Session Information
Session Type: Abstract Submissions (ACR)
Background/Purpose:
To identify and characterize subclinical synovitis in patients with rheumatoid arthritis in clinical remission using power Doppler ultrasound and serum levels of angiogenic factors.
Methods:
We selected patients with rheumatoid arthritis in clinical remission (defined as DAS28-ESR<2.6) tested by two independent rheumatologists. Clinical, epidemiological, demographic and serological data were analyzed. Ultrasonography of knees and hands (wrists, metacarpophalangeal [MCP], proximal interphalangeal [PIP], flexor and extensor tendons of the hand) was performed by a radiologist with an ultrasound scanner (Acuson Antares, Siemens AG, Erlangen, Germany) with a linear probe of 10.5 MHz. Synovial hypertrophy and power Doppler signal were scored (grades 0-3). Synovial hypertrophy >2 plus power Doppler signal was classified as active synovitis.
Serum levels of angiogenic factors were determined by Quantibody® Human Array (RayBiotech, Inc, Norcross, GA, USA).
Results:
Fifty-five patients were included of whom 25 (45.4%) met criteria for active synovitis. The most-affected joints were the wrist and second MCP. Patients with active synovitis on ultrasound had significantly higher DAS28-CRP (p=0.020) and only 12% were taking oral glucocorticoids (< 5 mg/day) compared with 40% of patients without active synovitis. No other clinical differences were found (Table 1). Patients with active synovitis had significantly-higher serum levels of angiogenic factors: angiopoietin-2 (p=0.038), VEGF-D (p=0.018), PIGF (p=0.043), SDF-1 (p=0.035), MMP-2 (p=0.027) and bFGF (p=0.007) (Table 1).
Table 1. Clinical, demographic and biological data of the 55 patients, stratified according the presence or not of active synovitis as defined by ultrasound*.
|
|
All n=55 |
HS + Doppler(active synovitis) n=25 |
No HS+Doppler (no active synovitis) n=30 |
p–value |
|
Age (years) |
52 (44-62) |
51 (43-61) |
55 (46-65) |
0.275 |
|
Women, n (%) |
42 (76) |
17 (68) |
25 (83) |
0.155 |
|
Disease duration (months) |
90.0 (56.2-150.3) |
86.3 (57.1-166.9) |
93.7 (50.8-148.9) |
0.649 |
|
RF, n (%) |
39 (71) |
18 (72) |
21 (70) |
0.555 |
|
ACPA, n (%) |
47 (86) |
23 (92) |
24 (80) |
0.193 |
|
DAS283v-ESR |
2.03 (1.67-2.44) |
2.24 (1.88-2.57) |
1.92 (1.55-2.21) |
0.060 |
|
DAS283v-CRP |
1.42 (1.37-1.59) |
1.54 (1.38-1.71) |
1.40 (1.17-1.49) |
0.020 |
|
mHAQ |
0.1 (0.0-0.4) |
0.1 (0.0-0.3) |
0.0 (0.0-0.4) |
0.564 |
|
ESR (mm/1h) |
9 (6-16) |
10 (7-20) |
9 (6-12) |
0.493 |
|
CRP (mg/dL) |
0.10 (0.03-0.35) |
0.11 (0.03-0.50) |
0.09 (0.04-0.27) |
0.722 |
|
Glucocorticoids, n (%) |
15 (27) |
3 (12) |
12 (40) |
0.020 |
|
Biological Therapy, n (%) |
23 (42) |
9 (36) |
14 (47) |
0.301 |
|
DMARDs, n (%) |
44 (80) |
21(84) |
23 (77) |
0.233 |
|
ANG-2 (pg/mL) |
726 (579-1027) |
880 (659-1152) |
702 (525-881) |
0.038 |
|
VEGF-D (pg/mL) |
32096 (17759-239749) |
63479 (26346-600000) |
27544 (9813-87872) |
0.018 |
|
PlGF (pg/mL) |
288 (147-994) |
452 (180-1501) |
237 (115-730) |
0.043 |
|
SDF-1 (pg/mL) |
280 (115-1648) |
750 (157-3420) |
165 (80-1127) |
0.035 |
|
MMP-2 (pg/mL) |
2738 (1909-4109) |
3762 (2101-5779) |
2403.5 (1870-3448) |
0.027 |
|
bFGF (pg/mL) |
314 (267-521) |
383 (285-762) |
295 (260-327) |
0.007 |
*Data are expressed as median (IQR) or as percentage. HS: synovial hypertrophy; RF: rheumatoid factor; ACPA: anti-citrullinated protein/peptide antibodies; DAS28: disease activity score; mHAQ: modified Health Status Questionnaire; ESR: erythrocyte sedimentation rate; DMARD: disease modifying anti-rheumatic drugs. ANG-2: angiopoietin-2; VEFG: vascular endothelial growth factor; PIGF: Placental Growth Factor. SDF: Stromal-cell derived factor-1; MMP-2: matrix metalloproteinase-2; bFGF: basic fibroblast growth factor.
Conclusion:
Around half of patients with RA in clinical remission presented active synovitis on ultrasound. These patients have greater disease activity and higher serum levels of angiogenic factors. These findings are clinically and physiopathologically consistent and may help identify active synovitis in RA patients in clinical remission.
This study is supported by a grant from Ministry of Economy, ISCIII, FIS 11/01890 and RD12/0006/0016 (JDC)
Disclosure:
J. Ramirez,
None;
V. Ruiz-Esquide,
None;
I. Pomés,
None;
R. Celis,
None;
J. Pomés,
None;
S. Cabrera,
None;
M. V. Hernández,
None;
O. M. Epis,
None;
J. L. Pablos,
None;
R. Sanmarti,
None;
J. D. Cañete,
None.
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