Antineoplastics
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Reactions 1478, p8 - 16 Nov 2013 S Antineoplastics Cardiotoxicity: case report A 31-year-old woman developed cardiotoxicity after receiving chemotherapy with cyclophosphamide, doxorubicin, ifosfamide and cytarabine [routes and durations of treatments to reaction onset not stated]. The woman was diagnosed with primary mediastinal large B-cell lymphoma. She started chemotherapy with two courses of rituximab, cyclophosphamide 0.75 g/m 2 , doxorubicin 50 mg/m 2 , vincristine and prednisolone (R-CHOP therapy). The effects of R-CHOP therapy were insufficient, so auto peripheral blood transplantation was planned. She received one course of ifosfamide 1500 mg/m 2 , carboplatin, etoposide and dexamethasone (DeVIC therapy). She later received two courses of cyclophosphamide 1.2 g/m 2 , etoposide, cytarabine 2 g/m 2 and prednisolone (CHASE therapy), and underwent peripheral blood stem cell harvest. The mediastinal mass significantly reduced in size. She then received high-dose chemotherapy comprising ranimustine for 2 days, then carboplatin, etoposide and cyclophosphamide 1.8 g/m 2 /day for 2 days, followed by peripheral blood stem cell transplantation. The total doses of cyclophosphamide and doxorubicin administered were 10.4g (7.6 g/m 2 ) and 100 mg/m 2 , respectively. After completing chemotherapy, she gradually 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. Echocardiography showed impaired systolic and diastolic dysfunction with pericardial effusion and left ventricular wall hypertrophy. She also had a worsening of renal and liver functions. The woman underwent pericardiocentesis. She was diagnosed with heart failure. Swan-Ganz catheterisation revealed mild pulmonary hypertension with increased pulmonary vascular resistance. After further tests, she was diagnosed with cyclophosphamide-induced cardiotoxicity. She received furosemide, carperitide, carvedilol, losartan and spironolactone. Her dyspnoea and fatigue improved, and she was discharged, although slight pericardial effusion and pulmonary 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 of doxorubicin and ifosfamide were lower than the reported cardiotoxic doses (anthracycline >550 mg/m 2 , ifosfamide >12.5 g/m 2 ), these agents can potentiate [cyclophosphamide]-induced cardiotoxicity. Moreover, cytarabine may also have contributed to the condition of this patient". Kusumoto S, et al. Cyclophosphamide-induced cardiotoxicity with a prolonged clinical 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 1 Reactions 16 Nov 2013 No. 1478 0114-9954/13/1478-0001/$14.95 Adis © 2013 Springer International Publishing AG. All rights reserved
Transcript of Antineoplastics
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
