Insulin resistance in early untreated rheumatoid arthritis patients

Shahin, Dina; Eltoraby, Ehab E; Mesbah, Abeer; Houssen, Maha E.

doi:10.1016/j.clinbiochem.2010.01.012

Cited by 60 publications

(66 citation statements)

References 34 publications

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“…There are suggestions that patients with early RA have higher fasting insulin levels and are more frequently insulin-resistant than controls, predisposing to CV events 54. Smoking is a clear risk factor for CV disease as well as anti-citrullinated protein antibody and rheumatoid factor (RF) positive RA,55 and smokers are more prevalent among RA patients than in the general population 56–58.…”

Section: Risk Factorsmentioning

confidence: 99%

How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?

et al. 2012

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Rheumatoid arthritis (RA) is a chronic inflammatory disease which is associated with an increased cardiovascular (CV) burden. Whether the risk is already present at the time of RA diagnosis remains a key area of debate. The aim of this review was to evaluate the existence of both subclinical CV changes, including endothelial dysfunction and atherosclerosis, CV risk factors, as well as CV disease manifestations such as coronary heart disease, myocardial infarction, congestive heart failure and CV death prior to RA diagnosis and during the first few years of the disease. The state of the endothelial function remains controversial in patients with newly diagnosed RA. Studies with impaired brachial artery vasodilatory responses at baseline showed a reversal of the dysfunction after 6-12 months of anti-inflammatory therapy. Morphological evidence of arterial wall atherosclerosis, measured by carotid artery intima-media thickness or the prevalence of carotid plaques, was already present during the first year following RA diagnosis. The risk of coronary heart disease and myocardial infarction is increased even prior to and, at the latest, within 1 year of the clinical onset of RA. The prevalence of hypertension was similar among patients with RA and controls. CV mortality may not increase within the first years of RA diagnosis. In conclusion, the CV risk seems to increase sooner after the RA diagnosis than previously thought. In addition to systematic CV risk assessment, patients with early RA might benefit from being targeted with stricter than conventional CV risk prevention and intervention.

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Section: Risk Factorsmentioning

confidence: 99%

How early in the course of rheumatoid arthritis does the excess cardiovascular risk appear?

et al. 2012

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“…RA patients, proportionally to the degree of infl ammatory activity [ 12 ] , as well as in other infl ammatory chronic diseases [ 13 ] . These facts support the contention that IR and infl ammatory response are linked conditions.…”

Section: Introduction ▼mentioning

confidence: 99%

Systemic Blockade of TNF-α does not Improve Insulin Resistance in Humans

Ferraz-Amaro¹,

Arce-Franco²,

Muñiz³

et al. 2011

Horm Metab Res

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The purpose of this study was to determine whether long-term modulation of inflammatory activity by tumor necrosis factor (TNF)-α inhibitors has some influence on insulin resistance (IR). 16 active rheumatoid arthritis (RA) patients without CV risk factors treated with anti-TNF-α agents were included in this study. RA activity by disease activity score 28, IR by HOMA2-IR, body composition by impedance analysis, physical activity by accelerometry, abdominal fat distribution by magnetic resonance imaging, and serum level of key adipokines by ELISA were measured at baseline and during a 1-year follow-up period. Patient body mass index increased significantly (26.94 ± 3.88 vs. 28.06 ± 4.57 kg/m2, p=0.02) after 1 year of treatment. Body composition, in terms of fat and fat-free mass, remained unchanged except for a significant elevation in body cell mass (25.50 ± 4.60 vs. 26.60 ± 3.17 kg, p=0.02). Basal levels of IR in the RA patients included in this study were significantly higher than healthy controls (1.6 ± 0.8 vs. 1.11 ± 0.56, p=0.011) but did not change during the follow-up. Nor did basal concentrations of adiponectin, visfatin, leptin, ghrelin, resistin, and apelin in response to anti-TNF-α treatment; only retinol-binding protein 4, showed a significant increase (51.7 ± 32.7 vs. 64.9 ± 28.4 μg/ml, p=0.03) at the end of the study. IR, adiposity distribution, and serum levels of most adipokines are not significantly affected by long-term inhibition of TNF-α in RA patients. Our data suggest that although systemic blockade of TNF-α exerts an anticachectic effect in RA patients, it does not seem to play a major role in IR.

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“…Glucocorticoids (GCs) impair hepatic and peripheral insulin sensitivity and induce β-cell dysfunction; however, the precise underlying mechanisms are still being investigated 3 4. Previously, patients with RA were shown to have impaired fasting insulin sensitivity (homoeostatic model assessment of insulin resistance (HOMA-IR) and fasting β-cell function (HOMA-B)), which correlated with disease activity and markers of inflammation 5–7. Consequently, prevalent diabetes was estimated to be up to 15–19% in patients with RA,8 9 an increased number as compared with the estimated T2DM prevalence of 4–8% in middle-aged men and women in the general population 10…”

Section: Introductionmentioning

confidence: 99%