Unpredicted Severe Toxicity after 5-Fluorouracil Treatment due to Dihydropyrimidine Dehydrogenase Deficiency.
10.3904/kjim.2006.21.1.43
- Author:
Jin Ho BAEK
1
;
Jong Gwang KIM
;
Shi Nae KIM
;
Dong Hwan KIM
;
Sang Kyun SOHN
;
Young Jun HONG
;
Kyu Bo LEE
Author Information
1. Department of Hematology/Oncology, Kyungpook National University Hospital, Daegu, Korea. jkk21c@knu.ac.kr
- Publication Type:Case Report
- Keywords:
Dihydrouracil dehydrogenase;
Fluorouracil;
Stomach neoplasms
- MeSH:
Stomach Neoplasms/complications/*drug therapy/surgery;
Risk Factors;
Risk Assessment;
Humans;
Fluorouracil/*adverse effects;
Female;
*Drug Toxicity;
Dihydrouracil Dehydrogenase (NADP)/*deficiency;
Chemotherapy, Adjuvant;
Antimetabolites, Antineoplastic/*adverse effects;
Adult;
Adenocarcinoma/complications/*drug therapy/surgery
- From:The Korean Journal of Internal Medicine
2006;21(1):43-45
- CountryRepublic of Korea
- Language:English
-
Abstract:
Dihydropyrimidine dehydrogenase (DPD) is the initial and rate-limiting enzyme in the catabolism of 5-fluorouracil (5-FU). Thus, patients with a DPD deficiency are at risk of developing severe 5-FU-associated toxicity. A 37-year-old female with gastric cancer underwent a curative operation, followed by adjuvant chemotherapy consisting of 5-FU and epirubicin. After the first cycle of chemotherapy, the patient manifested grade 2 mucositis and febrile neutropenia, and when her treatment was subsequently continued with doxifluridine she developed severe mucositis and febrile neutropenia. A PCR study revealed that her DPD mRNA level was lower than that in a control group. Thus, when considering the routine use of 5-FU for the treatment of cancer patients, an analysis of DPD activity or screening for DPD mutations is warranted in confined patients who experience unpredicted severe toxicity after initial 5-FU administration, even though DPD deficiency is a rare metabolic defect.
