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BMJ Case Reports 2009; doi:10.1136/bcr.08.2008.0718
  • Findings that shed new light on the possible pathogenesis of a disease or an adverse effect

Hypophosphataemic neuropathy during total parenteral nutrition

  1. Yohei Iguchi1,
  2. Keiko Mori1,
  3. Haruki Koike1,
  4. Kazuo Mano2,
  5. Yoji Goto2,
  6. Takashi Kato2,
  7. Tomonobu Nakano3,
  8. Gen Sobue1
  1. 1
    Nagoya University Graduate School of Medicine, Neurology, 65, Tsurumai-cho, showa-ku, Nagoya, 466-8550, Japan
  2. 2
    Japanese Red Cross Nagoya First Hospital, Neurology, 3-35 Michishitacho, Nakamuraku, Nagoya, Aichi, Japan
  3. 3
    Aichi Medical University, Stroke Center, Aichi 480-1195, Nagakute, Aichi, 480-1195, Japan
  1. sobueg{at}med.nagoya-u.ac.jp
  • Published 2 February 2009

Summary

Intravenous glucose administration is the most common cause of hypophosphataemia in hospitalised patients. While most of these cases are asymptomatic, severe hypophosphataemia, when combined with phosphorus depletion, can cause acute neuropathy that mimics Guillain–Barré syndrome. A malnourished patient who received intravenous hyperalimentation (IVH) without intravenous phosphate (IP) developed hypophosphataemia and acute sensorimotor neuropathy. F waves in the peripheral nerve trunk were absent or diminished, while nerve conduction velocities were nearly normal. The sural nerve biopsy revealed the presence of some subperineurial oedema and mild axonal atrophy. Prompt IP administration reversed the patients’ neurological symptoms and normalised F waves. Our data suggest that hypophosphataemia plays a role in the pathogenesis of neuropathy that develops in patients following IVH without IP.

Footnotes

  • Competing interests: None.

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