Compared with controls, patients with rheumatoid arthritis (RA), especially those with high disease activity, had increased insulin resistance and impaired beta-cell function, according to data presented at the American College of Rheumatology 2016 annual meeting in Washington, DC.
While it is well-recognized that patients with RA are at increased risk of systemic insulin resistance, the association been RA disease activity and beta-cell dysfunction has not been established.
They evaluated 127 participants without diabetes—90 with RA (mean age: 52.4 years; mean disease duration: 9 years) and 37 age and comorbidity-matched controls (mean age: 49.0 years). All patients with RA were receiving disease-modifying antirheumatic drug (DMARD) therapy, including methotrexate (93.3%), steroids (65.6%), and biologic therapy (27.8%).
Body mass index (BMI), waist circumference, blood pressure, disease activity, systemic inflammatory markers, lipids, glucose, specific insulin, and C-peptide were included in the clinical work-up. The updated-computer homeostasis model assessment was used to mark insulin resistance (HOMA2-IR) and beta-cell function (HOMA2-%B).
Nearly three-quarters of patients with RA (74.4%) had increased insulin resistance, defined by a logHOMA2-IR value greater than 1, as compared with 54.2% of controls (P =.025). Values of logHOMA2-IR were also higher among patients with RA vs controls (1.4 vs 1.2; P =.008). Impaired beta-cell function was also noted in those with RA vs controls (HOMA2-%B: 148 vs 141; P =.186).
All insulin resistance factors, including age, BMI, waist circumference, blood pressure, and triglycerides were associated with logHOMA2-IR in univariate analysis, but multivariate analysis identified RA, in addition to BMI and triglycerides, as an independent risk factor for insulin resistance (beta = 0.065; 95% CI, 0.019-0.112; P =.006).
Insulin resistance appeared to be more frequent in patients with a modified disease activity score 28 joints without acute-phase reactants (mDAS28-SE) of >5.1 compared with those who had lower scores (84.0% vs 63.6%; P =.021). These patients also had higher incidence rates of insulin resistance (P =.003) than those with lower disease activity, but results did not demonstrate a significant difference in beta-cell function between the 2 groups (P =.446).
“[Patients with RA]had higher log HOMA2-IR than controls, which was followed with impaired beta-cell function. More significant difference was demonstrated in patients with high disease activity compared to controls. RA itself was an independent risk factor for increased insulin resistance,” the researchers concluded.
Disclosures: The researchers report no relevant financial disclosures.
- Ristic G, Subota V, Stanisavljevic D, Glisic B, Petronijevic M, Stefanovic D. Rheumatoid arthritis is an independent risk factor for increased insulin resistance and impaired beta-cell function: Impact of disease activity [abstract]. Arthritis Rheumatol. 2016; 68 (suppl 10). http://acrabstracts.org/abstract/rheumatoid-arthritis-is-an-independent-risk-factor-for-increased-insulin-resistance-and-impaired-beta-cell-function-impact-of-disease-activity. Accessed November 8, 2016.
This article originally appeared on Rheumatology Advisor