Epithelial Neutrophil-Activating Peptide 78/C-X-C Motif Chemokine 5 in the Insulin Resistance of Patients with Rheumatoid Arthritis

Hiurma Sanchez-Perez¹, Beatriz-Segura Tejera², De Vera-González AM³, Alejandra González Delgado⁴, Jose M Olmos⁵, José Luis Hernandez⁶, Begoña Ubilla⁷, Raquel Lopez-Mejías⁸, Miguel Angel González-Gay⁹ and Ivan Ferraz-Amaro¹⁰, ¹Rheumatology, Rheumatology Division, Hospital Universitario de Canarias, La Laguna. Tenerife, Spain, ²Rheumatology section, Hospital Germans Trias i Pujol, Badalona, Spain, ³Central Laboratory Division, University Hospital of Canary Islands, Tenerife, Spain, ⁴Central Laboratory Division. Hospital Universitario de Canarias, Tenerife, Spain., Tenerife, Spain, ⁵Division of Internal Medicine. Hospital Universitario Marqués de Valdecilla, IDIVAL.Universidad de Cantabria. RETICEF, Santander, Spain, ⁶Internal Medicine, Hospital Universitario Marqués de Valdecilla. IDIVAL, Santander, Spain, ⁷Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, IDIVAL, Santander, Spain, ⁸Epidemiology, Genetics and Atherosclerosis Research Group on Systemic Inflammatory Diseases, Hospital Universitario Marqués de Valdecilla, IDIVAL, Santander, Spain, ⁹Rheumatology, Hospital Universitario Marqués de Valdecilla. IDIVAL. Santander. Universidad de Cantabria. Spain, Johannesburg, South Africa, ¹⁰Rheumatology, Hospital Universitario de Canarias, La Laguna, Tenerife, Spain

Meeting: ACR/ARHP Annual Meeting 2017

Date of first publication: September 18, 2017

Keywords: chemokines, insulin resistance and rheumatoid arthritis (RA)

Session Information

Date: Monday, November 6, 2017

Title: Rheumatoid Arthritis – Clinical Aspects Poster II: Pathophysiology, Autoantibodies, and Disease Activity Measures

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: It is known that the chemokine molecule CXCL5 (C-X-C motif chemokine 5 or epithelial neutrophil activating peptide 78 -ENA78-) is a link between obesity, inflammation, and insulin resistance (IR) in general population. Similarly, chronic inflammation has been found to deteriorate IR and impair pancreatic beta cell function in rheumatoid arthritis (RA) patients. The aim of this study was to explore the role of CXCL5 in the IR of RA patients.

Methods: Cross-sectional study that encompassed 141 non-diabetic patients with RA. IR by homeostatic model assessment (HOMA2), insulin and C-peptide serum levels and lipid profile, and CXCL5 serum levels were assessed in patients. A multivariable regression analysis, adjusted for IR related factors, was performed to evaluate how CXCL5 is related to IR, disease activity and disease characteristics in RA patients.

Results: Insulin and C peptide serum levels did strongly correlated between them (r2=0,913, p<0.001) but not with CXCL5 (insulin r2=-0.034, p= 0.69; C peptide r2=-0.050, p=0.56). Interestingly, while glucocorticoids were related with insulin (beta coef. 2.56 [95%CI 0.31-5.42], p=0.080), C-peptide serum levels (beta coef. 1.69 [95%CI 1.09-2.28], p=0.000), and HOMA2-IR (beta coef. 0.34 [95%CI -0.02-0.70], p=0.06) and HOMA2-%B-C peptide (beta coef. 51 [95%CI 31-70], p=0.000), the use of prednisone was not associated with CXCL5 serum levels (beta coef. -6 [95%CI -74-63], p=0.87). C reactive protein (beta coef. 0.2 [95%CI -1.4-1.9], p=0.80) and disease activity through DAS28 (beta coef. 13 [95%CI -14-41], p=0.34) also disclosed no relation with CXCL5. Other disease characteristics like disease duration, presence of rheumatoid factor or anti-citrullinated protein antibodies, or use of methotrexate or anti-TNF alpha therapies were not related with CXCL5 serum levels. Additionally, CXCL5 did neither explained HOMA2-IR (beta coef. -0.00 [95%CI -0.00-0.00], p=0.21) nor beta cell production, using HOMA2-%B-C peptide (beta coef. -0.05 [95%CI -0.12-0.02], p=0.17), through multivariable regression analysis.

Conclusion: CXCL5 is not related to RA disease characteristics or IR in RA patients. This could imply that the mechanisms that lead to IR of RA patients are different from those from general population.

Disclosure: H. Sanchez-Perez, None; B. S. Tejera, None; D. V. G. AM, None; A. González Delgado, None; J. M. Olmos, None; J. L. Hernandez, None; B. Ubilla, None; R. Lopez-Mejías, None; M. A. González-Gay, None; I. Ferraz-Amaro, None.

To cite this abstract in AMA style:

Sanchez-Perez H, Tejera BS, AM DVG, González Delgado A, Olmos JM, Hernandez JL, Ubilla B, Lopez-Mejías R, González-Gay MA, Ferraz-Amaro I. Epithelial Neutrophil-Activating Peptide 78/C-X-C Motif Chemokine 5 in the Insulin Resistance of Patients with Rheumatoid Arthritis [abstract]. Arthritis Rheumatol. 2017; 69 (suppl 10). https://acrabstracts.org/abstract/epithelial-neutrophil-activating-peptide-78c-x-c-motif-chemokine-5-in-the-insulin-resistance-of-patients-with-rheumatoid-arthritis/. Accessed .

ACR Meeting Abstracts - https://acrabstracts.org/abstract/epithelial-neutrophil-activating-peptide-78c-x-c-motif-chemokine-5-in-the-insulin-resistance-of-patients-with-rheumatoid-arthritis/