1994
DOI: 10.1016/s0140-6736(94)91839-2
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Prophylaxis and reversal of ifosfamide encephalopathy with methylene-blue

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Cited by 165 publications
(90 citation statements)
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“…MB itself has been used in medical practice for more than 100 years and is recognized as having very low tissue toxicity. Clinical uses of MB include the treatment of ifosfamide encephalopathy, methemoglobinemia, urolithiasis, and cyanide poisoning [22,23]. Even intravenous administration of MB is FDA approved for methemoglobinemia.…”
Section: Discussionmentioning
confidence: 99%
“…MB itself has been used in medical practice for more than 100 years and is recognized as having very low tissue toxicity. Clinical uses of MB include the treatment of ifosfamide encephalopathy, methemoglobinemia, urolithiasis, and cyanide poisoning [22,23]. Even intravenous administration of MB is FDA approved for methemoglobinemia.…”
Section: Discussionmentioning
confidence: 99%
“…Methylene blue was then administered as an i.v. bolus of 50 mg repeated at the same dose every 2 h, or as continuous infusion at 200 mg day À1 diluted in 5% dextrose, until the event resolved (Küpfer et al, 1994).…”
Section: Study Design and Treatment Planmentioning
confidence: 99%
“…Little is known about the toxicologic effects of glutaric acid. Elevated glutarate levels in the urine or blood have been described in patients with certain metabolic disorders (e.g., glutaric acidosis and glutaric aciduria) and after ifosfamide overdose [14][15][16][17][18]. In glutaric acidosis, an autosomal recessive disorder characterized by macrocephaly, dyskinesia, dystonia, opisthotonos, choreoathetoid movements, and delayed development, severe metabolic acidosis results from glutaric acid accumulation due deficiency of glutaryl-CoA dehydrogenase [19,20].…”
Section: Discussionmentioning
confidence: 99%
“…In glutaric acidosis, an autosomal recessive disorder characterized by macrocephaly, dyskinesia, dystonia, opisthotonos, choreoathetoid movements, and delayed development, severe metabolic acidosis results from glutaric acid accumulation due deficiency of glutaryl-CoA dehydrogenase [19,20]. After ifosfamide overdose, excessive urinary excretion of glutaric acid and sarcosine may occur, leading to defective mitochondrial fatty acid oxidation and acidemia [18]. Unfortunately, we were unable to obtain qualitative or quantitative confirmation of glutaraldehyde or its metabolites in this case, as laboratory facilities to measure these chemicals were not available.…”
Section: Discussionmentioning
confidence: 99%