title: Improvement of thyroid function in hypothyroid patients with rheumatoid arthritis after 6 months of adalimumab treatment: a pilot study.
abstract: OBJECTIVE
  Rheumatoid arthritis (RA) is characterized by high levels of cytokines such as tumor necrosis factor (TNF). TNF appears to have an etiologic role in thyroid dysfunction, and thyroid dysfunction is a common comorbidity in RA. Anti-TNF treatment might limit thyroid dysfunction. Thus, changes in thyroid hormones were studied during TNF-blocking therapy in patients with RA.
  
  
  METHODS
  At baseline and after 6 months' treatment with adalimumab, thyroid function [thyroid-stimulating hormone (TSH), free thyroxine (fT4), and antibodies against thyroid peroxidase (TPOabs)] were assessed in 138 consecutive adalimumab-treated patients with RA who were naive for TNF-blocking agents. Patients were categorized as hypothyroid, hyperthyroid, or euthyroid. In these groups, changes in thyroid function were determined.
  
  
  RESULTS
  Prevalences of hypothyroidism, hyperthyroidism, and TPOabs were 13%, 5%, and 15%, respectively. After 6 months, TPOabs decreased from 267 to 201 IU/ml (p = 0.048). In hypothyroid patients without concomitant L-thyroxine, a trend for declining levels of TSH was observed. Subgroup analysis revealed that in patients who were hypothyroid and TPOabs-positive and L-thyroxine-naive, TSH levels decreased significantly, from 12.5 (interquartile range 6.7-18.4) to 7.1 (interquartile range 4.9-13.8) mU/l (p = 0.043).
  
  
  CONCLUSIONS
  Anti-TNF treatment improves thyroid function in hypothyroid patients with RA (especially in those who are L-thyroxine-naive and TPOabs-positive), providing further evidence that inflammatory cytokines such as TNF have a pathogenic role in thyroid dysfunction.
authors.affiliation: Department of Rheumatology, VU University Medical Centre, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
authors.forename: Hennie G
authors.initials: HG
authors.lastname: Raterman
authors.forename: Anna
authors.initials: A
authors.lastname: Jamnitski
authors.forename: Willem F
authors.initials: WF
authors.lastname: Lems
authors.forename: Alexandre E
authors.initials: AE
authors.lastname: Voskuyl
authors.forename: Ben A C
authors.initials: BA
authors.lastname: Dijkmans
authors.forename: Wouter H
authors.initials: WH
authors.lastname: Bos
authors.forename: Suat
authors.initials: S
authors.lastname: Simsek
authors.forename: Paul
authors.initials: P
authors.lastname: Lips
authors.forename: Rob J
authors.initials: RJ
authors.lastname: van de Stadt
authors.forename: Margret H M T
authors.initials: MH
authors.lastname: de Koning
authors.forename: Michael T
authors.initials: MT
authors.lastname: Nurmohamed
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D005260:Female; D006801:Humans; D007037:Hypothyroidism / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D013960:Thyroid Function Tests; D013961:Thyroid Gland / Q000503:physiopathology*; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha; D013972:Thyrotropin; D000068879:Adalimumab; D013974:Thyroxine