Korean J Intern Med.  2014 Nov;29(6):807-813. 10.3904/kjim.2014.29.6.807.

Early effects of tumor necrosis factor inhibition on bone homeostasis after soluble tumor necrosis factor receptor use

Affiliations
  • 1Division of Rheumatology, Department of Internal Medicine, Inha University Hospital, Incheon, Korea. parkwon@inha.ac.kr
  • 2Department of Occupational and Environmental Medicine, Inha University Hospital, Incheon, Korea.

Abstract

BACKGROUND/AIMS
Our aim was to assess whether short-term treatment with soluble tumor necrosis factor (TNF) receptor affects circulating markers of bone metabolism in rheumatoid arthritis (RA) patients.
METHODS
Thirty-three active RA patients, treated with oral disease-modifying antirheumatic drugs (DMARDs) and glucocorticoids for > 6 months, were administered etanercept for 12 weeks. Serum levels of bone metabolism markers were compared among patients treated with DMARDs at baseline and after etanercept treatment, normal controls and naive RA patients not previously treated with DMARDs (both age- and gender-matched).
RESULTS
Bone-specific alkaline phosphatase (BSALP) and serum c-telopeptide (CTX)-1 levels were lower in RA patients treated with DMARDs than in DMARD-naive RA patients. After 12 weeks of etanercept treatment, serum CTX-1 and sclerostin levels increased. In patients whose DAS28 improved, the sclerostin level increased from 1.67 +/- 2.12 pg/mL at baseline to 2.51 +/- 3.03 pg/mL, which was statistically significant (p = 0.021). Increases in sclerostin levels after etanercept treatment were positively correlated with those of serum CTX-1 (r = 0.775), as were those of BSALP (r = 0.755).
CONCLUSIONS
RA patients treated with DMARDs showed depressed bone metabolism compared to naive RA patients. Increases in serum CTX-1 and sclerostin levels after short-term etanercept treatment suggest reconstitution of bone metabolism homeostasis.

Keyword

Arthritis, rheumatoid; Bone remodeling; TNFR-Fc fusion protein

MeSH Terms

Adult
Alkaline Phosphatase/blood
Arthritis, Rheumatoid/blood/diagnosis/*drug therapy
Biological Markers/blood
Bone Morphogenetic Proteins/blood
Bone Remodeling/*drug effects
Collagen Type I/blood
Female
Genetic Markers
Homeostasis
Humans
Immunoglobulin G/*administration & dosage
Immunosuppressive Agents/*administration & dosage
Inflammation Mediators/blood
Male
Middle Aged
Peptides/blood
Receptors, Tumor Necrosis Factor/*administration & dosage
Time Factors
Treatment Outcome
Tumor Necrosis Factor-alpha/antagonists & inhibitors
Alkaline Phosphatase
Biological Markers
Bone Morphogenetic Proteins
Collagen Type I
Genetic Markers
Immunoglobulin G
Immunosuppressive Agents
Inflammation Mediators
Peptides
Receptors, Tumor Necrosis Factor
Tumor Necrosis Factor-alpha
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