Inage Kazuhide, Orita Sumihisa, Yamauchi Kazuyo, Sakuma Yoshihiro, Kubota Go, Oikawa Yasuhiro, Sainoh Takeshi, Sato Jun, Fujimoto Kazuki, Shiga Yasuhiro, Takahashi Kazuhisa, Ohtori Seiji
Department of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Department of Orthopedic Surgery, National Hospital Organization Chiba Medical Center, Chiba, Japan.
Asian Spine J. 2015 Jun;9(3):338-43. doi: 10.4184/asj.2015.9.3.338. Epub 2015 Jun 8.
Retrospective study.
We conducted a study to investigate the time course changes in bone metabolic markers after the administration of the anti-receptor activator of nuclear factor-kappa B ligand (RANKL) antibody and to assess drug compliance among osteoporotic patients.
The anti-RANKL antibody is expected to provide an improvement in those with a bone metabolism disorder. However there are only a few clinical reports available on the effect of treatment.
We included 40 post-menopausal osteoporotic patients who received the anti-RANKL antibody. To determine the time course changes in the bone metabolic markers, we measured the serum tartrate-resistant acid phosphatase 5b (TRACP 5b; a bone resorption marker) and the serum N-terminal propeptide of type 1 collagen (P1NP; a bone formation marker) levels prior to and 1 month after administrating the anti-RANKL antibody. To evaluable drug compliance, we assessed the dropout rate during treatment and at 6 months after treatment.
The average TRACP 5b level significantly decreased from 574.8 mU/dL before treatment to 153.2 mU/dL 1 month after treatment (p<0.05). There was no significant difference in the average P1NP level, which was 56.9 µG/L and 35.1 µG/L before and 1 month after treatment, respectively (p>0.05). As for drug compliance, we did not have any dropouts during the treatment or after 6 months (dropout rate: 0%).
Our study suggests that anti-RANKL antibody treatment suppresses bone resorption and maintains bone formation.
