Éric Toussirot1,2,3,4,5,6, Laurent Mourot7,8, Barbara Dehecq9, Fabrice Michel10, Daniel Wendling3,5, Émilie Grandclément9, Gilles Dumoulin9,11. 1. INSERM CIC-1431, University Hospital of Besançon, Clinical Investigation Center in Biotherapy, Besançon, France. 2. Fédération Hospital-Universitaire INCREASE, University Hospital of Besançon, Besançon, France. 3. Department of Rheumatology, University Hospital of Besançon, Besançon, France. 4. Department of Therapeutics and UPRES EA 4266: "Pathogenic agents and Inflammation", University of Bourgogne Franche-Comté, Besancon, France. 5. University of Franche Comté, UPRES EA 4266 " Pathogens and Inflammation », Besançon, France. 6. LabEX LipSTIC, ANR-11-LABX-0021, Besançon cedex, France. 7. University Hospital of Besançon and University of Franche Comté, EA 4660 Culture Sport Health Society and Exercise Performance, Health, Innovation platform, Besançon, France. 8. University Hospital of Besançon, Clinical Investigation Center for Innovative Technologies INSERM CIC-1431, Place St Jacques, Besançon, France. 9. Department of Endocrine and Metabolic Biochemistry, University Hospital of Besançon, Besançon, France. 10. Department of Neuromuscular Examinations and Diseases, University Hospital of Besançon, Besançon, France. 11. University of Franche Comté, UPRES EA 3920, "Cardiovascular Pathophysiology and Prevention", Besançon France.
Abstract
OBJECTIVE: To examine the impact of long-term anti-TNFα therapy on bone mass, bone metabolism, and the trabecular bone score (TBS) in patients with rheumatoid arthritis (RA) or ankylosing spondylitis (AS). MATERIAL AND METHODS: In eight patients with RA and 12 with AS, bone mineral densities (BMDs) of the lumbar spine (LS), left and right femoral neck, and total skeleton were measured using dual X-ray absorptiometry at baseline and then at 6, 12, and 24 months after anti TNFα therapy. The TBS was also calculated. At baseline and at 1, 3, 6, 12, 18, and 24 months, bone metabolism was assessed by measurements of pro-collagen-I carboxyterminal propeptide (PICP), osteocalcin, and bone alkaline phosphatase levels in the serum, which are indicative of bone formation and β-isomerized carboxy-terminal telopeptide of type-I collagen (β-CTX-I) and serum isoform 5b of tartrate-resistant acid phosphatase (TRACP5b) levels in the serum, which are indicative of bone resorption. RESULTS: In patients with RA, the LS T-score increased (3.2%, p<0.001) and the TBS progressively decreased (-3.9%, p=0.03). In patients with AS, the LS BMD and T-score increased (4.3% and 6.2%, respectively; p<0.001) with no significant change in the TBS. Serum TRACP5b levels dramatically increased in both groups (227% in patients with RA and 150% in those with AS, p<0.001), while β-CTX-I levels did not change. Serum osteocalcin and PICP levels showed a transitory increase in patients with AS. CONCLUSION: Long-term anti-TNFα therapy increased LS bone mass and affected bone quality (TBS) with little impact on bone remodeling. Conversely, TRACP5b levels dramatically increased during anti-TNFα therapy but without any detrimental effect on bone mass.
OBJECTIVE: To examine the impact of long-term anti-TNFα therapy on bone mass, bone metabolism, and the trabecular bone score (TBS) in patients with rheumatoid arthritis (RA) or ankylosing spondylitis (AS). MATERIAL AND METHODS: In eight patients with RA and 12 with AS, bone mineral densities (BMDs) of the lumbar spine (LS), left and right femoral neck, and total skeleton were measured using dual X-ray absorptiometry at baseline and then at 6, 12, and 24 months after anti TNFα therapy. The TBS was also calculated. At baseline and at 1, 3, 6, 12, 18, and 24 months, bone metabolism was assessed by measurements of pro-collagen-I carboxyterminal propeptide (PICP), osteocalcin, and bone alkaline phosphatase levels in the serum, which are indicative of bone formation and β-isomerized carboxy-terminal telopeptide of type-I collagen (β-CTX-I) and serum isoform 5b of tartrate-resistant acid phosphatase (TRACP5b) levels in the serum, which are indicative of bone resorption. RESULTS: In patients with RA, the LS T-score increased (3.2%, p<0.001) and the TBS progressively decreased (-3.9%, p=0.03). In patients with AS, the LS BMD and T-score increased (4.3% and 6.2%, respectively; p<0.001) with no significant change in the TBS. Serum TRACP5b levels dramatically increased in both groups (227% in patients with RA and 150% in those with AS, p<0.001), while β-CTX-I levels did not change. Serum osteocalcin and PICP levels showed a transitory increase in patients with AS. CONCLUSION: Long-term anti-TNFα therapy increased LS bone mass and affected bone quality (TBS) with little impact on bone remodeling. Conversely, TRACP5b levels dramatically increased during anti-TNFα therapy but without any detrimental effect on bone mass.
Entities:
Keywords:
TNFα inhibitors; TRACP5b; bone markers; bone mineral density; trabecular bone score
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