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Subacute reversible toxic encephalopathy related to treatment with capecitabine: A case report with literature review and discussion of pathophysiology.
MedLine Citation:
PMID:  24631316     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
INTRODUCTION: Capecitabine, a 5-fluorouracil (5FU) pro-drug, is increasingly used in breast and gastrointestinal cancers due to its more convenient oral route of administration when compared to 5FU. Despite its widespread use, there are only a few reports on capecitabine CNS toxicity, while the pathogenic basis of such toxicity remains unclear.
CASE: A 69-year-old male presented with recurrent generalized seizures 2.5 months after preoperative chemoradiotherapy with capecitabine in locally advanced rectal cancer. Brain MRI revealed a diffuse, subcortical white matter alteration suggestive of vasogenic edema. The diagnosis of toxic encephalopathy was supported after elimination of alternative causes of the neurological dysfunction and complete resolution of clinical and imaging findings after 3 months of no further chemotherapy.
CONCLUSIONS: Given the expanding use of capecitabine, physicians should be aware of this potential complication when a neurological worsening occurs during or after treatment with this chemotherapeutic agent. In our case, as in previously described cases encephalopathy was characterized by a favorable course after cessation of the drug. Vasogenic edema rather than cytotoxic edema may play a pivotal pathogenetic role in this form of encephalopathy.
Authors:
E Lyros; S Walter; I Keller; P Papanagiotou; K Fassbender
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Publication Detail:
Type:  REVIEW     Date:  2014-3-11
Journal Detail:
Title:  Neurotoxicology     Volume:  -     ISSN:  1872-9711     ISO Abbreviation:  Neurotoxicology     Publication Date:  2014 Mar 
Date Detail:
Created Date:  2014-3-17     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905589     Medline TA:  Neurotoxicology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier B.V.
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