Capecitabine-induced cardiotoxicity: more evidence or clinical approaches to protect the patients&amp;#39; heart?

Fontanella, Caterina; Aita, Marianna; Cinausero, M.; Aprile, Giuseppe; Baldin, M.G.; Dusi, Veronica; Lestuzzi, Chiara; Fasola, Gianpiero; Puglisi, Fabio

doi:10.2147/ott.s65653

Cited by 14 publications

(3 citation statements)

References 45 publications

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“…These biomarkers are not highly sensitive to FP-related cardiovascular toxicity. Nevertheless, as cardiovascular toxicity develops, levels of these biomarkers increase abnormally [9,52,55]. In asymptomatic patients, Holter-ECG monitoring may be performed upon incidental findings of abnormal biomarker test results and can lead to successful diagnosis of FP-related cardiovascular toxicity.…”

Section: Biomarkersmentioning

confidence: 99%

Cardiotoxicities of 5-Fluorouracil and Other Fluoropyrimidines

Shiga

Hiraide

2020

Curr. Treat. Options in Oncol.

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This article is part of the Topical Collection on Cardio-oncology Keywords Fluoropyrimidine I 5-Fluorouracil I Endothelial dysfunction I Coronary spasm I Myocardial cell damage Opinion statement Fluoropyrimidine (FP) is used to treat a wide range of cancers; however, it is associated with drug-induced vascular toxicity, as well as angina pectoris and coronary spasm. FP has been administered for many years, although the incidence, mechanisms, and appropriate methods for managing its associated cardiovascular toxicities have not been clarified, and the management of these complications has not been standardized. This lack of evidence is not limited to FP. Many trials of anticancer agents have been conducted, excluding patients with heart diseases. Hence, there is a paucity of epidemiological data on cardiovascular adverse events caused by anticancer agents. There have been remarkable improvements in cancer treatment in recent years, with consequent improvements in prognosis. In this context, new cardiovascular toxicities related to new drugs have emerged. We are now compelled to respond to cardiovascular adverse events despite the lack of evidence regarding optimal management. The result has been establishment and rapid maturation of the new academic field of cardio-oncology. Despite the relative lack of evidence, we must review small pieces of evidence that have accumulated to date and make the utmost efforts to provide patients with effective evidence-based medical care. Simultaneously, we urgently need randomized clinical trials to build strong evidence.

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Section: Biomarkersmentioning

confidence: 99%

Cardiotoxicities of 5-Fluorouracil and Other Fluoropyrimidines

Shiga

Hiraide

2020

Curr. Treat. Options in Oncol.

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“…It has been shown that this compound has a variety of biological proprieties, involving anti-hyperglycaemic, anti-neoplastic, anti-inflammatory, and antioxidant actions ( Ang et al , 2010 ; Polk et al , 2016 ; Xu et al , 2019 ) . Production of inflammatory mediators is inhibited by BBR according to previous studies ( Lou et al , 2011 ; Fontanella et al , 2014 ). In addition, BBR appears to improve the antioxidant defense mechanism within the cell, involving the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) while decreasing oxidative stress variables such as malondialdehyde (MDA), NO levels, and protein carbonyl content ( Zhou and Zhou, 2011 ).…”

Section: Introductionmentioning

confidence: 70%

Ameliorative effects of berberine and selenium against paracetamol-induced hepatic toxicity in rats

Shams,

Allah,

Ezzat

et al. 2024

Open Vet J

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Background: Paracetamol (PCM) overdosing induces hepatotoxicity, which can result in death if the dose is high enough and the patients are not given N-acetyl cysteine. Berberine (BBR) has a variety of biological proprieties including anti-inflammatory and antioxidant activities. Aim: Assessment of the potential effect of BBR and selenium when used alone or together on the paracetamol–induced acute hepatic toxicity in rats. Methods: This research involved 40 clinically healthy mature adult male albino rats, their weights ranged from 150-200 g and housed in standard conditions. Our study involved evaluating the potential effect of BBR and selenium when used alone or together on the paracetamol–induced acute hepatic toxicity via estimation of the liver function tests, determination of the antioxidant enzyme activities, lipid peroxidation markers, immune-modulatory effects, liver histopathological and immunohistochemical studies. Results: Co-treatment of BBR (150 mg/kg BW) with selenium (5 mg/kg BW) showed significant improvement in the liver function parameters, the antioxidant enzyme activities, reduction in the nitric oxide, lysozyme, malondialdehyde, TNF-α, and TGF-β1 levels, and marked elevation in the IgM levels. Conclusion: Altogether, BBR, Selenium or both augment antioxidant activity and alleviate the paracetamol-induced hepatic toxicity.

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“…Once cardiotoxicity has occurred, the safety of a rechallenge with a modified 5-FU- or capecitabine-based regimen is uncertain, and no widely accepted recommendations have been released. [13] Saneeymehri et al rechallenged capecitabine with a patient who experienced chest pain with 5-FU administration. The cardiac symptoms subsided after initiation of capecitabine and the patient tolerated the treatment well.…”

Section: Discussionmentioning

confidence: 99%

Rechallenge capecitabine after fluoropyrimidine-induced cardiotoxicity in rectal cancer

Peng¹,

Ouyang²,

Tong³

2019

Medicine

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Rationale:Fluoropyrimidine-induced cardiotoxicity is a rare but potentially serious toxicity. The most common symptom is anginal chest pain.Patient concerns:A 35-year-old woman was diagnosed with rectal cancer with metastasis to the liver.Diagnosis:A computed tomography scan showed a 9.3 × 4.5-cm predominantly hypodense lesion within the left lobe of the liver and thickening of the rectum. Liver biopsy showed moderately differentiated adenocarcinoma with necrosis involving the liver parenchyma, and immunohistochemistry for mismatch repair proteins indicated that the tumor was positive for MutL Homolog 1, MutS Homolog 2, MutS Homolog 6, and Protein Homolog 2. Rectal biopsy indicated moderately differentiated adenocarcinoma.Interventions:She received chemotherapy of fluorouracil 1600 mg/m2, leucovorin 500 mg/m2, and irinotecan 100 mg/m2 every week. During the second cycle of chemotherapy, she developed severe anginal chest pain. We replaced fluorouracil with capecitabine 1500 mg (3 pills) a day every 2 weeks, with 1 week off, with irinotecan 100 mg/m2 on day 1 and bevacizumab 5 mg/kg at 200 ml/h for 30 min every 2 weeks. She was treated with chemotherapy for approximately 6 months.Outcomes:The liver lesion showed a significant response to chemotherapy, so she underwent resection of the liver tumor and rectum. After the surgery, she received radiation therapy to the rectal area, and 3 months of chemotherapy were administered prior to colostomy reversal.Lessons:Although the mechanism of fluoropyrimidine-induced cardiotoxicity is still uncertain, our case provides clinical evidence that cardiotoxicity could be a dose-related complication. Reducing the dose of fluoropyrimidine should be considered as a strategy after fluoropyrimidine-induced cardiotoxicity. However, this must be discussed with a multidisciplinary team including oncologists and cardiologists. Close monitoring of serial biomarkers and echocardiography are necessary for early diagnosis of cardiotoxicity.

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Capecitabine-induced cardiotoxicity: more evidence or clinical approaches to protect the patients' heart?

Cited by 14 publications

References 45 publications

Cardiotoxicities of 5-Fluorouracil and Other Fluoropyrimidines

Cardiotoxicities of 5-Fluorouracil and Other Fluoropyrimidines

Ameliorative effects of berberine and selenium against paracetamol-induced hepatic toxicity in rats

Rechallenge capecitabine after fluoropyrimidine-induced cardiotoxicity in rectal cancer

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