Saif Muhammad W, Smith Melissa, Maloney Antonio
Hematology/Oncology, Tufts Medical Center, Tufts University School of Medicine.
Oncology, Tufts Medical Center, Tufts University School of Medicine.
Cureus. 2016 Sep 14;8(9):e783. doi: 10.7759/cureus.783.
5-Fluorouracil (5-FU) is the backbone of the chemotherapy regimens approved for treatment of many malignancies, especially colorectal cancer (CRC). The incidence of cardiotoxicity associated with 5-FU ranges between 1.5% to 18% and is most commonly manifested as anginal symptoms. Cardiomyopathy is very rarely reported with 5-FU and capecitabine. A 35-year-old Caucasian male with T3, N1, M0 rectal cancer after the initial neoadjuvant chemoradiation with 5FU/LV followed by surgical abdominoperineal resection (APR), began mFOLFOX6 in the adjuvant setting. Following the first treatment, he developed severe cardiomyopathy, with a drop in ejection fraction (EF) to 19% from normal. The cardiac workup showed no ischemic or other etiologies to explain this cardiac event. He was a nonsmoker and only occasionally drank alcohol. He had no previous or family history of heart disease and had normal cholesterol level. He was treated for severe congestive heart failure (CHF). When the patient presented to us for second opinion, we decided to examine him for dihydropyrimidine dehydrogenase (DPD) deficiency and thymidylate synthase (TYMS) polymorphism. The patient was found to be heterozygous for the c.85T>C mutation, resulting in reduced DPYD enzymatic activity and homozygous for TYMS 5'TSER genotype 2R/2R *f. Our group first identified and reported P453L (1358C>T) type DPYD germline mutation in a patient who developed 5-FU induced cardiotoxicity. In this paper, we describe the first case of cardiomyopathy related to DPD deficiency and homozygous polymorphism of TYMS in a patient with colon cancer following 5-FU containing regimen. Fluorouracil-related cardiomyopathy has to be anticipated and treated to prevent the serious consequence of cardiac dysfunction. The prospective testing for DPD deficiency in patients might prevent DPD-deficient patients from severe toxicity or even death, and therefore the development of a unified screening method is warranted.
5-氟尿嘧啶(5-FU)是获批用于治疗多种恶性肿瘤,尤其是结直肠癌(CRC)的化疗方案的基础药物。与5-FU相关的心脏毒性发生率在1.5%至18%之间,最常见的表现为心绞痛症状。5-FU和卡培他滨很少导致心肌病。一名35岁的白种男性,患有T3、N1、M0期直肠癌,在接受初始新辅助放化疗(5FU/LV)后行腹会阴联合切除术(APR),术后在辅助治疗阶段开始使用mFOLFOX6方案。首次治疗后,他出现了严重的心肌病,射血分数(EF)从正常水平降至19%。心脏检查未发现缺血或其他病因来解释这一心脏事件。他不吸烟,偶尔饮酒。他既往无心脏病史,家族中也无心脏病史,胆固醇水平正常。他接受了严重充血性心力衰竭(CHF)的治疗。当该患者前来寻求我们的二次诊断时,我们决定对他进行二氢嘧啶脱氢酶(DPD)缺乏症和胸苷酸合酶(TYMS)基因多态性检测。发现该患者c.85T>C突变呈杂合子状态,导致DPYD酶活性降低,且TYMS 5'TSER基因型为2R/2R *f呈纯合子状态。我们团队首次在一名发生5-FU诱导心脏毒性的患者中鉴定并报告了P453L(1358C>T)型DPYD种系突变。在本文中,我们描述了首例在接受含5-FU方案治疗的结肠癌患者中与DPD缺乏和TYMS纯合子多态性相关的心肌病病例。必须对氟尿嘧啶相关心肌病进行预测和治疗,以防止心脏功能障碍的严重后果。对患者进行DPD缺乏症的前瞻性检测可能会防止DPD缺乏的患者发生严重毒性反应甚至死亡,因此有必要开发一种统一的筛查方法。