Early effects of tumor necrosis factor inhibition on bone homeostasis after soluble tumor necrosis factor receptor use.
10.3904/kjim.2014.29.6.807
- Author:
Mie Jin LIM
1
;
Seong Ryul KWON
;
Kowoon JOO
;
Min Jung SON
;
Shin Goo PARK
;
Won PARK
Author Information
1. Division of Rheumatology, Department of Internal Medicine, Inha University Hospital, Incheon, Korea. parkwon@inha.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Arthritis, rheumatoid;
Bone remodeling;
TNFR-Fc fusion protein
- MeSH:
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
- From:The Korean Journal of Internal Medicine
2014;29(6):807-813
- CountryRepublic of Korea
- Language:English
-
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.
