OP0243 PROTON PUMP INHIBITOR USE IS ASSOCIATED WITH IMPAIRED BONE MINERAL DENSITY BUT NOT BONE MICROARCHITECTURE IN PATIENTS WITH INFLAMMATORY RHEUMATIC AND MUSCULOSKELETAL DISEASES TAKING GLUCOCORTICOIDS

Background Patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs) are at increased risk of osteoporosis fragility fractures. For this population, the question whether proton pump inhibitor (PPI) intake contributes to that has not yet been definitively answered. Prior studies have yielded conflicting results, did account for over-the-counter use PPI, major confounders were unmeasured. In addition, bone microarchitecture as a potential mediator fracture studied. Objectives To assess effect regular PPI on mineral density (BMD) in patients iRMDs. Methods Cross-sectional baseline data from single center Rh-GIOP cohort (“Glucocorticoid-induced Osteoporosis Chronic Inflammatory Rheumatic Diseases or Psoriasis”) used. Briefly, iRMDs prospectively enrolled assessed DXA scans, laboratory testing, bone-health-related questionnaires since 2015. Regular glucocorticoid (GC) ascertained by both chart review patient self-report. Three co-primary outcomes (all reported T-scores) defined: BMD left femoral neck lumbar spine, trabecular score (TBS). The latter is measure correlating vertebrae’s measured subset. Inverse probability treatment weighting adjusted following confounders: age, sex, body mass index, iRMD type, C-reactive protein, current cumulative GC dose, NSAID use, smoking, alcohol consumption, functional status (Health Assessment Questionnaire), disease duration, bisphosphonate chronic kidney stage, presence diabetes mellitus, frequency exercise. We investigated dose-response relationships present (“high dose” >20mg/d vs. “low ≤20mg/d pantoprazole equivalent) conducted an additional analysis interaction term use. All analyses based linear regression models. Multiple imputation 100 imputations was used missing (~4%). A detailed prespecified statistical plan gatekeeping procedure testing followed. Results 1,495 (75.3% women; mean age 62.6 ± 13.1 years; 49.2% [of those: 63.1% high dose]) included. Most had diagnosis rheumatoid arthritis (37.5%), followed 25.3% connective tissue diseases, 16% vasculitides, 14.2% spondyloarthropathies, 7% others. 63.8% GCs (median dose 5mg/d). unadjusted analyses, users lower spine ( Table 1 ). Interestingly, differences between non-users only subset concurrently using (data shown). There no statistically significant difference when comparing low P ≥ 0.52). TBS (n = 389) similar Conclusion Loss (seen neck) rather than impairment seems be driving seen negative association appears dependent concurrent 1. No Contrast P-value Crude (unadjusted ) Left -1.24 (-1.36 -1.13) -1.01 (-1.12 -0.89) -0.24 (-0.11 -0.37) <0.001 Lumbar -0.87 (-1.06 -0.69) -0.64 (-0.79 -0.48) -0.23 (-0.05 0.42) 0.01 Trabecular 1.28 (1.24 1.31) 1.30 (1.26 1.33) -0.02 (-0.06 0.02) 0.35 Adjusted -1.08 (-1.27 -0.88) -0.17 (-0.35 0.01) 0.07 -0.62 (-0.83 -0.41) -0.25 (-0.47 -0.04) 0.02 1.27 0.00 (-0.04 0.04) 0.97 Numbers estimated marginal means 95% confidence intervals. Acknowledgements supported Abbvie, Amgen, Almirall, Biogen, BMS, Chugai, Galapagos, Generic Assays, GSK, Hexal, Horizon Therapeutics, Lilly, Medac, Mundipharma, Novartis, Pfizer, Roche, Sanofi-Genzyme. A.P:: Deutsche Autoimmun-Stiftung (“German Autoimmune Foundation”). Parker Institute: core grant Oak Foundation (OCAY-18-774-OFIL). J.Y.: NIH/NIAMS K24-AR-074534 P30-AR-070155. R.S.: NIH/NCATS through UCSF-CTSI Grant Number TL1 TR001871. Disclosure Interests Andriko Palmowski: None declared, Gabriela Schmajuk: Jinoos Yazdany: Patti Katz: Jing Li: Rachael Stovall: Emma Kersey: Sabrina Mai Nielsen: Robin Christensen: Henning Bliddal: Zhivana Boyadzhieva: Udo Schneider: Tobias Alexander: Burkhard Muche Speakers bureau: BM received consulting speaker honoraria and/or congress support UCB Pharma Germany, Amgen Stadapharm., Consultant of: Sandra Hermann: Edgar Wiebe EW reports consultancy fees, travel expenses Medac Novartis., Frank Buttgereit: declared.