OP0277 Effect of Disease Modifying Drugs on Bone Mineral Density in Patients with Rheumatoid Arthritis, Psoriatic Arthritis, Psoriasis, and Ankylosing Spondylitis: A Meta-Analysis

2014 ◽  
Vol 73 (Suppl 2) ◽  
pp. 166.2-167
Author(s):  
S. Siu ◽  
B. Haraoui ◽  
C. Roubille ◽  
V. Richer ◽  
T. Starnino ◽  
...  
2008 ◽  
Vol 56 (8) ◽  
pp. 1011-1018 ◽  
Author(s):  
Young Ho Lee ◽  
Jin-Hyun Woo ◽  
Seong Jae Choi ◽  
Jong Dae Ji ◽  
Gwan Gyu Song

BackgroundThe effects of long-term high-dose corticosteroids on bone mineral density (BMD) are clear, but the effects of low-dose corticosteroids in patients with rheumatoid arthritis (RA) remain controversial. The aim of this study was to assess the effects of low-dose corticosteroids on BMD in patients with RA.MethodsThe authors surveyed randomized controlled studies that examined the effects of low-dose corticosteroids on BMD in patients with RA using MEDLINE and the Cochrane Controlled Trials Register and by performing manual searches. Data were collected on BMD (end-of-period or change-from-baseline) after longest recorded treatment durations. Meta-analysis was performed using a random effects model; outcomes are presented as standardized mean differences (SMDs).ResultsSeven studies were included in this meta-analysis, which included 7 studies on lumbar BMD meta-analysis and 6 studies on femur BMD meta-analysis. Corticosteroids resulted in a moderate worsening in lumbar BMD compared with controls (SMD = −0.483; 95% confidence interval [CI], −0.815 to −0.151, P = 0.004), whereas the femoral BMD differences were not siginificant (SMD = −0.224; 95% CI, −0.663 to 0.215, P = 0.318). Subgroup analysis of BMD data performed on a change-from-baseline basis showed that corticosteroids had a clear effect on both lumbar and femoral BMDs (SMD = −0.354; 95% CI, −0.620 to −0.088, P = 0.009; SMD = −0.488; 95% CI, −0.911 to −0.065, P = 0.024, respectively).ConclusionsThis meta-analysis shows BMD loss after low-dose corticosteroid treatment in patients with RA. These findings have practical implications for the long-term management of patients with RA on low-dose corticosteroids.


2019 ◽  
Vol 39 (1) ◽  
pp. 167-175 ◽  
Author(s):  
Katalin Gulyás ◽  
Ágnes Horváth ◽  
Edit Végh ◽  
Anita Pusztai ◽  
Ágnes Szentpétery ◽  
...  

Abstract Objectives Rheumatoid arthritis (RA) and ankylosing spondylitis (AS) have been associated with generalized and localized bone loss. We conducted a comprehensive study using imaging (dual-energy X-ray absorptiometry, DXA) and laboratory biomarkers in order to determine bone health and to study the effects of anti-tumor necrosis factor (TNF) biologics in RA and AS. Patients and methods Thirty-six RA and 17 AS patients undergoing 1-year etanercept (ETN) or certolizumab-pegol (CZP) therapy were studied. Bone density was assessed by DXA at baseline and after 12 months. Serum C-reactive protein (CRP), calcium, phosphate, parathyroid hormone (PTH), vitamin D3, osteocalcin, procollagen type I N-propeptide (P1NP), C-terminal telopeptide (βCTX), osteoprotegerin, sclerostin (SOST), Dickkopf-1 (DKK-1), soluble receptor activator nuclear kappa B ligand (sRANKL), and cathepsin K (cathK) levels were determined at baseline and after 6 and 12 months. Results TNF-α inhibition was clinically effective. Anti-TNF-α halted further bone loss over 1 year. In general, anti-TNF therapy significantly increased P1NP, SOST levels, and the P1NP/βCTX ratios, while decreased DKK-1 and CathK production at different time points in most patient subsets. In the full cohort and in RA, baseline and/or 12-month bone mineral density (BMD) at multiple sites exerted inverse relationships with CRP and βCTX, and positive correlation with SOST. In AS, L2-4 BMD after 1-year biologic therapy inversely correlated with baseline βCTX, while femoral neck BMD rather showed inverse correlations with CRP. Conclusions Anti-TNF therapy slowed down generalized bone loss, in association with clinical improvements, in both diseases. TNF blockade may enhance bone formation and suppress joint destruction. Anti-TNF therapy may act inversely on DKK-1 and SOST. Independent predictors of BMD were SOST and βCTX in RA, whilst CRP in AS.Key Points• One-year anti-TNF therapy halted generalized bone loss in association with clinical improvement in arthritides.• Anti-TNF therapy may inversely act on DKK-1 and SOST.• Independent predictors of BMD were SOST and βCTX in RA, while CRP in AS.


2020 ◽  
Vol 9 (11) ◽  
pp. 3712
Author(s):  
Tai-Li Chen ◽  
Jing-Wun Lu ◽  
Yu-Wen Huang ◽  
Jen-Hung Wang ◽  
Kuei-Ying Su

Introduction: Awareness of psoriasis-related comorbidities has been established in the current guidelines; however, evidence regarding the association of bone density or bone fragility with psoriatic disease remains inconclusive. Methods: We conducted a systematic review and meta-analysis to assess bone mineral density and the risk of osteoporosis and fractures in patients with psoriatic disease, including those with cutaneous psoriasis and psoriatic arthritis. We searched electronic databases for published observational studies. A meta-analysis was performed using the random-effect model. Pooled estimates and their confidence intervals (CIs) were calculated. Small-study effects were examined using the Doi plot and Luis Furuya–Kanamori index. Results: The analysis of the standardized mean difference in the absolute value of bone mineral density at different measuring sites (lumbar spine, femoral neck, and total hip) revealed no significant difference between patients with psoriatic disease and non-psoriatic controls. The pooled results of the adjusted odds ratios (ORs) demonstrated no increased risk of osteoporosis in patients with psoriatic disease. Notably, patients with psoriatic disease had a higher OR of developing bone fractures (adjusted OR: 1.09; 95% CI: 1.06 to 1.12; I2: 0%). Conclusion: Patients with psoriatic disease may be more likely to develop fractures compared with non-psoriatic controls. This higher risk for fracture may not necessarily be associated with lower bone mineral density nor a higher risk for osteoporosis.


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