1. Severe but reversible neuropathy and encephalopathy due to vitamin E deficiency
- Author
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Yusuf A. Rajabally, Barbara Wysota, Sophia Michael, Fu Liong Hiew, and Charlotte Dawson
- Subjects
Vitamin ,medicine.medical_specialty ,Ataxia ,medicine.medical_treatment ,Encephalopathy ,medicine.disease_cause ,Gastroenterology ,03 medical and health sciences ,chemistry.chemical_compound ,0404 agricultural biotechnology ,0302 clinical medicine ,Internal medicine ,medicine ,Humans ,Vitamin E ,Cognitive Dysfunction ,Vitamin E Deficiency ,Exocrine pancreatic insufficiency ,Mutation ,business.industry ,Peripheral Nervous System Diseases ,04 agricultural and veterinary sciences ,General Medicine ,Middle Aged ,medicine.disease ,040401 food science ,medicine.anatomical_structure ,chemistry ,Peripheral nervous system ,Exocrine Pancreatic Insufficiency ,Female ,Surgery ,Neurology (clinical) ,Vitamin E deficiency ,medicine.symptom ,business ,030217 neurology & neurosurgery - Abstract
Vitamin E deficiency is known to result mainly in a spinocerebellar syndrome and involvement of the peripheral nervous system occurs less commonly. Most cases of vitamin E-deficient ataxic neuropathy reported relate to a genetically-mediated cause through mutation of the alpha-tocopherol transfer protein (TTPA) gene on chromosome 8q13 [1]. Severe subacute adult-onset rapidly disabling neuropathy due to vitamin E deficiency is not to our knowledge reported. Cognitive dysfunction is uncommon in this setting. Occurrence of isolated ymptomatic vitamin E deficiency due to pancreatic exocrine insufficiency (PEI) appears exceptional.
- Published
- 2017
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