Mitochondrial myopathy caused by arsenic trioxide therapy.
Blood
; 119(18): 4272-4, 2012 May 03.
Article
en En
| MEDLINE
| ID: mdl-22427206
ABSTRACT
Arsenic trioxide (ATO) has been successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decade. Here we report a patient with APL who developed a mitochondrial myopathy after treatment with ATO. Three months after ATO therapy withdrawal, the patient was unable to walk without assistance and skeletal muscle studies showed a myopathy with abundant cytoplasmic lipid droplets, decreased activities of the mitochondrial respiratory chain complexes, multiple mitochondrial DNA (mtDNA) deletions, and increased muscle arsenic content. Six months after ATO treatment was interrupted, the patient recovered normal strength, lipid droplets had decreased in size and number, respiratory chain complex activities were partially restored, but multiple mtDNA deletions and increased muscle arsenic content persisted. ATO therapy may provoke a delayed, severe, and partially reversible mitochondrial myopathy, and a long-term careful surveillance for muscle disease should be instituted when ATO is used in patients with APL.
Texto completo:
1
Bases de datos:
MEDLINE
Asunto principal:
Óxidos
/
Arsenicales
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Leucemia Promielocítica Aguda
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Protocolos de Quimioterapia Combinada Antineoplásica
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Miopatías Mitocondriales
Límite:
Aged
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Female
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Humans
Idioma:
En
Revista:
Blood
Año:
2012
Tipo del documento:
Article
País de afiliación:
Francia