Figure 1. Differences in values of nephropathy markers in the patients with early RA, depending on TNF-α level. REFERENCES: [1] Kizaki K, Yamashita T, Hayashi et al. Infliximab is equivalently suppressin- goxidative stress compared to tocilizumab among well-controlled patients withrheumatoid arthritis. Int J Rheum Dis 2016. doi: 10.1111/1756- 185X.12972 [2] Isaacs JD, Zuckerman A, Krishnaswami S, et al. Changes in serum creati- nine inthe patients with active rheumatoid arthritis treated with tofacitinib: resultsfrom clinical trials. Arthritis Res Ther 2014;16(4):158. doi: 10.1186/ ar4673 Acknowledgements: No Acknowledgements. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2018-eular.1713 SAT0136 THE INFLUENCE OF HDL-CHOLESTEROL AND CRP ON INCREASED INSULIN RESISTANCE AND IMPAIRED BETA-CELL FUNCTION IN PATIENTS WITH RHEUMATOIDARTHRITIS G. G. Ristić 1 , V. Subota 2 , D. Stanisavljević 3 , B. Glišić 1 , M. Petronijević 1 , D. Stefanović 1 . 1 Department of Rheumatology and Clinical Immunology; 2 Institute of Medical Biochemistry, Military Medical Academy; 3 Institute of Medical Statistics, Faculty of Medicine, University of Belgrade, Belgrade, Serbia Background: Increased CRP in RApts is associated with lower levels HDL cho- lesterol. HDL cholesterol may enhance insulin secretion and stimulate glucose up take into skeletal muscle, adipose tissue, and liver. Objectives: To investigate we therlow HDL, alone or in combination with CRP, could explain increased insulin resistance (IR) and impaired β-cell function in RA pts in comparison to healthy controls. Methods: The study population included 127 nondiabetic subjects (90 RA pts and 37 matched controls). We determined body mass index, waist circumference (WC), and presence of metabolic syndrome (MetS). All pts were on disease modi- fyingantirheumatic drugs, 65.6% on steroids (none on steroids >10 mg/day), and27.8% on biologic therapy. Laboratory analyses included hsCRP, glucose, insulin, and C-peptide (as a marker of insulin secretion). Insulin resistance(IR) was calculated using the updated Homeostasis Model Assessment (HOMA2-IR), based on fasting plasma glucose and specific insulin concentrations. The output of the HOMA2 model was calibrated to give IR of 1 as normal. HOMA2-B indicates the potential of β-cells to compensate increased IR. Lack of compensatory rise of HOMA2-B implied impaired β-cell function. Results: IR was detected in 74.4% of RA pts and in 54.2% controls, p=0.025. RA pts had significantly higher concentration of specific insulin, C peptide, and HOMA2-IR than controls, while HOMA2-B was not statistically different. Both groups were comparable regarding all other factors known to affect glucose metabolism (age, WC, presence ofMetS). We found significant differences in inflammation markers between RA pts and controls: ESR 29.5 (14-44) vs. 16.0 (10.0-20.0); hsCRP 5.5 (2.8-15) vs. 3.0(1.8-3.9); p<0.000 for both, as well as in lip- ids, especially HDL concentration 1.5±0.4 vs 1.60±0.3, p=0.027 and a number of the pts with low HDL (37.8 vs 13.5%, p=0.007). Univariant regression analysis revealed significant positive effect of HDL on logHOMA2-B (β 0.099,95%CI 0.029-0.169, p=0.006) and negative, but not significant effect on HOMA2-IR. In the logistic regression, after adjustment for HDL concentration, significant differ- ences for HOMA2-IR and insulin became less important but still persisted (Table), while significance for C peptide became more prominent. When we added the influence of inflammation, this favourable effect ofHDL-cholesterol on C-peptide disappeared. Conclusions: RA pts had higher IR and impaired β-cell function in comparison to healthy controls. The augmentation of statistical significance for C peptide, as a marker of insulinsecretion, after adjustment for low HDL-cholesterol and signifi- cant effect of HDL on logHOMA2-B implicate its important role in disturbances of glucosemetabolism in RA. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2018-eular.7479 SAT0136 THE INFLUENCE OF HDL-CHOLESTEROL AND CRP ON INCREASED INSULIN RESISTANCE AND IMPAIRED BETA-CELL FUNCTION IN PATIENTS WITH RHEUMATOID ARTHRITIS G. G. Ristić 1 , V. Subota 2 , D. Stanisavljević 3 , B. Glišić 1 , M. Petronijević 1 , D. Stefanović 1 . 1 Department of Rheumatology and Clinical Immunology, 2 Institute of Medical Biochemistry, Military Medical Academy, 3 Institute of Medical Statistics, Faculty of Medicine, University of Belgrade, Belgrade, Serbia Background: Increased CRP in RA pts is associated with lower levels HDL cho- lesterol. HDL cholesterol may enhance insulin secretion and stimulate glucose uptake into skeletal muscle, adipose tissue, and liver. Objectives: To investigate whether low HDL, alone or in combination with CRP, could explain increased insulin resistance (IR) and impaired b-cell function in RA pts in comparison to healthy controls. Methods: The study population included 127 nondiabetic subjects (90 RA pts and 37 matched controls). We determined body mass index, waist circumference (WC), and presence of metabolic syndrome (MetS). All pts were on disease modi- fying antirheumatic drugs, 65.6% on steroids (none on steroids >10 mg/day), and 27.8% on biologic therapy. Laboratory analyses included hsCRP, glucose, insulin, and C-peptide (as a marker of insulin secretion). Insulin resistance (IR) was calcu- lated using the updated Homeostasis Model Assessment (HOMA2-IR), based on fasting plasma glucose and specific insulin concentrations. The output of the HOMA2 model was calibrated to give IR of 1 as normal. HOMA2-B indicates the potential of b-cells to compensate increased IR. Lack of compensatory rise of HOMA2-B implied impaired b-cell function. Results: IR was detected in 74.4% of RA pts and in 54.2% controls, p=0.025. RA pts had significantly higher concentration of specific insulin, C peptide, and HOMA2-IR than controls, while HOMA2-B was not statistically different. Both groups were comparable regarding all other factors known to affect glucose metabolism (age, WC, presence of MetS). We found significant differences in inflammation markers between RA pts and controls: ESR 29.5 (14–44) vs. 16.0 (10.0–20.0); hsCRP 5.5 (2.8–15) vs. 3.0 (1.8–3.9); p<0.000 for both, as well as in lipids, especially HDL concentration 1.5±0.4 vs 1.60±0.3, p=0.027 and a number of the pts with low HDL (37.8 vs 13.5%, p=0.007). Univariant regression analysis revealed significant positive effect of HDL on logHOMA2-B (b 0.099, 95%CI 0.029–0.169, p=0.006) and negative, but not significant effect on HOMA2-IR. In the logistic regression, after adjustment for HDL concentration, significant differ- ences for HOMA2-IR and insulin became less important but still persisted (Table), while significance for C peptide became more prominent. When we added the influence of inflammation, this favourable effect of HDL-cholesterol on C-peptide disappeared. Laboratory parameters RA pts (N=90) Controls (N=37) P Adjusted for HDL Adjusted for CRP Adjusted for HDL+CRP Glucose (mmol/l) 4.8±0.6 4.7±0.8 ns / Insulin (pmol/ L) 68.5 (50.2– 102.7) 55.3 (36.0– 69.1) 0.008 0.018 0.048 0.054 C peptide (pmol/L) 785 (520– 1010) 600 (450–880) 0.046 0.025 0.078 0.066 HOMA2-IR 1.4 (1.0– 2.3) 1.2 (0.8– 1.4) 0.008 0.019 0.046 0.053 HOMA2-B 148 (116– 190) 141 (114–158) 0.186 0.136 0.258 0.165 HOMA2-IS 70 (46– 100) 84 (71.0– 132) 0.010 0.017 0.074 0.089 Conclusions: RA pts had higher IR and impaired b-cell function in comparison to healthy controls. The augmentation of statistical significance for C peptide, as a marker of insulin secretion, after adjustment for low HDL-cholesterol and signifi- cant effect of HDL on logHOMA2-B implicate its important role in disturbances of glucose metabolism in RA. Disclosure of Interest: None declared DOI: 10.1136/annrheumdis-2018-eular.7479 930 Saturday, 16 June 2018 Scientific Abstracts on May 28, 2020 by guest. 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