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CASE REPORT
DADS neuropathy associated with anti-TNF-α therapy
  1. Ronan Niall McGinty1,
  2. Brian McNamara2,
  3. Helena Moore3
  1. 1Department of Neurology, Cork University Hospital, Cork, Ireland
  2. 2Department of Neurophysiology, Cork University Hospital, Cork, Ireland
  3. 3Bon Secours Hospital, Tralee, Ireland
  1. Correspondence to Dr Ronan Niall McGinty, ronan.mcginty{at}hse.ie

Summary

A 52-year-old man with idiopathic Parkinson's disease and severe rheumatoid arthritis presented with a 1-year history of progressively worsening limb paraesthesia. Examination showed sensory loss in a glove and stocking distribution, absent reflexes and unsteady tandem gait. Nerve conduction studies suggested an acquired peripheral neuropathy with distal demyelination, which—together with the clinical phenotype—was consistent with a Distal Acquired Demyelinating Symmetric (DADS) neuropathy pattern. This was attributed to therapy with adalimumab, an antitumor necrosis factor (TNF)-α agent, which the patient had been taking for 2 years for rheumatoid arthritis. One month after discontinuing adalimumab, the limb paraesthesia had resolved completely and the patient had a normal tandem gait. Demyelinating disorders may rarely occur as complications of anti-TNF-α agents and therefore have implications for pretreatment counselling and ongoing monitoring. DADS neuropathy is a subtype of chronic inflammatory demyelinating polyradiculoneuropathy, which responds poorly to standard therapy and has not previously been described with anti-TNF-α therapy.

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