PO211 Severe neuropathy and cognitive disfunction secondary to vitamin e deficiency caused by pancreatic insufficiency – case presentation

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51 years old lady admitted to local DGH with 3 months history of vomiting, diarrhoea, weight loss, pr gressive unsteadiness and worsening cognitive function. Past medical history included type 2 diabetes, hypothyroidism and cholecystectomy. She was smoking 20 cigarettes per day and didn’t drink alcohol. Her CT TAP showed fatty pancreas, MRI head and spine was normal, PET scan was negative. During hospital stay patient’s neurological symptoms deteriorated so was referred to tertiary centre. On examination was severely confused, had widespread amyotrophy and muscles weakness but no fasciculations, profound sensory loss to all modalities, marked pseudoathetosis and sensory ataxia. All reflexes were absent, plantar reflexes were flexor. Blood tests showed abnormal LFTs: GGT 654, ALP 45, ALP 191, bilirubin and amylase was normal. CSF protein was 0.7, cells were normal. NCS and EMG showed absent upper limbs sensory potentials with reduced but present sural responses in keeping with ganglionopathy. Nutritional screen showed low vitamin E 1.1 [9.5–41.5] and A 0.57 [0.99–3.35]. Faecal elastase1 was low suggestive of pancreatic insufficiency. Patient was treated with Creon and high dose vitamin E. After 8 weeks of treatment patient’s cognitive function returned to normal, power and sensation improved, body weight increased

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