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dihydropyrimidine dehydrogenase deficiency/kusma

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NesneKlinik denemelerPatentler
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A neonate with recurrent vomiting and generalized hypotonia diagnosed with a deficiency of dihydropyrimidine dehydrogenase.

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Deficiency of dihydropyrimidine dehydrogenase (DPD) is a rare inborn error of pyrimidine metabolism. To date, only about 50 patients are known worldwide. The clinical picture is varied and is not yet fully described. Most patients are diagnosed at the age of 1-3 years. We present a patient diagnosed

Dihydropyrimidinase deficiency: the first feline case of dihydropyrimidinuria with clinical and molecular findings.

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Dihydropyrimidinase (DHP, EC 3.5.2.2) is the second enzyme of the pyrimidine degradation pathway and a deficiency of this enzyme is responsible for a rare inborn metabolic syndrome characterized by dihydropyrimidinuria. Here we report a cat with DHP deficiency, manifesting malnutrition, depression,

Delayed Presentation of DPD Deficiency in Colorectal Cancer.

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Case Study Mr. D., a 55-year-old male, presented to the medical oncology service with a diagnosis of stage III adenocarcinoma of the sigmoid colon. He presented 7 weeks post sigmoid colectomy with lymph node resection and was initiated on adjuvant chemotherapy with CAPOX (capecitabine [Xeloda] and

[A case of dihydropyrimidine dehydrogenase (DPD) deficiency with severe side effects from UFT/Uzel administration].

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5-FU is among the drugs most frequently used in the treatment of gastrointestinal malignancies. Also, it has been reported to reveal severe side effects in the case of a dihydropyrimidine dehydrogenase (DPD) deficiency. A 75-year-old man showed severe nausea and vomiting after administration of
OBJECTIVE The objective of this study was to evaluate the safety of using tegafur-uracil (UFT) in colorectal cancer patients with partial dihydropyrimidine dehydrogenase (DPD) deficiency. METHODS The study included five colorectal cancer patients who presented with acute toxicity (grades 3 and 4)
OBJECTIVE To describe the altered pharmacokinetics of 5-fluorouracil (5-FU) and its major catabolite 5-fluoro-5,6-dihydrouracil (5-FDHU) in a 52-year-old woman affected by a severe 5-FU toxicity. METHODS Toxicities were rated according to World Health Organization. 5-FU and 5-FDHU plasma

Age and sex are independent predictors of 5-fluorouracil toxicity. Analysis of a large scale phase III trial.

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BACKGROUND Cancer is most common in older age groups, but little information is available with regard to the impact of age on chemotherapy toxicity. This study was undertaken to determine if age is an independent risk factor for 5-fluorouracil (5-FU) toxicity. METHODS Toxicity data from a

DPYD variants as predictors of 5-fluorouracil toxicity in adjuvant colon cancer treatment (NCCTG N0147).

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BACKGROUND Previous studies have suggested the potential importance of three DPYD variants (DPYD*2A, D949V, and I560S) with increased 5-FU toxicity. Their individual associations, however, in 5-FU-based combination therapies, remain controversial and require further systematic study in a large
OBJECTIVE The aim of this study was to evaluate the use of plasma and saliva uracil (U) to dihydrouracil (UH2) metabolic ratio and DPYD genotyping, as a means to identify patients with dihydropyrimidine dehydrogenase (DPD) deficiency and fluoropyrimidine toxicity. METHODS Paired plasma and saliva

Phase II study of preoperative radiation plus concurrent daily tegafur-uracil (UFT) with leucovorin for locally advanced rectal cancer.

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BACKGROUND Considerable variation in intravenous 5-fluorouracil (5-FU) metabolism can occur due to the wide range of dihydropyrimidine dehydrogenase (DPD) enzyme activity, which can affect both tolerability and efficacy. The oral fluoropyrimidine tegafur-uracil (UFT) is an effective, well-tolerated
BACKGROUND Efficacy and toxicity of oxaliplatin (Eloxatin; Sanofi-Aventis, Paris, France) combined with irinotecan (IROX) were examined in 383 patients enrolled on the IROX arm of Intergroup Study N9741. METHODS This IROX regimen was oxaliplatin 85 mg/m(2) and irinotecan 200 mg/m(2) administered

Emergency use of uridine triacetate for the prevention and treatment of life-threatening 5-fluorouracil and capecitabine toxicity.

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Increased susceptibility to 5-fluorouracil (5-FU)/capecitabine can lead to rapidly occurring toxicity caused by impaired clearance, dihydropyrimidine dehydrogenase deficiency, and other genetic variations in the enzymes that metabolize 5-FU. Life-threatening 5-FU overdoses occur because of infusion
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