Cumulative incidence and risk factors of mitoxantrone-induced cardiotoxicity in childrena systematic review

VANDALEN, E; VANDERPAL, H; Bakker, P.M.; Caron, Huib N.; Kremer, L. C. M.

doi:10.1016/s0959-8049(03)01071-2

Cited by 9 publications

(6 citation statements)

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“…MTX ( Fig. 1) is an anthraquinone derivative that has been extensively investigated for the treatment of breast and prostate cancer but its clinical application has been limited due to severe cardiotoxicity (20). Solid lipid nanoparticles (21), liposomes (22) and polyester nanoparticles (23) have been investigated to improve MTX formulation but limited drug loading capacity and poorly controlled release hindered their utility.…”

Section: Introductionmentioning

confidence: 99%

Surface Functionalization of Mesoporous Silica Nanoparticles Controls Loading and Release Behavior of Mitoxantrone

et al. 2012

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Section: Introductionmentioning

confidence: 99%

Surface Functionalization of Mesoporous Silica Nanoparticles Controls Loading and Release Behavior of Mitoxantrone

et al. 2012

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“…Unfortunately, the therapeutic use of anthracyclines and anthracenedione is associated with cumulative cardiotoxicity caused by irreversible damage to the cardiac muscle [1,2]. The lifetime cumulative dose limit for doxorubicin is 450 to 550 mg/m 2 with a cumulative incidence of congestive heart failure (CHF) of 7.5% at a total doxorubicin dose of 550 mg/m 2 [3,4].…”

Section: Introductionmentioning

confidence: 99%

Pixantrone (BBR 2778) has reduced cardiotoxic potential in mice pretreated with doxorubicin: Comparative studies against doxorubicin and mitoxantrone

Cavalletti¹,

Crippa²,

Mainardi³

et al. 2007

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Anthracyclines and anthracenediones are important oncotherapeutics; however, their use is associated with irreversible and cumulative cardiotoxicity. A novel aza-anthracenedione, pixantrone (BBR 2778), was developed to reduce treatment-related cardiotoxicity while retaining efficacy. This study evaluates the cumulative cardiotoxic potential of pixantrone compared with equiactive doses of doxorubicin and mitoxantrone in both doxorubicin-pretreated and doxorubicin-naïve mice. CD1 female mice were given doxorubicin 7.5 mg/kg (once weekly for 3 weeks) followed 6 weeks later by either sterile 0.9% saline, doxorubicin 7.5 mg/kg, pixantrone 27 mg/kg, or mitoxantrone 3 mg/kg (once weekly for 3 weeks). A second group of CD1 female mice were given 2 cycles of either sterile 0.9% saline, pixantrone 27 mg/kg, doxorubicin 7.5 mg/kg, or mitoxantrone 3 mg/kg (once weekly for 3 weeks). Animals were sacrificed at different time points for histopathologic examination of the heart. In the doxorubicin-pretreated mice, further exposure to doxorubicin or mitoxantrone resulted in a significant worsening of pre-existing degenerative cardiomyopathy. In contrast, pixantrone did not worsen pre-existing cardiomyopathy in these animals. Only minimal cardiac changes were observed in mice given repeated cycles of pixantrone, while 2 cycles of doxorubicin or mitoxantrone resulted in marked or severe degenerative cardiomyopathy. These animal studies demonstrate the reduced cardiotoxic potential of pixantrone compared with doxorubicin and mitoxantrone. Exposure to pixantrone did not worsen pre-existing cardiomyopathy in doxorubicin-pretreated mice, suggesting that pixantrone may be useful in patients pretreated with anthracyclines.

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“…8,9 In a systematic review of 17 cohort studies, Van Dalen et al reported a cumulative incidence of mitoxantroneinduced cardiomyopathy ranging from 0 to 6.7% for clinical heart failure and from 0 to 80% for asymptomatic cardiac dysfunction. 7 These findings compare to a cumulative incidence of anthracyclineinduced cardiotoxicity ranging from 0 to 16% for symptomatic heart failure and from 0 to 57% for asymptomatic cardiac dysfunction.…”

Section: Discussionmentioning

confidence: 91%

“…5,6 Early or acute toxicity occurs during therapy or in the 1st year following therapy, whereas late cardiotoxicity occurs at least 1 year after the completion of therapy. [5][6][7] No specific treatment exists for anthracycline-induced cardiotoxicity other than supportive care, although some patients show variable recovery of ventricular function with conventional medical therapy for heart failure.…”

Section: Discussionmentioning

confidence: 99%

“…Mitoxantrone hydrochloride, an anthracenedione, is a non-cell-cycle-specific anthraquinone derivative, which has demonstrated significant antitumour activity similar to anthracyclines; unfortunately, in clinical studies, mitoxantrone has been shown to cause anthracycline-like cardiotoxicity 8 9 In a systematic review of 17 cohort studies, Van Dalen et al reported a cumulative incidence of mitoxantrone-induced cardiomyopathy ranging from 0 to 6.7% for clinical heart failure and from 0 to 80% for asymptomatic cardiac dysfunction 7 . These findings compare to a cumulative incidence of anthracycline-induced cardiotoxicity ranging from 0 to 16% for symptomatic heart failure and from 0 to 57% for asymptomatic cardiac dysfunction.…”

Section: Discussionmentioning

confidence: 99%

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Case report and review of the literature: the utilisation of a ventricular assist device as bridge to recovery for anthracycline-induced ventricular dysfunction

et al. 2017

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Ventricular assist devices are used in children with heart failure as a bridge to myocardial recovery or cardiac transplantation. Anthracyclines cause cardiac toxicity and may result in acute or long-term cardiac failure. We describe the use of a ventricular assist device as a bridge to recovery in a child with severe acute anthracycline-induced cardiomyopathy, and we review the associated literature. A 6-year-old girl was treated for acute myeloblastic leukaemia with daunorubicin and mitoxantrone. After 2 weeks her final dose of chemotherapy, her Left Ventricular Ejection Fraction decreased to 21%. Despite initiation of medical therapy, she had continued deterioration of left ventricular function and developed evidence of poor end-organ perfusion. She was not a candidate for cardiac transplantation, as the post-transplant immune suppression therapy would put her at risk for recurrence of her malignancy. We placed her on a short-term ventricular assist device as a bridge to ultimately placing her on a long-term ventricular assist device versus continuing medical therapy. Her left ventricular ejection fraction improved to 55% 24 days after ventricular assist device insertion. She was separated from the ventricular assist device 26 days after its insertion. She was discharged home 29 days later and is now 28 months after ventricular assist device implantation with stable ventricular function, as documented by a left ventricular ejection fraction of 55%, and normal end organ function. This case is one of the only reports known describing successful use of a short-term ventricular assist device as a bridge to recovery in a child with severe acute anthracycline-induced cardiotoxicity.

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Cumulative incidence and risk factors of mitoxantrone-induced cardiotoxicity in childrena systematic review

Cited by 9 publications

References 0 publications

Surface Functionalization of Mesoporous Silica Nanoparticles Controls Loading and Release Behavior of Mitoxantrone

Surface Functionalization of Mesoporous Silica Nanoparticles Controls Loading and Release Behavior of Mitoxantrone

Pixantrone (BBR 2778) has reduced cardiotoxic potential in mice pretreated with doxorubicin: Comparative studies against doxorubicin and mitoxantrone

Case report and review of the literature: the utilisation of a ventricular assist device as bridge to recovery for anthracycline-induced ventricular dysfunction

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