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Reversible cardiomyopathy in a patient with chronic myelomonocytic leukemia treated with decitabine/cedazuridine: a
Ankur Sheel1, Junu Bae2, Ashlee Asada1
1Department of Internal Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, 43210, USA.
Insights
A case study reports reversible cardiomyopathy in an 85-year-old female treated with oral decitabine-cedazuridine for chronic myelomonocytic leukemia (CMML). Cardiac function recovered after drug discontinuation, highlighting the need for further research into this adverse effect.
Area of Science:
- Hematology
- Pharmacology
- Cardiology
Background:
- Hypomethylating agents (HMAs) like decitabine treat hematological malignancies.
- Oral decitabine's bioavailability is limited by cytidine deaminase; cedazuridine inhibits this enzyme.
- Intravenous decitabine is linked to cardiomyopathy, but oral decitabine-cedazuridine's cardiac effects are less understood.
Purpose of the Study:
- To report a case of reversible cardiomyopathy in a patient receiving oral decitabine-cedazuridine.
- To investigate potential cardiotoxicity associated with the oral combination therapy.
Main Methods:
- A case study of an 85-year-old female with chronic myelomonocytic leukemia (CMML).
- The patient received 5 cycles of oral decitabine-cedazuridine therapy.
- Cardiac function and symptoms were monitored, with assessment after drug discontinuation.
Main Results:
- The patient developed cardiomyopathy and heart failure with reduced ejection fraction.
- Symptoms and cardiac function improved upon cessation of decitabine-cedazuridine treatment.
- This suggests a potential for reversible cardiotoxicity with the oral HMA combination.
Conclusions:
- Reversible cardiomyopathy occurred in a patient treated with oral decitabine-cedazuridine.
- Further trials are necessary to determine the prevalence of cardiomyopathy with this therapy.
- Research into preventative strategies for cardiotoxic effects is recommended.
Background:
Hypomethylating agents (HMAs) have shown efficacy in the treatment of hematological malignancies and are indicated for the treatment of chronic myelomonocytic leukemia (CMML). While the HMA decitabine, in its intravenous formulation, has been used since 2006 for the treatment of CMML, use of its oral formulation has been limited by poor bioavailability due to first-pass metabolism by the enzyme cytidine deaminase. The dose of intravenous decitabine is limited by toxicities such as cardiomyopathy and heart failure. Therefore, cedazuridine was developed as an inhibitor of cytidine deaminase. Cedazuridine decreases the first-pass metabolism of oral decitabine allowing therapeutic levels to be achieved at lower doses, and thus, the novel oral combination of cedazuridine with decitabine was developed. While cardiomyopathy and heart failure are well-established adverse effects associated with intravenous decitabine alone, there to our knowledge there have been no documented incidences of reversible cardiomyopathy in the literature or in patients who participated in the phase 2 and phase 3 clinical trials of oral decitabine-cedazuridine.
Case:
This case study presents an 85 year-old Caucasian female with CMML who developed cardiomyopathy and heart failure with reduced ejection fraction after completing 5 cycles of therapy with decitabine/cedazuridine. Furthermore, her symptoms and cardiac function recovered upon discontinuation of the drug.
Conclusions:
We present an occurrence of reversible cardiomyopathy in a patient who completed 5 cycles of decitabine/cedazuridine, an oral combination therapy developed to enhance oral bioavailability of decitabine thereby limiting its adverse effects. As the decitabine/cedazuridine combination therapy rises in popularity due to its convenient oral formulation, more trials are needed to understand the prevalence of cardiomyopathy with this drug and to discover preventative strategies for cardiotoxic effects.
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