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Abstract Number: 2259

Changes in serum  Soluble RANKL and Osteoprotegerin Levels after Teriparatide Administration in Rheumatic Disease Patients with Glucocorticoid-Induced Osteoporosis

Makoto Kaburaki, Kaichi Kaneko, Kotaro Shikano, Mai Kawazoe, Emiko Shindo, Hiroshi Sato, Natsuki Fujio, Sei Muraoka, Nahoko Tanaka, Tatsuhiro Yamamoto, Natsuko Kusunoki, Tomoko Hasunuma, Shinichi Kawai and Shotaro Masuoka, Division of Rheumatology, Department of Internal Medicine, School of Medicine, Faculty of Medicine, Toho University, Tokyo, Japan

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: osteoporosis, rheumatic disease and teriparatide

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Session Information

Session Title: Osteoporosis and Metabolic Bone Disease - Clinical Aspects and Pathogenesis: Osteoporosis: Treatment, Safety, and Long Term Outcomes

Session Type: Abstract Submissions (ACR)

Background/Purpose ,Osteoporosis is one of the serious complications of systemic glucocorticoid therapy. Reduced bone formation is the key process in patients with glucocorticoid-induced osteoporosis (GIOP), however, the significance of increased bone resorption in these patients is still under consideration. We reported that serum soluble receptor activator for nuclear factor-κB ligand (sRANKL) level might be a predictive factor in patients under glucocorticoid therapy (J Clin Endocrinol Metab. 97: E1909-917, 2012). Teriparatide, a recombinant form of parathyroid hormone, is an option of treatment for GIOP, especially to the severe cases. Its daily injection stimulates bone formation, resulting increase of bone volume and reduction of bone fracture. Thus, we observed the effect of teriparatide on serum sRANKL and osteoprotegerin (OPG) levels as bone resorption markers in patients with rheumatic disease under glucocorticoid therapy.The aim of this study is to evaluate the effect of teriparatide on serum sRANKL and OPG levels in patients under glucocorticoid therapy. 

Methods ,Patients were recruited at Toho University Omori Medical Center. This study was approved by the Ethics Committees at Toho University Omori Medical Center (approval number; 24-97). Twenty postmenopausal women (71±6 yr [mean ± SD]) with rheumatic diseases (rheumatoid arthritis 9, vasculitis syndrome 6, polymyalgia rheumatica 3, polymyositis 1, and systemic lupus erythematosus 1) were included in this study. All the patients were changed from oral bisphosphonates to daily s.c. injections of teriparatide (20 μg) for treatment of GIOP. Patients who received mean prednisolone at doses of 6.7±5.4 (SD) mg daily were eligible for this study. We measured serum sRANKL, OPG, bone formation markers (OC, ucOC, BAP, and P1NP), and bone resorption markers (TRACP-5b and NTX) during teriparatide treatment. The bone mineral density (BMD) was measured before and 6 months after start of teriparatide treatment. Data were expressed as the median with the interquartile range. 

Results ,Serum sRANKL levels were significantly decreased after teriparatide treatment (0.066 [0.0-0.188] to 0.0 [0.0-0.008] pmol/L, p < 0.05). In contrast, serum OPG levels were not changed after the treatment (6.71 [5.79-8.13] to 7.17 [5.69-8.92] pmol/L, p =0.584). All of serum bone formation markers (OC; 3.6 [2.9-5.8] to 10.0 [8.2-18.0] ng/mL, ucOC; 1.4 [0.9-4.6] to 5.2 [3.4-9.1] ng/mL, BAP; 10.9[8.8-16.0] to 15.5 [11.6-22.3] U/L, and P1NP; 26.8 [12.5-43.2] to 88.8 [48.1-196.0] ng/L) and resorption markers (TRACP-5b; 227 [171-506] to 353 [269-506] mU/L and NTX; 12.7 [10.7-22.4] to 21.9 [16.9-26.6] nmolBCE/L) were significantly (p < 0.05) increased after teriparatide treatment. Mean BMD was significantly increased when compared to that of pretreatment value (0.65 [0.59-0.71] to 0.72 [0.65-0.84], p < 0.05). 

Conclusion ,It is suggested that the improvement of bone density by teriparatide might be explained not only by activation of bone formation but also by decreased bone resorption due to reduction of sRANKL in patients under glucocorticoid therapy.


Disclosure:

M. Kaburaki,
None;

K. Kaneko,
None;

K. Shikano,
None;

M. Kawazoe,
None;

E. Shindo,
None;

H. Sato,
None;

N. Fujio,
None;

S. Muraoka,
None;

N. Tanaka,
None;

T. Yamamoto,
None;

N. Kusunoki,
None;

T. Hasunuma,
None;

S. Kawai,
None;

S. Masuoka,
None.

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