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Clin Rheumatol. 2019 Sep 14. doi: 10.1007/s10067-019-04771-3. [Epub ahead of print]

Effects of 1-year anti-TNF-α therapies on bone mineral density and bone biomarkers in rheumatoid arthritis and ankylosing spondylitis.

Author information

1
Division of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Nagyerdei str 98, Debrecen, 4032, Hungary.
2
Department of Sports Medicine, Debrecen, Hungary.
3
Department of Rheumatology, Uppsala University Hospital, Uppsala, Sweden.
4
Department of Rheumatology, St. Vincent's University Hospital and Conway Institute for Biomolecular Research, University College Dublin, Dublin, Ireland.
5
Department of Laboratory Medicine, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
6
Department of Oncology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
7
Department of Otolaryngology, Borsod County Teaching Hospital, Miskolc, Hungary.
8
Division of Rheumatology, Department of Internal Medicine, Faculty of Medicine, University of Debrecen, Nagyerdei str 98, Debrecen, 4032, Hungary. szekanecz.zoltan@med.unideb.hu.

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.

KEYWORDS:

Biologics; Bone loss; DKK-1; Erosion; JAK inhibitors; Osteoporosis; Osteoprotegerin; RANKL; Rheumatoid arthritis; Sclerostin; Spondyloarthritis; Syndesmophyte

PMID:
31522318
DOI:
10.1007/s10067-019-04771-3

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