Response to anti-tumour necrosis factor alpha blockade is associated with reduction of carotid intima-media thickness in patients with active rheumatoid arthritis.
OBJECTIVE
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-alpha 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 (DAS44), 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 cIMT 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-alpha blockade is associated with cIMT reduction in RA patients steadily responsive to therapy, probably by lowering inflammation.
Del Porto
F
F
Università La Sapienza, II Facoltà di Medicina e Chirurgia, Azienda Ospedaliera Sant'Andrea, Dipartimento di Scienze Mediche, Via di Grottarossa, Rome, Italy. flavia.delporto@uniroma1.it
Laganà
B
B
Lai
S
S
Nofroni
I
I
Tinti
F
F
Vitale
M
M
Podestà
E
E
Mitterhofer
A P
AP
D'Amelio
R
R
D000208:Acute Disease; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy*; D002340:Carotid Artery Diseases / Q000150:complications / Q000000981:diagnostic imaging; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use*; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use*; D018709:Statistics, Nonparametric; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography
D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068800:Etanercept