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Guillain-Barré syndrome as an early manifestation of angioimmunoblastic T-cell lymphoma
  1. Nicholas Araki Howell1,
  2. Sumedha Arya2,
  3. Peter C Tai3,
  4. Hamid Sadeghian3,
  5. Ali Sakhdari4,
  6. Robert Wu5 and
  7. Anca Prica2
  1. 1Department of Medicine, University of Toronto, Toronto, Ontario, Canada
  2. 2Division of Haematology, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada
  3. 3Division of Neurology, University of Toronto Temerty Faculty of Medicine, Toronto, Ontario, Canada
  4. 4Department of Laboratory Medicine & Pathobiology, Faculty of Medicine, University of Toronto, 1 King’s College Circle, Toronto, Ontario, Canada
  5. 5Division of General Internal Medicine, Department of Medicine, University of Toronto Faculty of Medicine, Toronto, Ontario, Canada
  1. Correspondence to Dr Nicholas Araki Howell; nicholas.howell{at}


Guillain-Barré syndrome (GBS) is a rare condition caused by autoimmune damage of peripheral nerves. We describe a case where a man in his 80s presented with subacute, progressive fatigue and weakness. He had received an outpatient work-up for possible haematological malignancy, but eventually presented to the emergency department for worsening weakness. A physical exam and cerebrospinal fluid analysis suggested a diagnosis of GBS. Subsequently, a pathological diagnosis of angioimmunoblastic T-cell lymphoma was made. The patient underwent intravenous immunoglobulin treatment for GBS and was started on cyclophosphamide, doxorubicin, vincristine and prednisone therapy. Prior research has suggested that incident malignancy may be associated with GBS, which may be caused by a paraneoplastic-type phenomenon, malignancy-associated immune dysregulation or an autoimmune reaction triggered by a common exposure. Clinicians should be aware of the possible association between these two conditions and should remain open minded to the possibility of non-infectious triggers for GBS.

  • haematology (incl blood transfusion)
  • neuromuscular disease
  • oncology

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  • Contributors NAH contributed towards the conception and design, acquisition of data, analysis and interpretation of data; he also was responsible for drafting the initial version of the article. SA, HS, AS and AP contributed towards the acquisition of data and the analysis and interpretation of the data. PT and RW contributed towards the analysis and interpretation of data. All authors critically revised the manuscript for important intellectual content, provided final approval of the manuscript and agreed to be accountable for the article.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.

  • Competing interests PT reports non-financial support from Aurora, outside the submitted work. NAH, SA, HS, RW and AP have nothing to declare.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.