“…For UFT, lower incidences of cardiotoxicity (1%) have been reported [41], but there are few published data regarding the cardiotoxicity from S-1. Yet, a case series of seven patients whom were successfully treated with S-1 after cardiotoxicity induced by capecitabine has been published [42]. The thymidylate synthase inhibitor, raltitrexed, is an alternative in patients with advanced colorectal cancer.…”
Background: Fluoropyrimidines are mainstay chemotherapeutics in the treatment of gastrointestinal cancers and are also used to treat breast cancer and head and neck cancers. However, 5-flourouracil (5-FU) and capecitabine may induce cardiotoxicity that mostly presents as acute coronary syndromes. We compared the incidence of cardiotoxicity induced by 5-FU and capecitabine in patients with colorectal cancer and sought to identify risk markers for cardiotoxicity. Methods: We reviewed all consecutive patients with colorectal cancer who received 5-FU or capecitabine at one institution in the neoadjuvant (2007-2016), adjuvant (2000-2016) or metastatic setting (2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016). Results: Totally, 995 patients received 5-FU and 1241 received capecitabine. The incidence of cardiotoxicity induced by 5-FU was 5.2% [95% confidence interval (CI): 3.8-6.6%] and 4.1% (95% CI: 3.0-5.2%) induced by capecitabine (p ¼ .21). The most common events were angina without ischemia (5-FU: 1.6%, capecitabine: 1.3%, p ¼ .53), angina with ischemia on ECG (5-FU: 0.9%, capecitabine: 0.8%, p ¼ .53), unspecified chest pain (5-FU: 0.9%, capecitabine: 0.6%, p ¼ .34), ST-elevation myocardial infarction (5-FU: 0.5%; capecitabine: 0.4%, p ¼ .76) and non-ST-elevation myocardial infarction (5-FU: 0.7%, capecitabine: 0.5%, p ¼ .50). Cardiac arrest or sudden death occurred in 0.5 and 0.4%, respectively (p ¼ 1). No risk markers for cardiotoxicity induced by 5-FU were identified. In the capecitabine group, ischemic heart disease was a risk marker (odds ratio: 2.9, 95% CI: 1.2-7.0, p ¼ .016). Conclusions: Five percent of patients treated with 5-FU developed cardiotoxicity and 4% treated with capecitabine. Ischemic heart disease was a risk marker for cardiotoxicity induced by capecitabine.
“…For UFT, lower incidences of cardiotoxicity (1%) have been reported [41], but there are few published data regarding the cardiotoxicity from S-1. Yet, a case series of seven patients whom were successfully treated with S-1 after cardiotoxicity induced by capecitabine has been published [42]. The thymidylate synthase inhibitor, raltitrexed, is an alternative in patients with advanced colorectal cancer.…”
Background: Fluoropyrimidines are mainstay chemotherapeutics in the treatment of gastrointestinal cancers and are also used to treat breast cancer and head and neck cancers. However, 5-flourouracil (5-FU) and capecitabine may induce cardiotoxicity that mostly presents as acute coronary syndromes. We compared the incidence of cardiotoxicity induced by 5-FU and capecitabine in patients with colorectal cancer and sought to identify risk markers for cardiotoxicity. Methods: We reviewed all consecutive patients with colorectal cancer who received 5-FU or capecitabine at one institution in the neoadjuvant (2007-2016), adjuvant (2000-2016) or metastatic setting (2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016). Results: Totally, 995 patients received 5-FU and 1241 received capecitabine. The incidence of cardiotoxicity induced by 5-FU was 5.2% [95% confidence interval (CI): 3.8-6.6%] and 4.1% (95% CI: 3.0-5.2%) induced by capecitabine (p ¼ .21). The most common events were angina without ischemia (5-FU: 1.6%, capecitabine: 1.3%, p ¼ .53), angina with ischemia on ECG (5-FU: 0.9%, capecitabine: 0.8%, p ¼ .53), unspecified chest pain (5-FU: 0.9%, capecitabine: 0.6%, p ¼ .34), ST-elevation myocardial infarction (5-FU: 0.5%; capecitabine: 0.4%, p ¼ .76) and non-ST-elevation myocardial infarction (5-FU: 0.7%, capecitabine: 0.5%, p ¼ .50). Cardiac arrest or sudden death occurred in 0.5 and 0.4%, respectively (p ¼ 1). No risk markers for cardiotoxicity induced by 5-FU were identified. In the capecitabine group, ischemic heart disease was a risk marker (odds ratio: 2.9, 95% CI: 1.2-7.0, p ¼ .016). Conclusions: Five percent of patients treated with 5-FU developed cardiotoxicity and 4% treated with capecitabine. Ischemic heart disease was a risk marker for cardiotoxicity induced by capecitabine.
“…Oteracil prevents the phosphorylation of 5-FU in the digestive tract in order to reduce gastrointestinal toxicities [2]. S-1 has shown comparable efficacy results compared to 5-FU and capecitabine in both Asian and in Western patients with metastatic colorectal cancer (mCRC) [3,4], but is associated with a lower incidence of handfoot syndrome (HFS) and cardiac toxicity compared with capecitabine [4][5][6]. In a retrospective analysis of 52 patients in whom capecitabine was discontinued and replaced with S-1 for reasons of severe symptoms of HFS, 94% of patients experienced a lower grade of HFS upon treatment with S-1 compared to the capecitabine-induced grade of HFS, with 56% of patients experiencing a complete resolution of HFS-related symptoms [7].…”
“…The results of the phase III SALTO trial, comparing S-1 to capecitabine in Western mCRC patients, demonstrated that first-line treatment with S-1 was associated with a significantly lower incidence of handefoot syndrome (HFS) compared with capecitabine, without compromising on efficacy, although the study was not powered to show non-inferiority [10,11]. Retrospective series in Western mCRC patients have shown the tolerability of S-1 in Western mCRC patients who discontinued treatment with capecitabine for reasons of HFS or cardiac toxicity [12,13]. Together, these data indicated that S-1 may be considered as a suitable alternative to capecitabine in Western mCRC patients, specifically in those with intolerance due to HFS or cardiac toxicity.…”
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