title: Diabetes mellitus risk in rheumatoid arthritis: reduced incidence with anti-tumor necrosis factor α therapy.
abstract: OBJECTIVE
  To examine the association of tumor necrosis factor α (TNFα) inhibitor use and the risk of developing diabetes mellitus in a rheumatoid arthritis (RA) inception cohort.
  
  
  METHODS
  Adults diagnosed with RA between January 1, 2001, and December 31, 2009, were identified (n = 1,881). Prevalent cases of diabetes mellitus (n = 294) were excluded. Information on sociodemographic data, medical history, body mass index (BMI), laboratory measures, and medications was collected from the electronic health record. Incident diabetes mellitus was defined using the 2010 American Diabetes Association criteria or physician-established diagnosis. Time-varying Cox proportional hazards regression models were used to adjust for age, sex, race, BMI, rheumatoid factor (RF) and anti-cyclic citrullinated peptide antibodies (anti-CCP), erythrocyte sedimentation rate (ESR), and use of nonsteroidal antiinflammatory drugs (NSAIDs), glucocorticoids, hydroxychloroquine, and methotrexate.
  
  
  RESULTS
  A total of 1,587 incident RA patients without diabetes mellitus were included. The anti-TNFα users (n = 522) had a lower median age but greater baseline BMI; maximum ESR, RF, and anti-CCP positivity; and NSAID, glucocorticoid, or methotrexate use. The median followup time for the ever and never TNFα inhibitor users was 44.9 months (interquartile range [IQR] 23.7-73.0 months) and 37.1 months (IQR 16.3-65.1 months), respectively (P < 0.001). Of the 91 patients developing diabetes mellitus, 16 were ever and 75 were never TNFα inhibitor users, yielding incidence rates of 8.6 and 17.2 per 1,000 person-years (P = 0.048), respectively. Adjusting for covariates, the hazard ratio for incident diabetes mellitus in TNFα inhibitor users was 0.49 (95% confidence interval 0.24-0.99, P = 0.049) compared to the never users.
  
  
  CONCLUSIONS
  In this inception RA cohort, anti-TNFα use was associated with a 51% reduction in risk of developing diabetes mellitus.
authors.affiliation: Geisinger Medical Center, Danville, Pennsylvania 17822, USA.
authors.forename: Jana L
authors.initials: JL
authors.lastname: Antohe
authors.forename: Androniki
authors.initials: A
authors.lastname: Bili
authors.forename: Jennifer A
authors.initials: JA
authors.lastname: Sartorius
authors.forename: H Lester
authors.initials: HL
authors.lastname: Kirchner
authors.forename: Stephanie J
authors.initials: SJ
authors.lastname: Morris
authors.forename: Sorina
authors.initials: S
authors.lastname: Dancea
authors.forename: Mary Chester M
authors.initials: MC
authors.lastname: Wasko
mesh_terms: D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology; D015897:Comorbidity; D003920:Diabetes Mellitus / Q000175:diagnosis / Q000453:epidemiology / Q000517:prevention & control; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010414:Pennsylvania / Q000453:epidemiology; D016016:Proportional Hazards Models; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D014409:Tumor Necrosis Factor-alpha