Initial dose effect of 5-fluorouracil: rapidly improving severe, acute toxic myopericarditis

Çalık, Ali Nazmi; Çeliker, Emel; Velibey, Yalçın; Çağdaş, Metin; Güzelburç, Özge

doi:10.1016/j.ajem.2010.10.025

Cited by 24 publications

(9 citation statements)

References 9 publications

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“…Additionally, the presence of these features in the setting of drug use, excludes the diagnosis of SCM, per Gothenburg Criteria 38. A similar presentation of reversible global hypokinesis associated with 5-FU has been previously described,39–45 and these cases do not meet the strict definition of SCM (table 1). Thus, these reports of 5-FU-related global hypokinesia, make us think about our current understanding of the underlying mechanism for this cardiotoxicity.…”

Section: Discussionmentioning

confidence: 69%

“…An important point to emphasise from our case is that even though the patient can be asymptomatic, the dysfunction of the LV is severe. Although the dysfunction is reversible and temporary in most cases,39 40 54 during the acute phase of cardiac dysfunction, the patient is at increased risk for grave complications like thrombus formation and fatal arrhythmia. Thus, it is warranted that patients be monitored closely for cardiac complications at least during the acute phase following 5-FU therapy.…”

Section: Discussionmentioning

confidence: 99%

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Acute reversible left ventricular systolic dysfunction associated with 5-fluorouracil therapy: a rare and increasingly recognised cardiotoxicity of a commonly used drug

et al. 2019

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5-Fluorouracil (5-FU) is the third most common chemotherapeutic agent for treating solid cancers and the second most common to cause cardiotoxicity. We present a rare case of acute reversible severe left ventricular systolic dysfunction associated with 5-FU. A 54-year-old woman with a history of stage IV gastric cancer presented with features of transient ischaemic attack after receiving the first dose of FLOT (5-FU, leucovorin, oxaliplatin and docetaxel). During the diagnostic workup, it was found that her ejection fraction was severely reduced to 15% with features of global hypokinesis, which later improved back to 65% within 13 days. These cases challenge our current understanding of the underlying mechanisms of this cardiotoxicity. Additionally, even though the patient did not experience any cardiac symptoms, it is important to monitor these patients closely as they are at high risk for fatal complications like arrhythmia and thrombus formation.

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Section: Discussionmentioning

confidence: 69%

Section: Discussionmentioning

confidence: 99%

Acute reversible left ventricular systolic dysfunction associated with 5-fluorouracil therapy: a rare and increasingly recognised cardiotoxicity of a commonly used drug

et al. 2019

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“…However, in some patients abnormalities of the left ventricular wall motion have been reported in areas not corresponding to coronary vessel distribution, suggesting a multifactorial cardiotoxicity mechanism: the occurrence of ischemia, secondary to coronary vasospasms, is only a component of the pathophysiological spectrum, which also includes the thrombosis of small vessels, direct toxicity on the myocardium and inflammation that could lead to myocarditis [46]. For example, Calik et al described an original case of acute toxic myopericarditis occurring after the first bolus dose of 5-FU [47]. Their patient, admitted to the ICCU with clinical features similar to ours, presented however inflammatory biomarkers elevation and echocardiography revealed global myocardial hypokinesia of the left ventricle.…”

Section: Underlying Pathogenic Mechanismsmentioning

confidence: 99%

What the Cardiologist Needs to Consider in the Management of Oncologic Patients with STEMI-Like Syndrome: A Case Report and Literature Review

et al. 2021

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In pre-hospital care, an accurate and quick diagnosis of ST-segment elevation myocardial infarction (STEMI) is imperative to promptly kick-off the STEMI network with a direct transfer to the cardiac catheterization laboratory (cath lab) in order to reduce myocardial infarction size and mortality. Aa atherosclerotic plaque rupture is the main mechanism responsible for STEMI. However, in a small percentage of patients, emergency coronarography does not reveal any significant coronary stenosis. The fluoropyrimidine agents such as 5-Fluorouracil (5-FU) and capecitabine, widely used to treat gastrointestinal, breast, head and neck cancers, either as a single agent or in combination with other chemotherapies, can cause potentially lethal cardiac side effects. Here, we present the case of a patient with 5-FU cardiotoxicity resulting in an acute coronary syndrome (ACS) with recurrent episodes of chest pain and ST-segment elevation.. Our case report highlights the importance of widening the knowledge among cardiologists of the side effects of chemotherapeutic drugs, especially considering the rising number of cancer patients around the world and that fluoropyrimidines are the main treatment for many types of cancer, both in adjuvant and advanced settings.

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“…Past studies have reported that cardiotoxicity cases have increased due to 5-FU (Polk et al, 2014). The 5-FU's themselves, or its metabolites, are toxic for myocytes (Ensley et al, 1986) and 5-FU has direct toxic effects on vascular endothelium that have been associated with a decrease of endothelial nitric oxide (NO) synthase, and the reduction of NO synthase leads to coronary spasms and endothelium-independent vasoconstriction via protein kinase C (Chong and Ghosh., 2019;Çalık et al, 2012;Dechant et al, 2012;Tsibiribi et al, 2006). It has been reported that cardiotoxicity is induced the cell damage and apoptosis occur due to increased oxidative stress in cardiomyocytes (Rashid et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

Analysis of Leaf Tolerance to Midvein Damage by a Simple Midvein Cut-Off Trial

2020

THE JAPS

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In this study, the protective effects of Quercetin (Q) and Rutin in 5-fluorouracil (5-FU)-induced cardiotoxicity in rats were investigated and used eighty-piece Sprague Dawley male rats. Rats were divided randomly to eight groups; control, 5-FU, Q50+5-FU, Q100+5-FU, Q100, Rutin50+5-FU, Rutin100+5-FU, Rutin100. The control group was given intragastric (ig) corn oil for 14 days. 5-FU group was injected intraperitoneal (ip) with a single dose of 50 mg/kg. The doses of Q (50 and 100 mg/kg) and Rutin (50 and 100 mg/kg) were administered for 14 days. Rat of the 5-FUadministered groups were sacrificed under anesthesia 72 hours after 5-FU administration. The other groups were sacrificed on the day 15 after the administration. The blood samples were collected from anesthetized rats and sera were isolated from the clotted blood. The cardiac tissues were used for biochemical, histopathological and immunohistochemical analysis. Cardiac enzyme levels were significantly increased in the 5-FU group. Malondialdehyde (MDA) level was significantly higher than control in the 5-FU group and decreased in the Q100+5-FU and Rutin100+5-FU. Superoxide dismutase (SOD) and glutathione (GSH) activities were significantly decreased in the 5-FU group compared to the control, Q100+5-FU and Rutin100+5-FU. 5-FU groups had degeneration of cardiac cells and myofibril. The intensity of β-MHC positivity was higher in the 5-FU group compared to the other groups. In conclusion, this study demonstrates that Q (50 and 100 mg/kg) and Rutin (50 and 100 mg/kg) have protective effects on the 5-FU-induced cardiotoxicity in rats.

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Initial dose effect of 5-fluorouracil: rapidly improving severe, acute toxic myopericarditis

Cited by 24 publications

References 9 publications

Acute reversible left ventricular systolic dysfunction associated with 5-fluorouracil therapy: a rare and increasingly recognised cardiotoxicity of a commonly used drug

Acute reversible left ventricular systolic dysfunction associated with 5-fluorouracil therapy: a rare and increasingly recognised cardiotoxicity of a commonly used drug

What the Cardiologist Needs to Consider in the Management of Oncologic Patients with STEMI-Like Syndrome: A Case Report and Literature Review

Analysis of Leaf Tolerance to Midvein Damage by a Simple Midvein Cut-Off Trial

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