Saito Yoshitaka, Takekuma Yoh, Yuki Satoshi, Komatsu Yoshito, Sugawara Mitsuru
Department of Pharmacy, Hokkaido University Hospital, Sapporo, Japan.
Department of Gastroenterology and Hepatology, Hokkaido University Hospital, Sapporo, Japan.
Case Rep Oncol. 2021 Mar 1;14(1):207-211. doi: 10.1159/000512820. eCollection 2021 Jan-Apr.
We had previously reported on S-1-induced hypertriglyceridemia. Here, we report fluorouracil-induced hypertriglyceridemia in a patient with capecitabine-induced hypertriglyceridemia and the corresponding therapeutic process. A woman in her forties who had experienced grade 3 hypertriglyceridemia due to oxaliplatin + capecitabine was administered fluorouracil ± oxaliplatin + levofolinate calcium + panitumumab; however, grade 4 hypertriglyceridemia occurred after the thirteenth administration. Bezafibrate normalized the elevation. Chemotherapy cessation resulted in its decrease to normal, and bezafibrate was stopped. Nine months after cessation, treatment with fluorouracil + irinotecan + levofolinate calcium + ramucirumab was initiated. After four cycles of treatment, her serum triglyceride levels increased again to grade 3, and then, fenofibrate was administered, resulting in a significant decrease to grade 1-2. Serum triglyceride levels significantly reduced after cessation of the prior fluorouracil-containing regimen, although its elevation was observed again following the latter treatment. Therefore, fluorouracil-induced hypertriglyceridemia was strongly speculated in this case. We have speculated that the most probable cause of tegafur and capecitabine-induced hypertriglyceridemia is fluorouracil or its metabolic enzymes since their end product is fluorouracil in the previous report. Results from this patient suggest that our supposition was correct. Fibrates administration, cessation of the treatment, and monitoring of serum triglyceride level was effective in this case as well as previous reports. Fluorouracil-induced hypertriglyceridemia is associated with the one caused by tegafur and capecitabine and presents the possibility of severe complications. Elucidation of its exact mechanism and epidemiological features is needed for better understanding.
我们之前曾报道过S-1诱导的高甘油三酯血症。在此，我们报告一例在接受卡培他滨诱导的高甘油三酯血症患者中发生氟尿嘧啶诱导的高甘油三酯血症及相应治疗过程。一名四十多岁的女性因奥沙利铂+卡培他滨出现3级高甘油三酯血症，接受氟尿嘧啶±奥沙利铂+亚叶酸钙+帕尼单抗治疗；然而，在第13次给药后出现了4级高甘油三酯血症。非诺贝特使血脂升高恢复正常。停止化疗后血脂降至正常，非诺贝特停药。停药9个月后，开始用氟尿嘧啶+伊立替康+亚叶酸钙+雷莫西尤单抗治疗。四个周期治疗后，她的血清甘油三酯水平再次升至3级，随后给予非诺贝特，使其显著降至1-2级。停用之前含氟尿嘧啶的治疗方案后血清甘油三酯水平显著降低，尽管在后续治疗中再次出现升高。因此，强烈推测该病例为氟尿嘧啶诱导的高甘油三酯血症。我们曾推测替加氟和卡培他滨诱导高甘油三酯血症最可能的原因是氟尿嘧啶或其代谢酶，因为在前一份报告中它们的终产物是氟尿嘧啶。该患者的结果表明我们的推测是正确的。在本病例以及之前的报告中，使用贝特类药物、停止治疗以及监测血清甘油三酯水平均有效。氟尿嘧啶诱导的高甘油三酯血症与替加氟和卡培他滨引起的高甘油三酯血症相关，且存在严重并发症的可能性。需要阐明其确切机制和流行病学特征以更好地理解。
