarker or diagnostic tool to unequivocally diagnose DILI. Glutamate dehydrogenase received renewed attention as being more specific than alanine aminotransferase. There were a few new reports of previously unrecognized hepatotoxins, including immune modulators and novel gene therapy drugs that we highlight. Updates and new developments of previously described hepatotoxins, such as immune checkpoint inhibitors and anti-tuberculosis drugs are reviewed. Finally, novel technologies such as organoid culture systems to better predict DILI preclinically may be coming of age and determinants of hepatocyte loss, such as calculating P ALT are poised to improve our current means of estimating DILI severity and the risk of acute liver failure.

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Severe and Late Acute Liver Injury Induced by Capecitabine

Cited by 3 publications

References 8 publications

Evaluation of Adjuvant Chemotherapy-Associated Steatosis (CAS) in Colorectal Cancer

Evaluation of Adjuvant Chemotherapy-Associated Steatosis (CAS) in Colorectal Cancer

Chemotherapy-Induced Liver Injury: Unveiling Emerging Mechanisms and Exploring Mitigation Strategies

Drug-Induced Liver Injury: Highlights and Controversies in the Recent Literature

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