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Tacrolimus treatment increases bone formation in patients with rheumatoid arthritis

Authors
Kang, Kwi YoungJu, Ji HyeonSong, Yeong WookYoo, Dae-HyunKim, Ho-YounPark, Sung-Hwan
Issue Date
Aug-2013
Publisher
Springer Verlag
Keywords
Tacrolimus; Calcineurin; Osteoblast; NFAT; Osteocalcin
Citation
Rheumatology International, v.33, no.8, pp 2159 - 2163
Pages
5
Indexed
SCI
SCIE
SCOPUS
Journal Title
Rheumatology International
Volume
33
Number
8
Start Page
2159
End Page
2163
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/162224
DOI
10.1007/s00296-012-2370-z
ISSN
0172-8172
1437-160X
Abstract
Tacrolimus is a calcineurin inhibitor, and it is used for the treatment of rheumatoid arthritis (RA). It works by inhibiting nuclear factor of activated T cells and inducting immunosuppression. This study aims to evaluate the influence of tacrolimus on the bone metabolism of patients with RA. Twenty-eight RA patients in three centers received tacrolimus 3 mg once daily for 24 weeks. Blood samples for evaluating bone metabolism and cytokines were collected at Weeks 0 and 24. We measured the serum C-telopeptide of type I collagen (sCTx-I), osteocalcin and inflammatory cytokines. We analyzed the data using the Kruskal-Wallis test and Spearman's correlation. IL-2 and IL-6 were significantly decreased after the administration of tacrolimus (p = 0.027 and p = 0.024). There was no significant difference in the serum level of sCTx-I before and after treatment. The level of serum osteocalcin at Week 24 was significantly increased compared to the level at Week 0 (p = 0.002). The increase of osteocalcin was correlated with the reductions of IL-2 and IFN-gamma (r = 0.405, p = 0.033 and r = 0.380, p = 0.046, respectively). Tacrolimus treatment increased bone formation markers in RA patients. This suggests that tacrolimus may play a role to inhibit bone erosion by increasing bone formation as well as improving the clinical symptoms of RA.
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