Mosijczuk A D, Ruymann F B, Mease A D, Bernier R D
Cancer. 1979 Nov;44(5):1582-7. doi: 10.1002/1097-0142(197911)44:5<1582::aid-cncr2820440507>3.0.co;2-h.
Two children with leukemia are presented, each demonstrating an unusual aspect of anthracycline-induced cardiomyopathy. In the first patient (a 7-month-old female with acute monocytic leukemia) extremely young age and previous chemotherapy with a podophyllotoxin derivative, VP-16, may have prediposed the patient to fatal congestive heart failure at a total Daunorubicin dose of only 225 mg/m2. In the second patient, a delay of 4 1/2 years was not sufficient in preventing congestive heart failure resulting from the administration of additional anthracycline chemotherapy. We conclude that extremely young age and, possibly, prior therapy with VP-16 may be addition risk factors in the development of anthracycline cardiomyopathy. Also, we suggest that once an anthracycline agent has reached a toxic threshold for the myocardium, the heart may always be at risk to injury from additional Adriamycin or Daunorubicin therapy.
本文介绍了两名白血病患儿,他们各自展现了蒽环类药物所致心肌病的一个不同寻常的方面。首例患者(一名7个月大的急性单核细胞白血病女婴),因其年龄极小且先前接受过鬼臼毒素衍生物VP - 16化疗,可能使患者在柔红霉素总剂量仅为225 mg/m²时就易发生致命性充血性心力衰竭。在第二例患者中,4年半的间隔时间不足以预防因再次给予蒽环类化疗而导致的充血性心力衰竭。我们得出结论,年龄极小以及可能先前接受过VP - 16治疗可能是蒽环类心肌病发生的额外危险因素。此外,我们认为一旦蒽环类药物达到对心肌的毒性阈值,心脏可能始终面临因额外使用阿霉素或柔红霉素治疗而受损的风险。