The effect of anti-TNF treatment on body composition and insulin resistance in patients with rheumatoid arthritis

Springer Science and Business Media LLC - Tập 41 - Trang 319-328 - 2020
I. A. M. van den Oever1, M. Baniaamam2,3, S. Simsek4, H. G. Raterman5, J. C. van Denderen2, I. C. van Eijk5, M. J. L. Peters6, I. E. van der Horst-Bruinsma1,7, Y. M. Smulders6, M. T. Nurmohamed1,2
1Department of Rheumatology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, the Netherlands
2Department of Rheumatology, Amsterdam Rheumatology and Immunology Center, Reade, Amsterdam, The Netherlands
3Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, Amsterdam, The Netherlands
4Department of Internal Medicine, Northwest Clinics, Alkmaar, The Netherlands
5Department of Rheumatology, Northwest Clinics, Alkmaar, The Netherlands
6Department of Internal Medicine, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands
7Amsterdam Rheumatology and Immunology Center, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands

Tóm tắt

Given the link between systemic inflammation, body composition and insulin resistance (IR), anti-inflammatory therapy may improve IR and body composition in inflammatory joint diseases. This study assesses the IR and beta cell function in rheumatoid arthritis (RA) patients with active disease compared to osteoarthritis (OA) patients and investigates the effect of anti-TNF treatment on IR, beta cell function and body composition in RA. 28 Consecutive RA patients starting anti-TNF treatment (adalimumab), and 28 age, and sex-matched patients with OA were followed for 6 months. Exclusion criteria were use of statins, corticosteroids, and cardiovascular or endocrine co-morbidity. Pancreatic beta cell function and IR, using the homeostasis model assessment (HOMA2), and body composition, using dual-energy X-ray absorptiometry (DXA) were measured at baseline and 6 months. At baseline, IR [1.5 (1.1–1.8) vs. 0.7 (0.6–0.9), 100/%S] and beta cell function (133% vs. 102%) were significantly (p < 0.05) higher in RA patients with active disease as compared to OA patients. After 6 months of anti-TNF treatment, IR [1.5 (1.1–1.8) to 1.4 (1.1–1.7), p = 0.17] slightly improved and beta cell function [133% (115–151) to 118% (109–130), p <0.05] significantly improved. Improvement in IR and beta cell function was most pronounced in RA patients with highest decrease in CRP and ESR. Our observations indicate that IR and increased beta cell function are more common in RA patients with active disease. Anti-TNF reduced IR and beta cell function especially in RA patients with highest decrease in systemic inflammation and this effect was not explained by changes in body composition.

Tài liệu tham khảo

Khovidhunkit W, Kim MS, Memon RA, Shigenaga JK, Moser AH, Feingold KR et al (2004) Effects of infection and inflammation on lipid and lipoprotein metabolism: mechanisms and consequences to the host. J Lipid Res 45:1169–1196 Tilg H, Moschen AR (2008) Inflammatory mechanisms in the regulation of insulin resistance. Mol Med 14:222–231 Wang Z, Nakayama T (2010) Inflammation, a link between obesity and cardiovascular disease. Mediators Inflamm. Article ID 535918. Liefmann R (1949) Endocrine imbalance in rheumatoid arthritis and rheumatoid spondylitis; hyperglycemia unresponsiveness, insulin resistance, increased gluconeogenesis and mesenchymal tissue degeneration; preliminary report. Acta Med Scand 136:226–232 Svenson KL, Lundqvist G, Wide L, Hallgren R (1987) Impaired glucose handling in active rheumatoid arthritis: effects of corticosteroids and antirheumatic treatment. Metabolism 36:944–948 Svenson KL, Lundqvist G, Wide L, Hallgren R (1987) Impaired glucose handling in active rheumatoid arthritis: relationship to the secretion of insulin and counter-regulatory hormones. Metabolism 36:940–943 Svenson KL, Pollare T, Lithell H, Hallgren R (1988) Impaired glucose handling in active rheumatoid arthritis: relationship to peripheral insulin resistance. Metabolism 37:125–130 Ferraz-Amaro I, Garcia-Dopico JA, Medina-Vega L, Gonzalez-Gay MA, Diaz-Gonzalez F (2013) Impaired beta cell function is present in nondiabetic rheumatoid arthritis patients. Arthritis Res Ther 15:R17 Tejera-Segura B, Lopez-Mejias R, de Vera-Gonzalez AM, Jimenez-Sosa A, Olmos JM, Hernandez JL et al (2019) Relationship between insulin sensitivity and beta-cell secretion in nondiabetic subjects with rheumatoid arthritis. J Rheumatol 46:229–236 Roubenoff R, Roubenoff RA, Ward LM, Holland SM, Hellmann DB (1992) Rheumatoid cachexia: depletion of lean body mass in rheumatoid arthritis. Possible association with tumor necrosis factor. J Rheumatol 19:1505–1510 Hotamisligil GS, Shargill NS, Spiegelman BM (1993) Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance. Science 259:87–91 Borst SE (2004) The role of tnf-alpha in insulin resistance. Endocrine 23:177–182 Krogh-Madsen R, Plomgaard P, Moller K, Mittendorfer B, Pedersen BK (2006) Influence of tnf-alpha and il-6 infusions on insulin sensitivity and expression of il-18 in humans. Am J Physiol Endocrinol Metab 291:E108–E114 Burska AN, Sakthiswary R, Sattar N (2015) Effects of tumour necrosis factor antagonists on insulin sensitivity/resistance in rheumatoid arthritis: a systematic review and meta-analysis. PLoS One 10:e0128889 Arnett FC, Edworthy SM, Bloch DA, McShane DJ, Fries JF, Cooper NS et al (1988) The american rheumatism association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31:315–324 Furst DE, Keystone EC, Kirkham B, Kavanaugh A, Fleischmann R, Mease P et al (2008) Updated consensus statement on biological agents for the treatment of rheumatic diseases. Ann Rheum Dis 67(3):2–25 Altman R, Alarcon G, Appelrouth D, Bloch D, Borenstein D, Brandt K et al (1990) The American college of rheumatology criteria for the classification and reporting of osteoarthritis of the hand. Arthritis Rheum 33:1601–1610 Prevoo ML, van’t Hof MA, Kuper HH, van Leeuwen MA, van de Putte LB, van Riel PL (1995) Modified disease activity scores that include twenty-eight-joint counts. Development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum 38:44–48 Fries JF, Spitz P, Kraines RG, Holman HR (1980) Measurement of patient outcome in arthritis. Arthritis Rheum 23:137–145 Levy JC, Matthews DR, Hermans MP (1998) Correct homeostasis model assessment (homa) evaluation uses the computer program. Diabetes Care 21:2191–2192 Otten J, Ahren B, Olsson T (2014) Surrogate measures of insulin sensitivity vs the hyperinsulinaemic-euglycaemic clamp: a meta-analysis. Diabetologia 57:1781–1788 Kim B, Choi HY, Kim W, Ahn C, Lee J, Kim JG et al (2018) The cut-off values of surrogate measures for insulin resistance in the korean population according to the korean genome and epidemiology study (koges). PLoS One 13:e0206994 Tang Q, Li X, Song P, Xu L (2015) Optimal cut-off values for the homeostasis model assessment of insulin resistance (homa-ir) and pre-diabetes screening: developments in research and prospects for the future. Drug Discov Ther 9:380–385 Wallace TM, Levy JC, Matthews DR (2004) Use and abuse of homa modeling. Diabetes Care 27:1487–1495 Kaul S, Rothney MP, Peters DM, Wacker WK, Davis CE, Shapiro MD et al (2012) Dual-energy X-ray absorptiometry for quantification of visceral fat. Obesity (Silver Spring) 20:1313–1318 Dessein PH, Joffe BI, Stanwix A, Botha AS, Moomal Z (2002) The acute phase response does not fully predict the presence of insulin resistance and dyslipidemia in inflammatory arthritis. J Rheumatol 29:462–466 WHO (2006) Definition and diagnosis of diabetes mellitus and intermediate hyperglycemia: report of a WHO/IDF consultation. WHO, Geneva Expert Panel on Detection E (2001) Treatment of high blood cholesterol in A. Executive summary of the third report of the national cholesterol education program (ncep) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel iii). JAMA 285:2486–2497 Masuko K (2014) Rheumatoid cachexia revisited: a metabolic co-morbidity in rheumatoid arthritis. Front Nutr 1:20 Straub RH (2014) Insulin resistance, selfish brain, and selfish immune system: an evolutionarily positively selected program used in chronic inflammatory diseases. Arthritis Res Ther 16(2):S4 Chen DY, Chen YM, Hsieh TY, Hsieh CW, Lin CC, Lan JL (2015) Significant effects of biologic therapy on lipid profiles and insulin resistance in patients with rheumatoid arthritis. Arthritis Res Ther 17:52 Peluso I, Palmery M (2016) The relationship between body weight and inflammation: lesson from anti-tnf-alpha antibody therapy. Hum Immunol 77:47–53 Bissell LA, Hensor EM, Kozera L, Mackie SL, Burska AN, Nam JL et al (2016) Improvement in insulin resistance is greater when infliximab is added to methotrexate during intensive treatment of early rheumatoid arthritis-results from the idea study. Rheumatology (Oxford) 55:2181–2190 Ursini F, Russo E, Ruscitti P, Giacomelli R, De Sarro G (2018) The effect of non-tnf-targeted biologics and small molecules on insulin resistance in inflammatory arthritis. Autoimmun Rev 17:399–404 Fernandes GS, Valdes AM (2015) Cardiovascular disease and osteoarthritis: common pathways and patient outcomes. Eur J Clin Invest 45:405–414