Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis

被引:189
作者
Popa, C
Netea, MG
Radstake, T
Van der Meer, JWM
Stalenhoef, AFH
van Riel, PLCM
Barerra, P
机构
[1] Univ Med Ctr St Radboud, Dept Rheumatol, NL-6500 HB Nijmegen, Netherlands
[2] Univ Med Ctr St Radboud, Dept Internal Med, Nijmegen, Netherlands
关键词
D O I
10.1136/ard.2004.023119
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Tumour necrosis factor (TNF) is known to increase the concentrations of interleukin (IL) 6 and C reactive protein (CRP) and to induce proatherogenic changes in the lipid profile and may increase the cardiovascular risk of patients with rheumatoid arthritis (RA) and other inflammatory disorders. Objective: To assess whether anti-TNF therapy modifies the cardiovascular risk profile in patients with RA. Methods: The lipoprotein spectrum and the inflammation markers CRP and IL6 were investigated in 33 patients with RA treated with human anti-TNF monoclonal antibodies (D2E7, adalimumab, Humira) and 13 patients with RA given placebo, before and after 2 weeks' treatment. Results: In the anti-TNF treated group, the mean (SD) concentrations of HDL-cholesterol were significantly higher after 2 weeks' treatment (0.86 (0.30) mmol/l v 0.98 (0.33) mmol/l, p<0.01), whereas LDL and triglyceride levels were not significantly changed. Additionally, a significant decrease in CRP (86.1 (54.4) mg/l v 35.4 (35.0) mg/l, p<0.0001), and IL6 (88.3 (60.5) pg/ml v 42.3 (40.7) pg/ml, p<0.001) concentrations was seen in this group. No changes in lipid profile, IL6, or CRP levels were seen in the placebo group. Conclusions: TNF neutralisation with monoclonal anti-TNF antibodies increased HDL-cholesterol levels and decreased CRP and IL6 levels after 2 weeks. Therefore this treatment may improve the cardiovascular risk profile of patients with RA.
引用
收藏
页码:303 / 305
页数:3
相关论文
共 15 条
[1]   Drug survival, efficacy and toxicity of monotherapy with a fully human anti-tumour necrosis factor-α antibody compared with methotrexate in long-standing rheumatoid arthritis [J].
Barrera, P ;
van der Maas, A ;
van Ede, AE ;
Kiemeney, BALM ;
Laan, RFJM ;
van de Putte, LBA ;
van Riel, PLCM .
RHEUMATOLOGY, 2002, 41 (04) :430-439
[2]  
Cauza E, 2002, WIEN KLIN WOCHENSCHR, V114, P1004
[3]   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
[4]  
Demacker PNM, 1997, CLIN CHEM, V43, P663
[5]   TUMOR-NECROSIS-FACTOR, CYTOKINES, AND THE HYPERLIPIDEMIA OF INFECTION [J].
GRUNFELD, C ;
FEINGOLD, KR .
TRENDS IN ENDOCRINOLOGY AND METABOLISM, 1991, 2 (06) :213-219
[6]   Anti-tumor necrosis factor-α treatment improves endothelial function in patients with rheumatoid arthritis [J].
Hürlimann, D ;
Forster, A ;
Noll, G ;
Enseleit, F ;
Chenevard, R ;
Distler, O ;
Béchir, M ;
Spieker, LE ;
Neidhart, M ;
Michel, BA ;
Gay, RE ;
Lüscher, TF ;
Gay, S ;
Ruschitzka, F .
CIRCULATION, 2002, 106 (17) :2184-2187
[7]  
Jacobsson LTH, 2003, ARTHRITIS RHEUM, V48, pS241
[8]   Infection and inflammation-induced proatherogenic changes of lipoproteins [J].
Khovidhunkit, W ;
Memon, RA ;
Feingold, KR ;
Grunfeld, C .
JOURNAL OF INFECTIOUS DISEASES, 2000, 181 :S462-S472
[9]   CHOLESTEROL AND CORONARY HEART-DISEASE - PREDICTING RISKS BY LEVELS AND RATIOS [J].
KINOSIAN, B ;
GLICK, H ;
GARLAND, G .
ANNALS OF INTERNAL MEDICINE, 1994, 121 (09) :641-647
[10]   Infliximab and methotrexate in the treatment of rheumatoid arthritis [J].
Lipsky, PE ;
van der Heijde, DMFM ;
St Clair, EW ;
Furst, DE ;
Breedveld, FC ;
Kalden, JR ;
Smolen, JS ;
Weisman, M ;
Emery, P ;
Feldmann, M ;
Harriman, GR ;
Maini, RN .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 343 (22) :1594-1602