Impact of TNF inhibition on insulin resistance and lipids levels in patients with rheumatoid arthritis

被引:160
作者
Tam, Lai-Shan [1 ]
Tomlinson, Brian [1 ]
Chu, Tanya T. [1 ]
Li, Tena K. [1 ]
Li, Edmund K. [1 ]
机构
[1] Chinese Univ Hong Kong, Dept Med & Therapeut, Hong Kong, Peoples R China
关键词
insulin resistance; lipid profile; rheumatoid arthritis; TNF blocker;
D O I
10.1007/s10067-007-0539-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Patients with rheumatoid arthritis (RA) have increased cardiovascular mortality. TNF-alpha is a critical mediator of inflammation and metabolic response in patients with RA. Increased insulin resistance and dyslipidemia were known risk factors in patients with active RA, however, the regulation of these metabolic parameters by TNF-alpha is poorly understood. Neutralization of TNF-alpha with infliximab offers a unique opportunity to study TNF-alpha-mediated regulation of these metabolic parameters in RA. The aim of the study was to assess the in vivo TNF-alpha-mediated regulation of insulin resistance and lipids levels in RA. Nineteen patients with active RA treated with infliximab were prospectively followed for 14 weeks. Plasma lipids levels and insulin resistance were measured at baseline, 6 and 14 weeks after infliximab treatment. At week 14, the disease activity (DAS-28 score) improved significantly (p<0.000), with a significant reduction in both C-reactive protein (p=0.007) and erythrocyte sedimentation rate (p=0.006) levels. The body weight did not change during the study period. After infliximab treatment, insulin resistance improved as reflected by the significant reduction in the Homeostasis Model Assessment Index. Total cholesterol, HDL-cholesterol, LDL-cholesterol, triglycerides, and apolipoprotein B (apoB) levels all increased significantly from baseline. Nonetheless, the atherogenic index, LDL-cholesterol/HDL-cholesterol ratio, and the LDL/apoB ratio remained unchanged. Infliximab improves insulin sensitivity and alters lipid profile in patients with active RA.
引用
收藏
页码:1495 / 1498
页数:4
相关论文
共 19 条
[1]   Effects of repeated infliximab therapy on serum lipid profile in patients with refractory rheumatoid arthritis [J].
Allanore, Y ;
Kahan, A ;
Sellam, J ;
Ekindjian, OG ;
Borderie, D .
CLINICA CHIMICA ACTA, 2006, 365 (1-2) :143-148
[2]  
Cauza E, 2002, WIEN KLIN WOCHENSCHR, V114, P1004
[3]   MECHANISM OF THE HYPERTRIGLYCERIDEMIA INDUCED BY TUMOR NECROSIS FACTOR ADMINISTRATION TO RATS [J].
CHAJEKSHAUL, T ;
FRIEDMAN, G ;
STEIN, O ;
SHILONI, E ;
ETIENNE, J ;
STEIN, Y .
BIOCHIMICA ET BIOPHYSICA ACTA, 1989, 1001 (03) :316-324
[4]   Conversion towards an atherogenic lipid profile in rheumatoid arthritis patients during long-term infliximab therapy [J].
Dahlqvist, SR ;
Engstrand, S ;
Berglin, E ;
Johnson, O .
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY, 2006, 35 (02) :107-111
[5]   Insulin resistance and impaired beta cell function in rheumatoid arthritis [J].
Dessein, Patrick H. ;
Joffe, Barry I. .
ARTHRITIS AND RHEUMATISM, 2006, 54 (09) :2765-2775
[6]   Effects of disease modifying agents and dietary intervention on insulin resistance and dyslipidemia in inflammatory arthritis: a pilot study [J].
Dessein, PH ;
Joffe, BI ;
Stanwix, AE .
ARTHRITIS RESEARCH, 2002, 4 (06) :R12
[7]   Role of cytokines in rheumatoid arthritis [J].
Feldmann, M ;
Brennan, FM ;
Maini, RN .
ANNUAL REVIEW OF IMMUNOLOGY, 1996, 14 :397-440
[8]  
Gonzalez-Gay MA, 2006, CLIN EXP RHEUMATOL, V24, P83
[9]   Definition of metabolic syndrome - Report of the National Heart, Lung, and Blood Institute/American Heart Association Conference on Scientific Issues Related to Definition [J].
Grundy, SM ;
Brewer, HB ;
Cleeman, JI ;
Smith, SC ;
Lenfant, C .
CIRCULATION, 2004, 109 (03) :433-438
[10]   IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance [J].
Hotamisligil, GS ;
Peraldi, P ;
Budavari, A ;
Ellis, R ;
White, MF ;
Spiegelman, BM .
SCIENCE, 1996, 271 (5249) :665-668