Session Information
Date: Monday, November 14, 2016
Title: Rheumatoid Arthritis – Clinical Aspects II: Risk and Impact of Comorbidity
Session Type: ACR Concurrent Abstract Session
Session Time: 2:30PM-4:00PM
Background/Purpose: Increased insulin resistance and impaired β-cell function have been demonstrated in pts with rheumatoid arthritis (RA). The aim of our study was to investigate these metabolic disturbances in RA pts compared to controls and analyze its association with disease activity.
Methods: The study population included 127 non-diabetic subjects: 90 RA pts (mean age 52.4±9.9 yrs, disease duration 9 yrs, range 4-13) and 37 matched controls (mean age 49.0±7.5 yrs). All pts were on disease modifying anti-rheumatic drugs (methotrexate 93.3%, steroids 65.6% (5 mg/day, range 5-10, none on steroids >10 mg/day), biologic therapy 27.8%). Clinical work-up included determination of the body mass index (BMI), waist circumference (WC), blood pressure (BP), disease activity (mDAS28-SE), inflammation markers, lipids, glucose, specific insulin, and C peptide. The updated-computer Homeostasis Model Assessment was used to calculate insulin resistance (HOMA2-IR) and β-cell function (HOMA2-%B). HOMA2-IR>1 was defined as increased insulin resistance. Lack of compensatory rise of HOMA2-%B implied impaired β-cell function.
Results: Increased insulin resistance (logHOMA2-IR>1) was detected in 74.4% of RA pts and in 54.2% controls, p=0.025. RA pts also had higher values of logHOMA2-IR than controls 1.4 (range 1.0-2.3) vs. 1.2 (range 0.8-1.4); p=0.008; followed with impaired β cell function: HOMA2-%B 148 (116-190) vs.141 (114-158) p=0.186. Univariate regression revealed association of logHOMA2-IR with all insulin resistance risk factors: age, BMI, WC, BP, and triglycerides, while multivariate analysis demonstrated that beside BMI and triglycerides, RA itself was an independent risk factors for logHOMA2-IR (β 0.065, 95% CI 0.019-0.112, p=0.006). Increased insulin resistance was more frequent in pts with DAS28-SE≥5.1 than DAS28-SE<5.1 (84.0% vs. 63.6%, p=0.021). Importantly, these groups were comparable regarding all insulin resistance risk factors and anti-inflammatory treatment including glycocorticoids. Pts with high disease activity also had higher levels of logHOMA2-IR (1.7 (1.2-2.5) vs. 1.3 (0.9-1.9) (p=0.003) while HOMA2-%B was not different 150 (118-195) vs.133 (115-184) p=0.446. In comparison with controls, both RA groups were not different regarding insulin resistance risk factors (Table 1). Parameters of glucose metabolism were comparable between controls and pts with DAS28-SE<5.1. Significant difference of logHOMA2-IR and logHOMA2-IR>1 was found between controls and pts with DAS-SE≥5.1. This was not followed with increase of HOMA2-%B.
Conclusion: RA pts had higher logHOMA2-IR than controls which was followed with impaired β cell function. More significant difference was demonstrated in pts with high disease activity compared to controls. RA itself was an independent risk factor for increased insulin resistance
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Table 1. Parameters of Insulin Resistance in RA pts with Different Levels of Disease Activity and Controls |
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| Laboratory |
RA pts with DAS28≥5.1 (N=46) |
RA pts with DAS28<5.1 (N=44) |
Controls (N=37) |
Controls vs. RA pts with DAS-SE≥5.1 |
Controls vs. RA pts with DAS-SE<5.1 |
| Age (years) |
52.8±10.7 |
52.2±9.2 |
49.0±7.5 |
ns |
ns |
| BMI (kg/m2) |
25.6±4.7 |
25.7±3.8 |
26.2±4.3 |
ns |
ns |
| Hypertension (%) |
12/46 (26.1) |
16/44 (36.4) |
8/37 (21.6) |
ns |
ns |
| Triglycerides (mmol/L) |
1.2 (0.8-1.6) |
1.2 (0.8-1.5) |
1.0 (0.8-1.4) |
ns |
ns |
| Blood glucose (mmol/L) |
5.0±0.6 |
4.7±0.6 |
4.7±0.8 |
ns |
ns |
| Insulin (pmol/L) |
79 (58-120) |
57 (39-91) |
55.3 (36-69) |
0.000 |
ns |
| C-peptide (pmol/L) |
960 (680-1130) |
700 (465-860) |
600 (450-880) |
0.005 |
ns |
| logHOMA2-IR |
1.7 (1.2-2.5) |
1.3 (0.9-1.9) |
1.2 (0.8-1.4) |
0.000 |
ns |
| HOMA2-IR>1 (%) |
39/46 (84.8) |
28/44 (63.6) |
20/37 (54.16) |
0.002 |
ns |
| HOMA2-%B |
150 (118-195) |
143 (115-184) |
141 (114-158) |
ns |
ns |
To cite this abstract in AMA style:
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). https://acrabstracts.org/abstract/rheumatoid-arthritis-is-an-independent-risk-factor-for-increased-insulin-resistance-and-impaired-beta-cell-function-impact-of-disease-activity/. Accessed .« Back to 2016 ACR/ARHP Annual Meeting
ACR Meeting Abstracts - https://acrabstracts.org/abstract/rheumatoid-arthritis-is-an-independent-risk-factor-for-increased-insulin-resistance-and-impaired-beta-cell-function-impact-of-disease-activity/