作者: C. H. Takimoto , R. B. Diasio , A. Bastian , G. B. Morrison , T. Dela Rosa
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摘要: PURPOSE/OBJECTIVES To describe the pharmacogenetic syndrome of dihydropyrimidine dehydrogenase (DPD) deficiency, which predisposes patients with cancer to potentially lethal adverse reactions following 5-fluorouracil (5-FU)-based chemotherapy. DATA SOURCES Published articles, abstracts, and conference proceedings. SYNTHESIS Genetic deficiencies in DPD, rate-limiting enzyme responsible for 5-FU catabolism, may occur 3% or more putting them at increased risk unusually severe (e.g., diarrhea, stomatitis, mucositis, myelosuppression, neurotoxicity) standard doses 5-FU. Diagnosis DPD deficiency must be confirmed by specialized laboratory tests. The principle treatment DPD-deficient acute is supportive care; however, administration thymidine reverse 5-FU-induced neurologic symptoms such as encephalopathy coma. CONCLUSIONS Early recognition this serious allow modification future chemotherapy, thus avoiding further life-threatening toxicities. IMPLICATIONS FOR NURSING PRACTICE Nurses understand pharmacology, mechanism action, clinical presentation, risks, traumatic psychosocial stresses experienced receiving therapy order develop timely interventions alternative plans care.