Background/Purpose:  Insulin resistance (IR) may contribute to an increase in cardiovascular risk. The aim of this study was to examine the association between IR and disease activity, disease phenotypes, drug exposure and subclinical atherosclerosis in patients with SLE.

Methods:  Cross-sectional study that encompassed 332 non-diabetes individuals; 102 SLE patients and 220 age/sex-matched controls. IR by homeostatic model assessment (HOMA2), insulin, C-peptide serum levels and lipid profile were assessed in both groups. Activity (SLEDAI), severity (Katz) and damage (SLICC) scores, carotid intima-media thickness (cIMT) and carotid plaques were assessed in SLE patients. A multivariable regression analysis, adjusted for IR related factors, was performed to evaluate the differences between groups in IR indexes and, in SLE patients, the interrelation between IR and disease activity/characteristics.

Results:  Median disease duration was 16 (IQR 9-28) years. Body mass index and abdominal circumference did not differ between groups. HOMA-IR-C-peptide (mean difference [IQR], 1.26 [0.77-1.74], p=0.00) and HOMA-%B-C-peptide (56 [4-71], p=0.00) were increased in SLE patients compared to controls. Similarly, insulin sensitivity through HOMA-S% was inferior in SLE patients (-44 [-28-61], p=0.00). Forty percent of patients were in no activity SLEDAI score, while 32, 21 and 9% were in mild, moderate and high/very high activity respectively. Patients in the SLEDAI high or very high activity category disclosed a higher HOMA-IR level (4.8 ± 4.8 vs. 2.07 ± 1.40, p= 0.00) when compared to those in the no activity category. SLICC index was also clearly associated with IR indexes; higher index values were related with higher HOMA-IR (beta coef. 0.27 [0.08-0.46], p=0.01) and lower HOMA-S% (beta coef. -6 [-10–3], p=0.00) levels. These associations remained significant after adjustment for age, gender, smoking, hypertension, and dyslipidemia. Katz severity index did not revealed relation with IR indexes. Use of prednisone was positively associated with HOMA-IR both when it was considered binary (beta coef 1.75 [1.37-2.12], p=0.00) and continuous (beta coef 0.15 [0.07-0.23] per mg, p=0.00). Hydroxychloroquine/other DMARDs use was not related with IR indexes. Patients with higher anti-DNA titers and those with lower complement serum levels did not reach higher IR levels. 28% of the SLE patients had carotid plaques. The presence of carotid plaque was associated with higher HOMA-IR-C-peptide (3.75 ± 3.62 vs. 1.86-1.19, p=0.00). This difference remained significant after adjustment for demographics or cardiometabolic risk factors (1.50 [0.34-2.66], p=0.01).

Conclusion: IR is present in a significant proportion of SLE patients. Disease activity and damage are SLE-related factors that lead to IR development IR is independently associated with subclinical artheriosclerosis in SLE patients.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/association-between-insulin-resistance-subclinical-artheriosclerosis-and-activitydamage-status-in-systemic-lupus-erythematosus-patients/