Reactions 1478, p8 - 16 Nov 2013

SAntineoplastics

Cardiotoxicity: case reportA 31-year-old woman developed cardiotoxicity after

receiving chemotherapy with cyclophosphamide, doxorubicin,ifosfamide and cytarabine [routes and durations of treatmentsto reaction onset not stated].

The woman was diagnosed with primary mediastinal largeB-cell lymphoma. She started chemotherapy with two coursesof rituximab, cyclophosphamide 0.75 g/m2, doxorubicin50 mg/m2, vincristine and prednisolone (R-CHOP therapy).The effects of R-CHOP therapy were insufficient, so autoperipheral blood transplantation was planned. She receivedone course of ifosfamide 1500 mg/m2, carboplatin, etoposideand dexamethasone (DeVIC therapy). She later received twocourses of cyclophosphamide 1.2 g/m2, etoposide, cytarabine2 g/m2 and prednisolone (CHASE therapy), and underwentperipheral blood stem cell harvest. The mediastinal masssignificantly reduced in size. She then received high-dosechemotherapy comprising ranimustine for 2 days, thencarboplatin, etoposide and cyclophosphamide 1.8 g/m2/dayfor 2 days, followed by peripheral blood stem celltransplantation. The total doses of cyclophosphamide anddoxorubicin administered were 10.4g (7.6 g/m2) and100 mg/m2, respectively. After completing chemotherapy, shegradually developed general fatigue and exertional dyspnoea,and was referred to a hospital 2 months later. Upon admission,she had a gallop rhythm and mild pretibial oedema. A chest x-ray showed mild pulmonary congestion and cardiomegaly,while ECG showed sinus tachycardia. Echocardiographyshowed impaired systolic and diastolic dysfunction withpericardial effusion and left ventricular wall hypertrophy. Shealso had a worsening of renal and liver functions.

The woman underwent pericardiocentesis. She wasdiagnosed with heart failure. Swan-Ganz catheterisationrevealed mild pulmonary hypertension with increasedpulmonary vascular resistance. After further tests, she wasdiagnosed with cyclophosphamide-induced cardiotoxicity.She received furosemide, carperitide, carvedilol, losartan andspironolactone. Her dyspnoea and fatigue improved, and shewas discharged, although slight pericardial effusion andpulmonary hypertension remained. Six months later,pericardial effusion disappeared, and cardiotoxicity improved.At last follow-up, she had no deterioration of heart failure.

Author comment: "Although the total doses ofdoxorubicin and ifosfamide were lower than the reportedcardiotoxic doses (anthracycline >550 mg/m2, ifosfamide>12.5 g/m2), these agents can potentiate[cyclophosphamide]-induced cardiotoxicity. Moreover,cytarabine may also have contributed to the condition of thispatient".Kusumoto S, et al. Cyclophosphamide-induced cardiotoxicity with a prolongedclinical course diagnosed on an endomyocardial biopsy. Internal Medicine 52:2311-2315, No. 20, 2013. Available from: URL: http://dx.doi.org/10.2169/internalmedicine.52.0347 - Japan 803095672

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Reactions 16 Nov 2013 No. 14780114-9954/13/1478-0001/$14.95 Adis © 2013 Springer International Publishing AG. All rights reserved