Background/Purpose: To compare the profile of adult-onset diabetes in patients with rheumatoid arthritis (RA) or osteoarthritis (OA), two chronic diseases leading to disability differing by their joint and systemic inflammation levels, and identify the disease characteristics associated with insulin resistance and metabolic control.

Methods: Observational, multicenter, cross-sectional usual-care study, including 7 rheumatology centers. This study included over a 24-month period consecutive patients with type-2 diabetes (T2D) and RA, fulfilling the 2010 ACR / EULAR criteria, and diabetic patients with osteoarthritis (OA). The following data were collected: demographics, disease activity and severity indices, current treatment for RA and diabetes, history and complications of diabetes. A systematic blood test was performed, assessing inflammatory (CRP levels) and metabolic (fasting glycemia and insulin levels, HbA1c) parameters. The HOMA2%B (insulin secretion) and HOMA2%S (tissue insulin sensitivity) indices (HOMA calculator, © Diabetes Trials Unit, University of Oxford) were used to assess insulin resistance.

Results: We included 122 RA patients (74% women, mean age 64±11 years, mean disease duration 15±11 years, 75% with positive ACPA antibodies and 64% with erosive disease). 64% of RA patients were treated with oral corticosteroids < 10 mg/day, 65% received Methotrexate and 53% received targeted biological therapies. We recruited 54 diabetic controls (75% women) with OA (33 knee OA and 21 hip OA), who were significantly older (68.5±11.9 years, p=0.031) and had a significantly higher BMI (31.5±6.3 kg/m2 vs. 27.7±5.5 kg/m2, p< 0.001) than patients with RA.

OA and RA patients had severe T2D with suboptimal metabolic control (mean HbA1c: 7.3%±1.29% and 7.0% ± 1.19%, respectively) and a biological profile of insulin resistance.

Insulin resistance was significantly higher in RA than OA patients after stratification on age and body mass index (HOMA2-S: 69.4±31.6 vs. 98.4±69.2, p=0.002).

The DAS28 negatively correlated with HOMA2-S (r=-0.29, p=0.011) and patients with moderate or high disease activity, had significantly decreased HOMA2-S (Figure 1). In multivariate analysis, HOMA2-S was independently associated with DAS28 (OR: 3.93, 95% CI 1.02-15.06). T2D metabolic control was not related to disease activity and functional impairment, but HbA1c levels were independently associated with bone erosions (OR: 4.43, 95% CI 1.18-16.61). Treatment with low-dose corticosteroids was not associated with decreased insulin sensitivity or increased HbA1c levels. Treatment with TNF-α inhibitors was associated with increased insulin sensitivity compared to patients not receiving biologics (101.3±58.71 vs. 60.0±32.5, p=0.001).

Conclusion: OA and RA patients with adult-onset diabetes display a clinical profile of severe T2D with suboptimal metabolic control.  RA patients displayed a biological profile of insulin resistance associated with joint and systemic inflammatory inflammation. These findings may have therapeutic implications, with the potential targeting of insulin resistance through the treatment of joint and systemic inflammation.

Figure 1: Insulin sensitivity assessed by the HOMA2-S according to the disease activity score (DAS)-28 HOMA2-S was evaluated in these subgroups after excluding patients with Latent Autoimmune Diabetes in Adults and T2D patients treated with insulin. Statistical test: Kruskal-Wallis test with Dunn correction, *p < 0.05

« Back to ACR Convergence 2020

ACR Meeting Abstracts - https://acrabstracts.org/abstract/influence-of-inflammatory-and-non-inflammatory-rheumatic-disorders-on-the-clinical-and-biological-profile-of-adult-onset-diabetes/