Share This Article:

Effect of Anti-TNF Therapy on Resistance to Insulin in Patients with Rheumatoid Arthritis

Abstract Full-Text HTML Download Download as PDF (Size:147KB) PP. 167-171
DOI: 10.4236/ojra.2013.33026    3,099 Downloads   4,815 Views   Citations

ABSTRACT

Objective: To evaluate the effect of anti-TNF therapy on resistance to insulin in patients with rheumatoid arthritis (RA) compared with patients with RA being treated with non-biological DMARDs. Methods: Inactive patients diagnosed with RA (ACR 1987 criteria) (DAS 28 < 2.6) were included, being treated with anti-tumor necrosis factor inhibitors (anti-TNF) (cases) and non-biological disease-modifying anti-rheumatic drugs (DMARD) (controls), without risk factors for insulin resistance (administration of steroids, body mass index > 25 kg/m2, diabetes mellitus or use of glucose lowering agents, systemic arterial hypertension or use of anti-hypertensive drugs, triglycerides > 150 mg/dl, hypercholesterolemia > 200 mg/dl, high-density lipoproteins < 40 mg/dl in men and < 50 mg/in women, or with lipids lowering agents, waist measurement > 88 cm in women and > 102 cm in men). We used HOMA (Homeostasis Model Assessment) to determine insulin resistance in both groups, HOMA being defined as >1 and sensitivity to insulin using QUICKI (Insulin Sensitivity Check Index), ≥0.38 being considered as normal. The Mann Whitney U was used for the statistical analysis. Results: A total of 28 patients, 15 being treated with non-biological DMARDs and 13 with anti-TNF therapy, were evaluated; 89.7%, of which were women. Average age: 43.5 (range 21 - 62); the average HOMA index of the non-biological DMARD group was 1.58 (range 0.7 - 5.4), compared with patients treated with anti-TNF therapy, 1.18 (range 0.2 - 4.3) (P = 0.5). The average QUICKI index was 0.36 (range 0.30 - 0.42) in patients treated with non-biological DMARD, compared with0.37 inpatients treated with anti-TNF therapy (range 0.30 - 0.51) (P = 0.8). Conclusion: Resistance to insulin manifested itself in both groups, although there was a greater trend of less insulin resistance and greater sensitivity in the anti-TNF group; this was probably not statistically significant due to the sample size.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

M. Pérez, R. Ariza, R. Asencio, A. Camargo, H. Garcia, M. Vazquez and L. Barile-Fabris, "Effect of Anti-TNF Therapy on Resistance to Insulin in Patients with Rheumatoid Arthritis," Open Journal of Rheumatology and Autoimmune Diseases, Vol. 3 No. 3, 2013, pp. 167-171. doi: 10.4236/ojra.2013.33026.

References

[1] J. Zwerina, K. Redlich, G. Schett and J. S. Smolen, “Pathogenesis of Rheumatoid Arthritis: Targeting Cytokines,” Annals of the New York Academy of Sciences, Vol. 1051, 2005, pp. 716-729. doi:10.1196/annals.1361.116
[2] S. Van Doornum, G. McColl and I. P. Wicks, “Accelerated Atherosclerosis: An Extraarticular Feature of Rheumatoid Arthritis?” Arthritis & Rheumatism, Vol. 46, No. 4, 2002, pp. 862-873. doi:10.1002/art.10089
[3] M. Boers, B. Dijkmans, S. Gabriel, H. Maradit-Kremers, J. O’Dell and T. Pincus, “Making an Impact on Mortality in Rheumatoid Arthritis: Targeting Cardiovascular Comorbidity,” Arthritis & Rheumatism, Vol. 50, No. 6, 2004, pp. 1734-1739. doi:10.1002/art.20306
[4] G. Paolisso, G. Valentini, D. Guigliamo, G. Mavrazzo, R. Tirri, M. Gallo, et al., “Evidence for Peripheral Impaired Glucose Handling in Patients with Connective Tissue Diseases,” Metabolism, Vol. 40, 1991, pp. 902-907. doi:10.1016/0026-0495(91)90064-4
[5] K. L. G. Svenson, T. Pollare, H. Lithell and R. Hallgren, “Impaired Glucose Handling in Active Rheumatoid Arthritis: Relationship to Peripheral Insulin Resistance,” Metabolism, Vol. 37, 1998, pp. 125-130. doi:10.1016/S0026-0495(98)90005-1
[6] G. La Montagna, F. Cacciapuoti, R. Buono, D. Manzella, G. Mennillo, A. Arciello, G. Valentini and G. Paolisso, “Insulin Resistance Is and Independent Risk Factor for Atherosclerosis in Rheumatoid Arthritis,” Diabetes and Vascular Disease Research, Vol. 4, No. 2, 2007, pp. 130-135. doi:10.3132/dvdr.2007.031
[7] J. P. Despres, B. Lamarche and P. Mauriege, “Hyperinsulinemia as an Independent Risk Factor for Ischemic Heart Disease,” New England Journal of Medicine, Vol. 334, No. 15, 1996, pp. 952-957. doi:10.1056/NEJM199604113341504
[8] P. Libby, G. Sukhova, R. T. Lee and Z. S. Galis, “Cytokines Regulate Vascular Functions Related to Stability of the Atherosclerotic Plaque,” Journal of Cardiovascular Pharmacology, Vol. 25, Suppl 2, 1995, pp. S9-S12. doi:10.1097/00005344-199500252-00003
[9] C. Book, T. Saxne and L. T. Jacobsson, “Prediction of Mortality in Rheumatoid Arthritis Based on Disease Activity Markers,” Journal of Rheumatology, Vol. 32, No. 3, 2005, pp. 430-434.
[10] S. Wallberg-Jonsson, H. Johansson, M. L. Ohman and S. Rantapaa-Dahlqvist, “Extent of Inflammation Predicts Cardiovascular Disease and Overall Mortality in Seropositive Rheumatoid Arthritis. A Retrospective Cohort Study from Disease Onset,” Journal of Rheumatology, Vol. 26, No. 12, 1999, pp. 2562-2571.
[11] G. S. Hotamisligil and B. M. Spiegelman, “Tumor Necrosis Factor Alpha: A Key Component of the Obesity-Diabetes Link,” Diabetes, Vol. 43, No. 11, 1994, pp. 1271-1278. doi:10.2337/diabetes.43.11.1271
[12] G. S. Hotamisligil, P. Arner, J. F. Caro, R. L. Atkinson and B. M. Spiegelman, “Increased Adipose Tissue Expression of Tumor Necrosis Factor-Alpha in Human Obesity and Insulin Resistance,” Journal of Clinical Investigation, Vol. 95, No. 5, 1995, pp. 2409-2415. doi:10.1172/JCI117936
[13] M. Saghizadeh, J. M. Ong, W. T. Garvey, R. R. Henry and P. A. Kern, “The Expression of TNF Alpha by Human Muscle. Relationship to Insulin Resistance,” Journal of Clinical Investigation, Vol. 97, No. 4, 1996, pp. 1111-1116. doi:10.1172/JCI118504
[14] G. S. Hotamisligil, N. S. Shargill and B. M. Spiegelman, “Adipose Expression of Tumor Necrosis Factor Alpha: Direct Role in Obesity-Linked Insulin Resistance,” Science, Vol. 259, No. 5091, 1993, pp. 87-91. doi:10.1126/science.7678183
[15] T. Saxne, M. A. Palladino Jr., D. Heinegard, N. Talal and F. A. Wollheim, “Detection of Tumor Necrosis Factor Alpha But Not Tumor Necrosis Factor Beta in Rheumatoid Arthritis Synovial Fluid and Serum,” Arthritis & Rheumatism, Vol. 31, 1988, pp. 1041-1045. doi:10.1002/art.1780310816
[16] D. N. Kiortsis, A. K. Mavridis, S. Vasakos, S. N. Nikas and A. A. Drosos, “Effects of Infliximab Treatment on Insulin Resistance in Patients with Rheumatoid Arthritis and Ankylosing Spondylitis,” Annals of the Rheumatic Diseases, Vol. 64, No. 5, 2005, pp. 765-766. doi:10.1136/ard.2004.026534
[17] M. A. Gonzalez-Gay, J. M. De Matias, C. Gonzalez-Juanatey, C. Garcia-Porrua, A. Sanchez-Andrade, J. Martin and J. Llorca, “Anti-Tumor Necrosis Factor-Alpha Blockade Improves Insulin Resistance in Patients with Rheumatoid Arthritis,” Clinical and Experimental Rheumatology, Vol. 24, No. 1, 2006, pp. 83-86.
[18] F. C. Arnett, S. M. Edworthy, D. A. Bloch, D. J. Mc-Shane, J. F. Fries, N. S. Cooper, L. A. Healey, S. R. Kaplan, M. H. Liang, H. S. Luthra, et al., “The American Rheumatism Association 1987 Revised Criteria for the Classification of Rheumatoid Arthritis,” Arthritis & Rheumatism, Vol. 31, No. 3, 1988, pp. 315-324. doi:10.1002/art.1780310302
[19] A. Rosenvinge, R. Krogh-Madsen, B. Baslund and B. K. Pedersen, “Insulin Resistance in Patient with Rheumatoid Arthritis: Effect of Anti-TNFalpha Therapy,” Scandinavian Journal of Rheumatology, Vol. 36, No. 2, 2007, pp. 91-96. doi:10.1080/03009740601179605
[20] F. M. Oguz, A. Oguz and M. Uzunlulu, “The Effect of Infliximab Treatment on Insulin Resistance in Patients with Rheumatoid Arthritis,” Acta Clinica Belgica, Vol. 62, No. 4, 2007, pp. 218-222.
[21] L. S. Tam, B. Tomlinson, T. T. Chu, T. K. Li and E. K. Li, “Impact of TNF Inhibition on Insulin Resistance and Lipids Levels in Patients with Rheumatoid Arthritis,” Clinical Rheumatology, Vol. 26, No. 9, 2007, pp. 1495-1498. doi:10.1007/s10067-007-0539-8

  
comments powered by Disqus

Copyright © 2019 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.