Response to anti-tumour necrosis factor alpha blockade is associated with reduction of carotid intima-media thickness in patients with active rheumatoid arthritis

被引:123
作者
Del Porto, F.
Lagana, B.
Lai, S.
Nofroni, I.
Tinti, F.
Vitale, M.
Podesta, E.
Mitterhofer, A. P.
D'Amelio, R.
机构
[1] Univ Roma La Sapienza, Azienda Osped Sant Andrea, Fac Med & Chirurg 2, Dipartimento Sci Med, I-00161 Rome, Italy
[2] Univ Roma La Sapienza, Azienda Osped Sant Andrea, Fac Med Clin, I-00161 Rome, Italy
[3] Univ Roma La Sapienza, Azienda Osped Sant Andrea, Dipartimento Med Clin, I-00161 Rome, Italy
[4] Univ Roma La Sapienza, Azienda Osped Sant Andrea, Dipartimento Med Sperimentale, I-00161 Rome, Italy
关键词
rheumatoid arthritis; cytokines; cardiovascular diseases; atherosclerosis; drug therapy; TNF-alpha blockers;
D O I
10.1093/rheumatology/kem089
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objectives. To determine whether tumour necrosis factor (TNF)-alpha blockers may reduce carotid intima-media thickness (cIMT) in patients with active rheumatoid arthritis (RA) steadily responsive to such therapy. Methods. From 287 consecutive RA patients attending our out-patient clinic and diagnosed on the basis of the American College of Rheumatology (ACR) criteria, 49 without traditional cardiovascular risk factors and meeting the requirements for TNF-alpha blockers therapy were selected. Among them, 39 actually started TNF-a blockers, but only 30, who reached at least a response on the ACR 20% improvement criteria at 14 weeks, maintained during the whole year of treatment, were finally considered (group A). The remaining 10/49, homogeneous for age, sex, traditional cardiovascular risk factors, socioeconomic status, disease activity and duration, who did not consent to TNF-alpha-blocker administration, were used as controls (group B). Disease activity score in 44 joints (DAS(44)), erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were evaluated before starting the study, and 3, 6, 12 months thereafter; cIMT was measured by ultrasound before and 12 months thereafter only. Results. Patients in group A showed a very significant clMT reduction (P < 0.0001 and P < 0.0001, on the right and left side, respectively), preceded by an early and lasting significant decrease in DAS44, ESR and CRP. Moreover, a significant correlation was found between cIMT and DAS44 (r= 0.435, P < 0.05). Conclusions. These results demonstrate that TNF-a blockade is associated with cIMT reduction in RA patients steadily responsive to therapy, probably by lowering inflammation.
引用
收藏
页码:1111 / 1115
页数:5
相关论文
共 52 条
[1]   THE AMERICAN-RHEUMATISM-ASSOCIATION 1987 REVISED CRITERIA FOR THE CLASSIFICATION OF RHEUMATOID-ARTHRITIS [J].
ARNETT, FC ;
EDWORTHY, SM ;
BLOCH, DA ;
MCSHANE, DJ ;
FRIES, JF ;
COOPER, NS ;
HEALEY, LA ;
KAPLAN, SR ;
LIANG, MH ;
LUTHRA, HS ;
MEDSGER, TA ;
MITCHELL, DM ;
NEUSTADT, DH ;
PINALS, RS ;
SCHALLER, JG ;
SHARP, JT ;
WILDER, RL ;
HUNDER, GG .
ARTHRITIS AND RHEUMATISM, 1988, 31 (03) :315-324
[2]   Common carotid intima media thickness as an indicator of atherosclerosis at other sites of the carotid artery - The Rotterdam study [J].
Bots, ML ;
Hofman, A ;
deJong, PTVM ;
Grobbee, DE .
ANNALS OF EPIDEMIOLOGY, 1996, 6 (02) :147-153
[3]   Mechanisms of disease - The many roles of chemokines and chemokine receptors in inflammation [J].
Charo, IF ;
Ransohoff, RM .
NEW ENGLAND JOURNAL OF MEDICINE, 2006, 354 (06) :610-621
[4]   Methotrexate and mortality in patients with rheumatoid arthritis:: a prospective study [J].
Choi, HK ;
Hernán, MA ;
Seeger, JD ;
Robins, JM ;
Wolfe, F .
LANCET, 2002, 359 (9313) :1173-1177
[5]   Mechanisms of disease: Cytokine pathways and joint inflammation in rheumatoid arthritis. [J].
Choy, EHS ;
Panayi, GS .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 344 (12) :907-916
[6]  
COEN G, 2003, BMC NEPHROL, V4, P1
[7]   Association between carotid atherosclerosis and markers of inflammation in rheumatoid arthritis patients and healthy subjects [J].
del Rincón, I ;
Williams, K ;
Stern, MP ;
Freeman, GL ;
O'Leary, DH ;
Escalante, A .
ARTHRITIS AND RHEUMATISM, 2003, 48 (07) :1833-1840
[8]  
DELRINCON I, 2006, ATHEROSCLEROSIS, DOI DOI 10.1016/J.ARTHEROSCLEROSIS.2006.09.027
[9]   Biomarkers of endothelial dysfunction, cardiovascular risk factors and atherosclerosis in rheumatoid arthritis [J].
Dessein, PH ;
Joffe, BI ;
Singh, S .
ARTHRITIS RESEARCH & THERAPY, 2005, 7 (03) :R634-R643
[10]   THE AMERICAN-COLLEGE-OF-RHEUMATOLOGY PRELIMINARY CORE SET OF DISEASE-ACTIVITY MEASURES FOR RHEUMATOID-ARTHRITIS CLINICAL-TRIALS [J].
FELSON, DT ;
ANDERSON, JJ ;
BOERS, M ;
BOMBARDIER, C ;
CHERNOFF, M ;
FRIED, B ;
FURST, D ;
GOLDSMITH, C ;
KIESZAK, S ;
LIGHTFOOT, R ;
PAULUS, H ;
TUGWELL, P ;
WEINBLATT, M ;
WIDMARK, R ;
WILLIAMS, HJ ;
WOLFE, F .
ARTHRITIS AND RHEUMATISM, 1993, 36 (06) :729-740