dihydropyrimidine dehydrogenase deficiency/i̇shal

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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

Severe adverse events due to dihydropyrimidine dehydrogenase deficiency in a Japanese patient with colon cancer taking capecitabine: a case report.

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Fluoropyrimidine has been commonly used not only in unresectable cases of metastatic colorectal cancer, but also in adjuvant therapy. Dihydropyrimidine dehydrogenase (DPD) is an enzyme encoded by the DPYD gene, which is responsible for the rate-limiting step in pyrimidine catabolism and

High-resolution melting analysis of the common c.1905+1G>A mutation causing dihydropyrimidine dehydrogenase deficiency and lethal 5-fluorouracil toxicity.

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Dihydropyrimidine dehydrogenase (DPD) deficiency is a pharmacogenetic syndrome associated with life-threatening toxicity following exposure to the fluoropyrimidine drugs 5-fluorouracil (5-FU) and capecitabine (CAP), widely used for the treatment of colorectal cancer and other solid tumors. The most

[Suspected dihydropyrimidine dehydrogenase deficiency in a patient receiving capecitabine as adjuvant chemotherapy after colon resection].

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We report here the case of a 75-year-old male patient who developed severe side effects after treatment with capecitabine (Xeloda®) that he received as adjuvant chemotherapy. He was suspected to have partial dihydropyrimidine dehydrogenase (DPD) deficiency. The patient underwent sigmoidectomy for

Dihydropyrimidine dehydrogenase deficiency: a pharmacogenetic defect causing severe adverse reactions to 5-fluorouracil-based chemotherapy.

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OBJECTIVE 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. METHODS Published articles, abstracts, and conference

Prolonged severe 5-fluorouracil-associated neurotoxicity in a patient with dihydropyrimidine dehydrogenase deficiency.

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5-Fluorouracil (5-FU) is an analogue of pyrimidine nucleosides that is widely used in the treatment of head and neck, breast, ovarian, and colon cancer. Stomatitis, diarrhea, dermatitis, and myelosuppression are the main toxicities of 5-FU. A less frequent side effect that is becoming more

DPYD2A mutation: the most common mutation associated with DPD deficiency*.

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BACKGROUND Dihydropyrimidine dehydrogenase (DPD) enzyme is responsible for the elimination of approximately 80% of administered dose of 5-FU. DPD deficiency has been associated with severe 5-FU toxicity. Syndrome of DPD deficiency manifests as diarrhea, stomatitis, mucositis, and neurotoxicity and

[Dihydropyrimidine dehydrogenase deficiency causes severe adverse effects of capecitabine].

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We report the case of a 61-year-old man who experienced severe adverse effects of capecitabine because of dihydropyrimidine dehydrogenase (DPD) deficiency. In 2016, he visited our hospital for adenocarcinoma of the gastroesophageal junction and was prescribed neoadjuvant chemotherapy with

Cytomegalovirus enterocolitis in a patient with dihydropyrimidine dehydrogenase deficiency after capecitabine treatment: A case report.

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5-Fluorouracil (5-FU) is widely used for cancer treatment. The reduced activity of dihydropyrimidine dehydrogenase (DPD), the key enzyme in 5-FU inactivation, increases a patient's risk of developing severe 5-FU related toxicity. However, screening for DPD deficiency is rarely

Protein intake and 5-fluorouracil toxicity in tumor-bearing animals.

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The administration of chemotherapy is limited in clinical situations by lack of selective antineoplastic activity resulting in significant host toxicity. Although it has been suggested that nutrition support can reduce chemotherapy-related toxicity, few controlled studies exist to document this

DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENCY (DPD) IN GI MALIGNANCIES: EXPERIENCE OF 4-YEARS.

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OBJECTIVES: 5-Fluorouracil (5-FU) is an integral part of treatment of GI malignancies. While normal DPD enzyme activity is rate limiting in 5-FU catabolism, its deficiency could increase concentrations of bioavailable 5-FU anabolic products leading to 5-FU related toxicity syndrome. METHODOLOGY:

Severe 5-fluorouracil toxicity associated with a marked alteration of pharmacokinetics of 5-fluorouracil and its catabolite 5-fluoro-5,6-dihydrouracil: a case report.

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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

A pharmacokinetic-based test to prevent severe 5-fluorouracil toxicity.

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OBJECTIVE Dihydropyrimidine dehydrogenase (DPD) plays a key role in the catabolism of 5-fluorouracil (5-FU) to 5-fluoro-5,6-dihydrouracil (5-FDHU), and as such, an impairment of DPD has been recognized as an important factor for altered 5-FU and 5-FDHU pharmacokinetics, predisposing patients to the

[Severe bone marrow suppression during adjuvant chemotherapy for gastric cancer by S-1 and its possible relationship to dihydropyrimidine dehydrogenase deficiency].

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The patient was a 70-year-old woman, who had undergone total gastrectomy and splenectomy with D2 lymph node dissection, for stage II gastric cancer. We admitted S-1 of 80 mg/day in adjuvant chemotherapy on postoperative day 28. There were no adverse events for one week, and she was discharged.

Predictive testing for DPD deficiency in a patient with familial history of fluoropyrimidine-associated toxicity.

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Reduced activity of DPD leads to severe toxicity in cancer patients receiving standard doses of fluoropyrimidines, particularly in the case of combination regimens. We describe a 38-year-old man with a resectable metastasis from hereditary nonpolyposis colorectal cancer, with indication of

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Herbal & Natural Medicine

Bilim tarafından desteklenen en eksiksiz şifalı otlar veritabanı

55 dilde çalışır
Bilim destekli bitkisel kürler
Görüntüye göre bitki tanıma
Etkileşimli GPS haritası - bölgedeki bitkileri etiketleyin (yakında)
Aramanızla ilgili bilimsel yayınları okuyun
Şifalı bitkileri etkilerine göre arayın
İlgi alanlarınızı düzenleyin ve haber araştırmaları, klinik denemeler ve patentlerle güncel kalın

Bir belirti veya hastalık yazın ve yardımcı olabilecek bitkiler hakkında bilgi edinin, bir bitki yazın ve karşı kullanıldığı hastalıkları ve semptomları görün.
* Tüm bilgiler yayınlanmış bilimsel araştırmalara dayanmaktadır

dihydropyrimidine dehydrogenase deficiency/i̇shal

Delayed Presentation of DPD Deficiency in Colorectal Cancer.

Severe adverse events due to dihydropyrimidine dehydrogenase deficiency in a Japanese patient with colon cancer taking capecitabine: a case report.

High-resolution melting analysis of the common c.1905+1G>A mutation causing dihydropyrimidine dehydrogenase deficiency and lethal 5-fluorouracil toxicity.

[Suspected dihydropyrimidine dehydrogenase deficiency in a patient receiving capecitabine as adjuvant chemotherapy after colon resection].

Dihydropyrimidine dehydrogenase deficiency: a pharmacogenetic defect causing severe adverse reactions to 5-fluorouracil-based chemotherapy.

Prolonged severe 5-fluorouracil-associated neurotoxicity in a patient with dihydropyrimidine dehydrogenase deficiency.

DPYD*2A mutation: the most common mutation associated with DPD deficiency.

[Dihydropyrimidine dehydrogenase deficiency causes severe adverse effects of capecitabine].

Cytomegalovirus enterocolitis in a patient with dihydropyrimidine dehydrogenase deficiency after capecitabine treatment: A case report.

Protein intake and 5-fluorouracil toxicity in tumor-bearing animals.

DIHYDROPYRIMIDINE DEHYDROGENASE DEFICIENCY (DPD) IN GI MALIGNANCIES: EXPERIENCE OF 4-YEARS.

Severe 5-fluorouracil toxicity associated with a marked alteration of pharmacokinetics of 5-fluorouracil and its catabolite 5-fluoro-5,6-dihydrouracil: a case report.

A pharmacokinetic-based test to prevent severe 5-fluorouracil toxicity.

[Severe bone marrow suppression during adjuvant chemotherapy for gastric cancer by S-1 and its possible relationship to dihydropyrimidine dehydrogenase deficiency].

Predictive testing for DPD deficiency in a patient with familial history of fluoropyrimidine-associated toxicity.

Bilim tarafından desteklenen en eksiksiz şifalı otlar veritabanı

DPYD2A mutation: the most common mutation associated with DPD deficiency*.