The effect of tumor necrosis factor-α inhibitor on bone mineral density of active rheumatoid arthritis patients with low bone mass

Abstract

Objective To explore the effect of tumor necrosis factor (TNF)-α inhibitors therapy on bone mineral density (BMD) in active rheumatoid arthritis (RA) patients with low bone mass. Methods Sixty-two active RA patients with low bone mass were treated with a standard treatment of calcium carbonate 0.5 g/d and alfacalcidol 0.25 μg/d, and were divided into two groups. Patients of the control group were treated with methotrexate 10 mg per week, while patients of the experimental group were treated with combined recombinant human type Ⅱ tumor necrosis factor receptor-antibody fusion protein 50 mg per week or adalimumab 40 mg/2 week subcutaneously for 12 months with methotrexate. BMD of lumbar spine (L2-4) , femoral neck, trochanter and Ward's triangle region by dual energy X-ray absorptiometry (DEXA), as well as the bone turnover markers serum C telopeptide of type-Ⅰ collagen (CTX-Ⅰ) and serum procollagen type-Ⅰ N propeptide (PINP) were measured by enzyme-linkedimmunosorbent assay (ELISA) in both groups at the baseline, treatment for six-month and twelve-month. T test and Chi-square test was used to process the data. Results ① After 6 months of treatment, the BMD of lumbar spine, femoral neck and trochanter in the group with TNF-α inhibitors were higher than the control group [(0.68±0.08) g/cm2vs (0.65±0.06) g/cm2, t=2.269, P=0.027; (0.63±0.08) g/cm2vs (0.58±0.09) g/cm2, t=2.111, P=0.040; (0.61±0.10) g/cm2vs (0.56±0.07) g/cm2, t=2.203, P=0.032; respectively]. And after 12 months, the BMD of all regions were significantly higher than the control group [spine, (0.68±0.07) g/cm2vs (0.62±0.08) g/cm2, t=5.115, P=0.000; femoral neck, (0.63±0.08) g/cm2vs (0.56±0.08) g/cm2, t=3.475, P=0.001; Ward's triangle region (0.60±0.08) g/cm2vs (0.56±0.08) g/cm2, t=2.309, P=0.025; trochanter, (0.61±0.10) g/cm2vs (0.53±0.08) g/cm2, t=3.254, P=0.002; respectively]. ② Compared to the baseline, BMD of lumbar spine was significantly decreased in the control group after 12 months. While in the group of TNF-α inhibitors, BMD of lumbar spine was increased[(0.66±0.08) g/cm2vs (0.68±0.07) g/cm2, t=3.411, P=0.001]. ③ Compared to the baseline, CTX-Ⅰ, a marker of bone resorption was significantly decreased at 6 months and 12 months in the group with TNF-αinhibitors [6 months, (0.33±0.2) ng/ml vs (0.46±0.22) ng/ml, t=5.548, P<0.01; 12 months, (0.31±0.21) ng/ml vs (0.46±0.22) ng/ml, t=5.974, P<0.01], while this decline was not found in the control group. PINP, a marker of bone formation was stable in both 2 groups during the study. Conclusion In active RA patients with low bone mass, loss of BMD in the spine and hip can be arrested by the treatmentof TNF-α inhibitors. Key words: Tumor necrosis factor-α inhibitor; Arthritis, rheumatoid; Bone mass; Bone mineral density