Etanercept Normalizes Systemic Bone Metabolism in Rheumatoid arthritis

초록

Background Rheumatoid arthritis (RA) is a chronic inflammatory disease accompanied by bone loss. Etanercept is soluble TNF-α receptor which is effective in suppressing RA activity. Objective Our aim is to assess bone metabolism in TNF naïve RA patients and to figure out effects of etanercept on bone turnover markers and inflammatory mediators. Methods Twenty-one RA patients (19 women and 2 men; age 46.29 ± 11.6 years) were included. They were required to be active RA, thus meeting the criteria of DAS28 ≥ 3.2 and either ESR ≥ 28mm/hr or CRP ≥ 2.0 mg/dL and morning stiffness ≥ 45 minutes. Age and sex matched control group were recruited. Etanercept was administered at standard dose, twice a week. Venous blood was drawn at baseline in both groups and at week 14-16 after etanercept use in RA patient. Bone metabolism was assessed using bone specific alkaline phosphatase (BSAP), osteoprotegerin (OPG), sclerostin for bone formation and receptor activator for nuclear factor ĸB ligand (RANKL), serum c-telopeptide (CTX) for bone resorption. Serum level of inflammatory mediators including ESR, CRP and IL-6 were also determined. Differences between two groups were examined for statistical difference by Wilkoxon signed ranks test. A p value of less than 0.05 was denoted statistically significant. Results At baseline the sclerostin level was significantly decreased in RA patients than in control group while serum CTX was decreasing. However after etanercept use, both serum CTX and sclerostin markedly increased(Table 1). BSAP and OPG were slightly affected by etanercept. RANKL mildly decreased after treatment. Inflammatory mediators responded to the treatment as ESR, CRP and IL-6 all significantly decreased (Table 2).