Background Some cases in RA, the use of biologics improved bone quality and formation. We try to demonstrate the TCZ suppresses RA activity and promotes bone formation.
Objectives TCZ was administered to RA patients to suppress the inflammatory cytokine IL-6, and the correlation of clinical assessment (DAS28-ESR) with bone/cartilage markers (MMP-3, IL-6, OC, NTX, osteoprotegerin [OPG], Dickkopf-1 [DKK-1], CTX-2) and the Spearman rank-correlation coefficient (ρ) were examined.
Methods Each marker and overall assessment was done pre-administration and at 12, 24 and 52 weeks in 20 RA patients from 2010 to 2012 at facilities associated with Kinki University. The subjects were 7 men and 13 women, average age 57.0±18.2 years, stages I (5), II (5), III (1) and IV (9), classes I (4), II (14), III (2) and IV (0), with disease duration of 8.8±8.0 years, rate of MTX use of 35% (7 patients) at 6.5±1.8 mg/week, rate of PSL use of 70% (14 patients) at 4.0±1.4 mg, with 11 subjects having used other biological agent.
Results DAS28-ESR at 52 weeks (LOCF) significantly decreased from pre-administration 5.1±1.4 to 1.9±0.9, with 90% achieving the remission criteria, and of 9 patients using TCZ as the first-line choice, 8 met the remission criteria and 1 met the criteria for low disease activity. MMP-3 significantly decreased from pre-administration 192±174 ng/mL to 102±86 ng/mL, as well as PSL use to 2.5±2.1 mg. OC and DKK-1 significantly changed at 24 weeks, when the DKK-1 and OC/NTX ratio showed negative correlation by the Spearman rank-correlation coefficient (ρ): -0.8593 (p<0.0001). Similarly, sigificant negative correlation of ρ=-0.4908 (p=0.0329) was also seen at 52 weeks (LOCF). DKK-1 at 52 weeks had significanly decreased from pre-administration 3194±797 pg/mL to 2451±734 pg/mL by TCZ administration, while the OC/NTX ratio increased 1.5 times from pre-administration. CTX-2, NTX and OPG showed no significant differences during this time. These changes related to bone formation were marked in first-line TCZ cases, and decrease was significantly greater in the remission group than in the non-remission group (p value). TCZ suppresses IL-6, which has various actions, and it may act on RANKL and have inhibitory effect on bone destruction through Wnt signal inhibitors. TCZ shows association with multiple mutual factors affecting inflammation, bone, joints, etc., and it was suggested that TCZ administration suppresses RA disease activity and promotes bone formation (particularly first-line choice & early choice > later choice).
Conclusions TCZ suppresses RA activity and promotes bone formation.
Disclosure of Interest None Declared
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