Adalimumab significantly reduces inflammation and serum DKK-1 level but increases fatty deposition in lumbar spine in active ankylosing spondylitis.
OBJECTIVE
To investigate whether adalimumab is effective for active ankylosing spondylitis (AS) patients and whether it has an impact on the formation of fatty deposition lesions (FDL) and serum Dickkopf homolog 1 (Dkk-1) level in AS patients.


METHODS
This was a randomized, double-blind, placebo-controlled study. Active AS patients received 40 mg adalimumab (n = 26) or placebo (n = 20) every other week during an initial 12-week double-blind period, and all switched to adalimumab treatment for another 12 weeks. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Function Index (BASFI), C-reactive protein (CRP), Ankylosing Spondylitis Disease Activity Scores (ASDAS) and serum DKK-1 levels were measured and magnetic resonance imaging (MRI) of both the lumbar spine and sacroiliac joints were obtained at baseline, week 12 and week 24. Spinal and sacroiliac joint inflammations were evaluated using the Spondyloarthritis Research Consortium of Canada (SPARCC) MRI index, and FDL were assessed in a dichotomous manner.


RESULTS
Obvious improvements in clinical assessments (BASDAI, BASFI, CRP and ASDAS reduced, all P < 0.05), as well as MRI inflammation measurements (both lumbar spine and sacroiliac joints SPARCC scores decreased, all P < 0.05) were shown in active AS patients treated by adalimumab for 12 weeks, but FDL in the lumbar spine seen by MRI increased significantly (P < 0.05) accompanied by decrease of serum DKK-1 levels (P < 0.05), while FDL remained stable after the treatment of placebo in AS patients.


CONCLUSIONS
Our study found that adalimumab was highly effective in reducing inflammation in active AS patients, but it was accompanied by the formation of FDL in the lumbar spine and decrease in serum DKK-1 levels.
Department of Rheumatology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou.
Zaiying
Z
Hu
Manlong
M
Xu
Qiuxia
Q
Li
Zhiming
Z
Lin
Zetao
Z
Liao
Shuangyan
S
Cao
Qiujing
Q
Wei
Yan Li
YL
Zhang
Tianwang
T
Li
Ou
O
Jin
Jianlin
J
Huang
Yunfeng
Y
Pan
Yuqiong
Y
Wu
Xinghe
X
Deng
Jieruo
J
Gu
D000068879:Adalimumab; D000273:Adipose Tissue / Q000187:drug effects* / Q000378:metabolism; D000328:Adult; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D004311:Double-Blind Method; D004359:Drug Therapy, Combination; D005260:Female; D006304:Health Status; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000097:blood*; D007596:Joints / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D050356:Lipid Metabolism / Q000187:drug effects*; D008159:Lumbar Vertebrae / Q000378:metabolism / Q000473:pathology; D008297:Male; D011788:Quality of Life; D020127:Recovery of Function; D012720:Severity of Illness Index; D013167:Spondylitis, Ankylosing / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism; D016896:Treatment Outcome
D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; C501126:DKK1 protein, human; D036341:Intercellular Signaling Peptides and Proteins; D000068879:Adalimumab