Background: Mitoxantrone has been extensively used as a disease-modifying therapy for multiple sclerosis. However, estimates of the associated risk of therapy-related acute leukaemia and cardiomyopathy have been derived from short-term studies. This study aimed to ascertain the long-term risk of therapy-related acute leukaemia or cardiomyopathy after mitoxantrone therapy for multiple sclerosis.
Methods: Between 2002 and 2010, 50 patients were treated with mitoxantrone at a single centre using a standard protocol (12 mg/m(2) body surface area monthly for 6 months as tolerated to a maximum of 72 mg/m(2) body surface area). Follow-up haematologic and echocardiographic data were collected in March 2011.
Results: Fifteen patients (30%) were excluded from analysis either because of lack of follow-up data, death due to non-cardiac and non-haematologic causes, or comorbid cardiovascular disease. The remaining 35 patients (70%) were followed for a median of 75 months (range: 9-103). The median cumulative mitoxantrone dose given was 72 mg/m(2) body surface area (range: 24-123). At the end of follow-up, no patients had developed therapy-related acute leukaemia. One patient suffered an asymptomatic drop in left ventricular ejection fraction from 55 to 47%.
Conclusion: This series of patients followed for up to 8.5 years suggests that the risk of either therapy-related acute leukaemia or cardiomyopathy after mitoxantrone therapy for multiple sclerosis is low when patients are treated within standard protocol.
While earlier post-mortem studies show involvement of the central nervous system in 71% of patients with chronic lymphocytic leukemia (CLL), involvement intravitam is rare. A 72-year-old man with untreated, minimally symptomatic CLL developed subacute-onset encephalopathy and presented with severe hyponatremia and stress-induced cardiomyopathy. His initial head computed tomography scan was unremarkable.
A 63-year-old woman with a history of acute myeloid leukemia followed by stem cell transplantation presented with acute heart failure. Transthoracic echocardiography revealed a preserved left ventricular ejection fraction with severe ventricular hypertrophy and signs of elevated filling pressures indicating infiltrative cardiomyopathy. She died from cardiac arrest due to cardiogenic shock.
Dilated cardiomyopathy (DCM) is a heart condition that causes enlarged and weakened left ventricles and affects the heart's ability to pump blood effectively. Most genetic etiology still needs to be understood. Previously, we have used the known germline hereditary fusion genes (HFGs) to identify HFGs associated with multiple myeloma and leukemia.
Loeffler's endocarditis (LE) is linked to hypereosinophilic syndrome, presenting in a 45-year-old woman with severe right-sided heart failure and an extreme eosinophil count of 20.9 × 10.*
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Imaging showed significant damage to the right ventricle, and biopsies revealed extensive endocardial fibrosis and eosinophil-rich thrombi, though no specific gene mutations were linked to abnormal blood conditions.*
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The patient underwent treatment with ruxolitinib, followed by heart transplantation due to irreversible damage, and after a challenging recovery phase, she improved despite facing ICU-acquired weakness and depression.*
