Abstract
Objective
To assess the effect of proton pump inhibitor (PPI) use on bone mineral density (BMD) and bone microarchitecture as measured by the trabecular bone score (TBS) in patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs).
Methods
Cross-sectional data from a prospective single-center cohort (2015 to 2022) of patients with iRMDs were used to evaluate 3 co-primary outcomes: BMD of the left femoral neck and the lumbar spine (as T-scores) and the TBS. Inverse probability weighting adjusted for numerous confounders including age, sex, body mass index, current and cumulative glucocorticoid (GC) dose, C-reactive protein levels, disability, and others. Analyses were based on general linear models, following a prespecified statistical analysis plan.
Results
The study included 1495 patients (75% women; mean age, 62.6±13.1 years; 49% and 63% with regular PPI and GC use, respectively). The PPI users had lower BMD at both spine (adjusted contrast −0.25; 95% CI, −0.47 to −0.04; P =.02) and femoral neck (−0.17 [−0.35 to 0.01]; P =.07). Differences between PPI users and nonusers were statistically significant only in patients concurrently using GCs at more than 7.5 mg/d prednisone equivalent. The TBS was similar in PPI users and nonusers (adjusted contrast, 0.00 [−0.04 to 0.04]; P =.97).
Conclusion
Our results suggest that PPIs lead to a loss of BMD rather than an impairment of bone microarchitecture in patients with iRMDs. The negative association between PPI use and BMD appears to be dependent on concurrent GC use. Clinicians should carefully review the indication for PPI use in patients with iRMDs, especially in those receiving higher dose GCs
To assess the effect of proton pump inhibitor (PPI) use on bone mineral density (BMD) and bone microarchitecture as measured by the trabecular bone score (TBS) in patients with inflammatory rheumatic and musculoskeletal diseases (iRMDs).
Methods
Cross-sectional data from a prospective single-center cohort (2015 to 2022) of patients with iRMDs were used to evaluate 3 co-primary outcomes: BMD of the left femoral neck and the lumbar spine (as T-scores) and the TBS. Inverse probability weighting adjusted for numerous confounders including age, sex, body mass index, current and cumulative glucocorticoid (GC) dose, C-reactive protein levels, disability, and others. Analyses were based on general linear models, following a prespecified statistical analysis plan.
Results
The study included 1495 patients (75% women; mean age, 62.6±13.1 years; 49% and 63% with regular PPI and GC use, respectively). The PPI users had lower BMD at both spine (adjusted contrast −0.25; 95% CI, −0.47 to −0.04; P =.02) and femoral neck (−0.17 [−0.35 to 0.01]; P =.07). Differences between PPI users and nonusers were statistically significant only in patients concurrently using GCs at more than 7.5 mg/d prednisone equivalent. The TBS was similar in PPI users and nonusers (adjusted contrast, 0.00 [−0.04 to 0.04]; P =.97).
Conclusion
Our results suggest that PPIs lead to a loss of BMD rather than an impairment of bone microarchitecture in patients with iRMDs. The negative association between PPI use and BMD appears to be dependent on concurrent GC use. Clinicians should carefully review the indication for PPI use in patients with iRMDs, especially in those receiving higher dose GCs
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Mayo Clinic Proceedings |
| Vol/bind | 99 |
| Udgave nummer | 7 |
| Sider (fra-til) | 1046-1057 |
| Antal sider | 12 |
| ISSN | 0025-6196 |
| DOI | |
| Status | Udgivet - 2024 |
| Udgivet eksternt | Ja |
Bibliografisk note
Funding Information:Grant Support: A.P. was supported by a research grant from the Deutsche Autoimmun-Stiftung (German Autoimmune Foundation). Rh-GIOP is or was supported by a joint funding of AbbVie, Amgen, Almirall, Biogen, BMS, Chugai, Galapagos, Generic Assays, GSK, Hexal, Horizon Therapeutics, Lilly, Medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi-Genzyme. The Parker Institute is supported by a core grant from the Oak Foundation (OCAY-18-774-OFIL). J.Y. is supported by NIH/NIAMS K24-AR-074534 and P30-AR-070155. R.S. is supported by NIH/NCATS through UCSF-CTSI grant TL1 TR001871.
Publisher Copyright:
© 2023 Mayo Foundation for Medical Education and Research
Finansiering
Grant Support: A.P. was supported by a research grant from the Deutsche Autoimmun-Stiftung (German Autoimmune Foundation). Rh-GIOP is or was supported by a joint funding of AbbVie, Amgen, Almirall, Biogen, BMS, Chugai, Galapagos, Generic Assays, GSK, Hexal, Horizon Therapeutics, Lilly, Medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi-Genzyme. The Parker Institute is supported by a core grant from the Oak Foundation (OCAY-18-774-OFIL). J.Y. is supported by NIH/NIAMS K24-AR-074534 and P30-AR-070155. R.S. is supported by NIH/NCATS through UCSF-CTSI grant TL1 TR001871.
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