Key result
Dexrazoxane linked to an absolute ~13% reduction in cardiac dysfunction vs anthracycline alone.
Why the study?
Anthracycline-based chemotherapy is used in 50%-60% of childhood cancers despite its well-known cardiotoxicity, prompting evaluation of dexrazoxane as a cardioprotective agent in children receiving anthracyclines.
Does dexrazoxane combined with anthracycline chemotherapy attenuate left ventricular ejection fraction decline and reduce the incidence of cardiac dysfunction (LVEF <50%) compared to anthracycline alone in children aged 0-18 years treated for childhood cancer?
Cohort (n=142)
No
Does dexrazoxane combined with anthracycline chemotherapy attenuate left ventricular ejection fraction decline and reduce the incidence of cardiac dysfunction (LVEF <50%) compared to anthracycline alone in children aged 0-18 years treated for childhood cancer?
In pediatric cancer patients treated with anthracyclines, concomitant dexrazoxane administration significantly attenuated early LVEF decline and prevented the development of cardiac dysfunction (0% vs. 12.6% in controls), even after accounting for differences in follow-up duration.
Answers are grounded in this paper and cite their sources.
Dexrazoxane was associated with preserved LVEF in this pediatric cohort; hypothesis-generating and should not yet change practice.
Objective: Anthracycline-based chemotherapy is used in 50%-60% of childhood cancers despite well-known cardiotoxicity. The authors evaluated dexrazoxane (DEX) as a cardioprotective agent in children receiving anthracyclines. Methods: The authors retrospectively analyzed 142 children aged 0-18 years treated for childhood cancer. The control group comprised 87 patients who received anthracycline alone (2009-2019) and the case group 55 patients who received DEX + anthracycline (2019-2022, after DEX was licensed in Türkiye). Cardiac dysfunction was defined as a left ventricular ejection fraction (LVEF) below 50%. Results: Baseline LVEF was comparable. Mean LVEF fell by 0.71 Å} 6.55 points with DEX vs. 6.44 Å} 9.76 in controls (Time Å~ Group interaction F(1,140) = 14.77, P < .001), and the difference persisted after adjustment for follow-up duration and treatment covariates (β = +4.60, 95% CI = 1.10-8.10, P = .010). Cardiac dysfunction developed in 11 of 87 controls (12.6%) and in none of the 55 DEX patients (P = .007; log-rank P = .040); this held in a 36-month landmark analysis (0 of 52 vs. 4 of 25, P = .009). Mortality was higher in controls (21.8% vs. 5.5%, P = .009) and in patients with cardiac dysfunction (54.5% vs. 17.1%, P = .012). Conclusion: Dexrazoxane attenuated the early decline in LVEF and reduced the incidence of anthracycline-induced cardiotoxicity, and this persisted after adjustment for the difference in follow-up duration. With a median DEX follow-up of only 22.8 months, these data support early cardioprotection; longer follow-up is needed to assess protection against late-onset cardiotoxicity.
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Türker et al. (2026) conducted a cohort in Childhood cancer treated with anthracycline-based chemotherapy (n=142). Dexrazoxane plus anthracycline vs. Anthracycline alone was evaluated on Cardiac dysfunction (defined as absolute left ventricular ejection fraction [LVEF] <50%) (HR 0.60, 95% CI 0.24-1.47, p=0.007). Dexrazoxane plus anthracycline reduced cardiac dysfunction (LVEF <50%) to 0% vs 12.6% with anthracycline alone (P=0.007) and attenuated LVEF decline (-0.71 vs -6.44 points, P<0.001).
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