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Neuropatía periférica en pacientes tratados con dimesilato de almitrina
Lancet (London, England)
|June 1, 1985
Resumen
Cinco pacientes desarrollaron neuropatía sensorial periférica después de tomar dimesilato de almitrina. Los síntomas incluyeron pérdida sensorial de las piernas y reducción de los tirones de tobillo, lo que indica una axonopatía distal, potencialmente relacionada con la pérdida de peso.
Área de la Ciencia:
- Neurología Neurología.
- Toxicología Toxicología.
Sus antecedentes:
- El dimesilato de almitrina es un medicamento utilizado para la estimulación respiratoria.
- La neuropatía periférica es un efecto adverso potencial de ciertos medicamentos.
Objetivo del estudio:
- Para reportar el desarrollo de neuropatía sensorial periférica en pacientes tratados con dimesilato de almitrina.
- Investigar las características clínicas y electrofisiológicas de esta neuropatía.
Principales métodos:
- Serie de casos de 5 pacientes tratados con dimesilato de almitrina (60-100 mg/día).
- Se realizaron exámenes clínicos, análisis del líquido cefalorraquídeo y estudios electrofisiológicos e histológicos.
Principales resultados:
- Los 5 pacientes desarrollaron pérdida sensorial insidiosa y simétrica en las piernas (distribución de las piernas) y pérdida de los tirones de tobillo.
- Los hallazgos electrofisiológicos e histológicos fueron consistentes con la axonopatía distal.
- El inicio de los síntomas ocurrió 2-4 meses después del inicio del dimesilato de almitrina en 4 pacientes.
- Se observó una pérdida de peso significativa (4-15 kg) en todos los pacientes antes del inicio de los síntomas.
Conclusiones:
- El dimesilato de almitrina puede causar neuropatía sensorial periférica, caracterizada por axonopatía distal.
- La pérdida de peso puede desempeñar un papel en el desarrollo de la neuropatía al liberar dimesilato de almitrina previamente unido.
- Se requiere una mayor investigación sobre los efectos neurotóxicos del dimesilato de almitrina.
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