Abstract
Objective: To evaluate the effect of anti-TNF therapy on resistance to insulin in patients with rheumatoid arthritis (RA) compared with patients with RA being treated with non-biological DMARDs. Methods: Inactive patients diagnosed with RA (ACR 1987 criteria) (DAS 28 2.6) were included, being treated with anti-tumor necrosis factor inhibitors (anti-TNF) (cases) and non-biological disease-modifying anti-rheumatic drugs (DMARD) (controls), without risk factors for insulin resistance (administration of steroids, body mass index > 25 kg/m2, diabetes mellitus or use of glucose lowering agents, systemic arterial hypertension or use of anti-hypertensive drugs, triglycerides > 150 mg/dl, hypercholesterolemia > 200 mg/dl, high-density lipoproteins 40 mg/dl in men and 50 mg/in women, or with lipids lowering agents, waist measurement > 88 cm in women and > 102 cm in men). We used HOMA (Homeostasis Model Assessment) to determine insulin resistance in both groups, HOMA being defined as >1 and sensitivity to insulin using QUICKI (Insulin Sensitivity Check Index), ≥0.38 being considered as normal. The Mann Whitney U was used for the statistical analysis. Results: A total of 28 patients, 15 being treated with non-biological DMARDs and 13 with anti-TNF therapy, were evaluated; 89.7%, of which were women. Average age: 43.5 (range 21 - 62); the average HOMA index of the non-biological DMARD group was 1.58 (range 0.7 - 5.4), compared with patients treated with anti-TNF therapy, 1.18 (range 0.2 - 4.3) (P = 0.5). The average QUICKI index was 0.36 (range 0.30 - 0.42) in patients treated with non-biological DMARD, compared with0.37 inpatients treated with anti-TNF therapy (range 0.30 - 0.51) (P = 0.8). Conclusion: Resistance to insulin manifested itself in both groups, although there was a greater trend of less insulin resistance and greater sensitivity in the anti-TNF group; this was probably not statistically significant due to the sample size.
Highlights
Rheumatoid arthritis (RA) is the most common form of chronic inflammatory joint disease that brings about osseous destruction
Inactive patients diagnosed with rheumatoid arthritis (RA) (ACR 1987 criteria) (DAS 28 < 2.6) were included, being treated with anti-tumor necrosis factor inhibitors and non-biological disease-modifying anti-rheumatic drugs (DMARD), without risk factors for insulin resistance
The average quantitative insulin sensitivity check index (QUICKI) index was 0.36 in patients treated with non-biological DMARD, compared with 0.37 in patients treated with anti-tumor necrosis factor (TNF) therapy (P = 0.8)
Summary
Rheumatoid arthritis (RA) is the most common form of chronic inflammatory joint disease that brings about osseous destruction. The inflammatory process causes thickening and hyperplasia of the synovium, which is infiltrated by numerous cells that produce pro-inflammatory cytokines, including IL-1, IL-6 and tumor necrosis factor (TNF) [1]. This inflammation plays an important part in the pathogenesis of atherosclerosis and contributes to the cardiovascular morbidity and mortality found in patients with RA [2]. Cardiovascular disease is twice as common in patients with RA, in comparison with the general population [3]. An increase in insulin resistance has been reported in patients with auto-immune diseases, including patients with RA [5,6]. In a case-control study it was found that insulin resistance of patients with RA
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