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Tumour necrosis factor blockade mediates altered serotonin transporter availability in rheumatoid arthritis: a clinical, proof-of-concept study
  1. Jonathan Cavanagh1,
  2. Carolyn Paterson1,
  3. John McLean1,
  4. Sally Pimlott2,
  5. Moira McDonald2,
  6. James Patterson2,
  7. David Wyper1,
  8. Iain McInnes1
  1. 1University of Glasgow, Sackler Institute of Psychobiological Research, Southern General Hospital, Glasgow, UK
  2. 2NHS Greater Glasgow & Clyde, Glasgow, UK
  1. Correspondence to Dr Jonathan Cavanagh, Sackler Institute of Psychobiological Research, Faculty of Medicine University of Glasgow, Southern General Hospital, Glasgow G51 4TF, UK; Jonathan.Cavanagh{at}clinmed.gla.ac.uk

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Depression in those who are ill is 5–10 times more common than in the general population. Increasing evidence implicates bidirectional biological mechanisms linking mood disorders and medical conditions.1 Depressive symptoms are significantly more common in rheumatoid arthritis (RA) than in the general population. Conservative estimates suggest major depressive disorder in between 13% and 17% of patients with RA. However, prevalence exceeding 40% has been reported in a recent study, with up to 11% of patients experiencing suicidal ideation.1 Major depressive disorder is an independent risk factor for both work disability and mortality in patients with RA.2

Cytokine dysregulation is central to the pathogenesis of RA with functional implications for breach of tolerance and autoimmunity, subsequent inflammation and articular dysfunction.3 Tumour necrosis factor (TNF), in particular, appears to be of pivotal importance in pathogenesis, based …

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