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Acute autonomic and sensory neuropathy after interferon α-2b therapy for chronic hepatitis C
  1. T IRIOKA,
  2. M YAMADA,
  3. M YAMAWAKI,
  4. Y SAITO,
  5. H MIZUSAWA
  1. Department of Neurology and Neurological Science
  2. Graduate School of Medicine
  3. Tokyo Medical and Dental University
  4. 1–5–45 Yushima Bunkyo-ku
  5. Tokyo 113–8519, Japan
  6. Department of Neurology
  7. Kanazawa University School of Medicine, Japan
  8. Department of Internal Medicine, Social Insurance Chuo General Hospital, Japan
  1. Dr T Irioka irioka{at}tc4.so-net.ne.jp
  1. M YAMADA
  1. Department of Neurology and Neurological Science
  2. Graduate School of Medicine
  3. Tokyo Medical and Dental University
  4. 1–5–45 Yushima Bunkyo-ku
  5. Tokyo 113–8519, Japan
  6. Department of Neurology
  7. Kanazawa University School of Medicine, Japan
  8. Department of Internal Medicine, Social Insurance Chuo General Hospital, Japan
  1. Dr T Irioka irioka{at}tc4.so-net.ne.jp
  1. H MIURA
  1. Department of Neurology and Neurological Science
  2. Graduate School of Medicine
  3. Tokyo Medical and Dental University
  4. 1–5–45 Yushima Bunkyo-ku
  5. Tokyo 113–8519, Japan
  6. Department of Neurology
  7. Kanazawa University School of Medicine, Japan
  8. Department of Internal Medicine, Social Insurance Chuo General Hospital, Japan
  1. Dr T Irioka irioka{at}tc4.so-net.ne.jp

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Acute autonomic and sensory neuropathy (AASN) is a disorder characterised by acute autonomic and sensory nerve dysfunctions, and well preserved motor nerve function.1 Although the pathomechanism of AASN is not clear, autonomic and sensory ganglion neuron cell bodies may be the main target of the immune mediated process underlying AASN.2 On the other hand, patients treated with interferon may develop neurological complications including neuropathy.3 We report the first case of AASN which can be associated with interferon α-2b therapy for chronic hepatitis C.

A 57 year old Japanese man with chronic hepatitis C had been treated with interferon α-2b since June 1998. On 3 September, a skin eruption abruptly emerged on his chest and rapidly spread over his whole body. There was no history of exposure to toxins and drugs other than the interferon. The interferon therapy was stopped on 7 September; after a total dose of 390 000 000 units. The skin eruption gradually resolved, but 1 week later, numbness appeared in his limbs. Subsequently he became unable to walk and stand. Further, he developed urinary overflow incontinence and bowel distension. He was then transfered to our neurology department on 2 October.

Physical examination disclosed orthostatic hypotension without secondary tachycardia (120/60 mm Hg lying, 85/52 mm Hg sitting, fixed pulse rate 60 bpm) and paralytic ileus. …

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