AB0948 Tumour necrosis factor inhibitors and their impact on diabetes mellitus among patients with psoriatic arthritis
Authors: S. Mantravadi, M. George, A. Ogdie
Journal: Annals of the Rheumatic Diseases (2018)

<h3>Background</h3> Tumour necrosis factor is a key inflammatory cytokine in the pathogenesis of psoriatic arthritis (PsA) and diabetes mellitus (DM). <sup>1,2</sup>Tumor necrosis factor inhibitors (TNFi) have been shown to be associated with a decreased incidence of DM, but it is unknown whether treatment of PsA with TNFi has off-target therapy benefits for patients with DM. <sup>3</sup> <h3>Objectives</h3> To determine whether initiation of a TNFi, compared to initiation of methotrexate (MTX) or metformin, results in a decrease in Haemoglobin A1c (HbA1c) in patients with PsA, DM, and elevated HbA1c. <h3>Methods</h3> A retrospective cohort study was conducted in OptumInsight, a de-identified administrative claims database that includes laboratory values for approximately 10% of patients. Data from 2000–2014 was included. We identified patients with PsA and DM (defined by ICD-9CM codes), with an HbA1c≥7 and examined change in HbA1c among new initiators of a TNFi (etanercept, adalimumab, certolizumab, or golimumab), MTX, and metformin (positive control). A baseline period of 12 months prior to the index date was required to capture potential confounders. All patients were required to have one HbA1c in the six months prior to and one HbA1c in the 6 months after drug initiation. We evaluated median HbA1c change in each group and then assessed statistical differences using the Wilcoxon Rank Sum test (unadjusted). We then used linear regression models to determine the relative differences in HbA1c change using MTX as the reference and adjusted for age, sex, baseline A1c, DM medications, and comorbidities in the baseline period, with clustering to account for multiple new drug initiations per patient. <h3>Results</h3> Among 914 drug initiations in 756 patients with PsA and available HbA1c values, HbA1c was ≥7 before 125 (44%) of TNFi initiations, 90 (43%) of MTX initiations, and 233 (55%) of metformin initiations. The average time between baseline and follow-up HbA1c values was 231 days. Median HbA1c change was −0.50 (IQR −1.30, 0.30) after TNFi initiation, −0.40 (IQR −1.50, 0.10) after MTX initiation, and −0.90 (IQR −1.80, 0) after metformin initiation (figure 1). In adjusted analyses, TNFi initiators had a similar decrease in HbA1c compared to MTX initiators, β 0.02 (95%CI: −0.29, 0.33). Metformin initiators had a significantly greater change in HbA1c than MTX patients, β −0.43 (95%CI: −0.72, −0.13). <h3>Conclusions</h3> TNFi and MTX initiation lead to a decline in HbA1c by half as much as metformin. Changes in HbA1c were not different among patients initiating TNFi versus MTX. <h3>References</h3> [1] Coates LC, et al. Semin Arthritis Rheum201612;46(3):291–304. [2] Solomon SS, et al. Horm Metab Res2010;42:115–121. [3] Solomon D, et al. JAMA2011;305(24):2525–2531. <h3>Disclosure of Interest</h3> S. Mantravadi: None declared, M. George Grant/research support from: Bristol Myers Squibb, A. Ogdie Grant/research support from: Pfizer and Novartis, Consultant for: Abbvie, Bristol Myers Squibb, Lilly, Pfizer, Novartis, and Takeda