Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Capecitabine is used to treat advanced breast and gastrointestinal malignancies. A single case of encephalopathy and three cases of peripheral neuropathy are the only neurotoxicities reported. The authors report five additional cases of capecitabine-induced multifocal leukoencephalopathy.
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PMID:Capecitabine-induced multifocal leukoencephalopathy: a report of five cases. 1623 30

Capecitabine is now-a-days rapidly replacing 5-Fluorouracil in daily clinical practice. Neurologic toxicity during a treatment with fluoropyrimidines, as 5-fluorouracil, represents a well-known side-effect, largely described in literature. Central nervous system (CNS) toxicity, mainly encephalopathy with or without seizures, occurs occasionally even when conventional doses are used. CNS toxicity incidence increases markedly when the blood-brain barrier is either overwhelmed or bypassed (Hildebrand J. Neurological complications of cancer chemotherapy. Curr Opin Oncol 2006; 18: 321-324). Peripheral nervous system (PNS) toxicity is more common because proximal and distal extremities of the peripheral nerves are not protected by a blood-brain like barrier and peripheral neuropathy remains a major limiting factor for the administration of conventional doses of several agents (Saif W, Wood TE, McGee PJ and Diasio RB. Peripheral neuropathy associated with capecitabine, Anticancer Drugs 2004;15: 767-771). Capecitabine is a prodrug of 5-fluorouracil, more easily administered by mouth; its transformation in 5-fluorouracil is performed in the liver. There are only a few reports on the toxic neurological side-effects of capecitabine. We describe in our report a rare case of toxic encephalopathy in a 82-year-old female, with a brief review of literature. In the literature reviewed, we found 12 neurologic episodes due to capecitabine lasting between a few days till some months. All clinical symptoms of the cases described in literature, obtained a complete regression with the discontinuation of capecitabine. A relation was not found with dihydropyrimidine dehydrogenase (DPD) mutation, also if pharmacologic and pharmacogenetic assessment should be done for this drug, especially in old patients. Toxic encephalopathy represents a rare event during capecitabine treatment and on the bases of the data found, is fairly managed in the clinical setting. The knowledge of the natural history of the toxic effect allows the use of the drug also in old patients.
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PMID:Toxic encephalopathy in elderly patients during treatment with capecitabine: literature review and a case report. 2092 54

A 55-year-old woman with a 3-year and 4-month history of liver metastasis from breast cancer underwent chemotherapy with capecitabine and cyclophosphamide for following 10-months. She did not have hypertension and was not pregnant. She showed dysarthria and mild somnolence, and her conscious level developed to semicoma after 6 days. She had pyrexia. Cerebrospinal fluid (CSF) demonstrated increased cell-count and elevated protein but no evidence of positive cytological finding and cultivation of bacteria was found in the CSF. Brain magnetic resonance imaging (MRI) revealed multiple lesions with hyperintensity in the brain stem, bilateral middle cerebellar peduncles, left splenium of corpus callosum, bilateral basal ganglia, bilateral thalami, bilateral corona radiata, and bilateral subcortical white matters of parietal lobes on the T(2) weighted and fluid attenuated inversion recovery (FLAIR) images. These lesions demonstrated mild hyperintensity on the diffusion weighted images but did not demonstrate hypointensity on the T(1) weighted images. Capecitabine and cyclophosphamide were discontinued at 4th day after onset of symptoms, and her conscious disturbance showed improvement slowly since day 12 after cessation of these drugs and hyperintensity areas detected on FLAIR image of MRI showed decreasing intensity after three weeks of onset. Capecitabine is an oral prodrug converted to 5-fluorouracil (5-FU). 5-FU and cyclophosphamide are known to induce leukoencephalopathy. Reversible multiple lesions with leukoencephalopathy on brain MRI which is called as a posterior reversible encephalopathy syndrome (PRES). Capecitabine is also reported to induce PRES in rare cases. Combination of these drugs was considered for the possible cause to induce leukoencephalopathy like PRES. Usually leukoencephalopathy occurs in relatively early time after start of chemotherapy with capecitabine or cyclophosphamide, but we consider that late-onset leukoencephalopathy can be induced by long-term chemotherapy with these drugs. It is necessary to observe leukoencephalopathy by brain MRI regularly when these drugs are used.
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PMID:[Late-onset leukoencephalopathy induced by long-term chemotherapy with capecitabine and cyclophosphamide for liver metastasis from breast cancer]. 2253 58

Mania-like states occurring due to neurological, metabolic or toxic conditions, without a primary mood disorder have been reported in scientific literature as secondary mania. A major clinical problem in such situations often stems from the difficulty to understand if the mood disturbance is indeed secondary to an organic cause or a coincidental primary mood disorder. Chemotherapy regimens have been associated with multiple psychiatric complications, including psychosis, mania and anxiety. Capecitabine is implicated to be associated with encephalopathy whose clinical presentation often mimics that of psychosis. However, presentations with mania have not been reported until with the capecitabine and oxaliplatin combination chemotherapy regimen. In this report, we describe a case of secondary mania in a patient suffering from carcinoma colon on treatment with chemotherapy regimen of capecitabine and oxaliplatin.
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PMID:Secondary mania following cancer chemotherapy with capecitabine. 2959 81