Welcome to Open Science
Contact Us
Home Books Journals Submission Open Science Join Us News
Remission of Uncontrolled Type 2 Diabetes Mellitus in a Patient Treated with Tumor Necrosis Factor-Inhibitor: A Case Report
Current Issue
Volume 2, 2015
Issue 1 (February)
Pages: 10-13   |   Vol. 2, No. 1, February 2015   |   Follow on         
Paper in PDF Downloads: 9   Since Aug. 28, 2015 Views: 1943   Since Aug. 28, 2015
Authors
[1]
Srikanta Banerjee, Health Sciences Department, University of Roehampton, London, United Kingdom.
[2]
Raxit Patel, Department of Internal Medicine, Christus Spohn Hospital, Alice, TX, United States.
Abstract
Biological agents that have recently been an important treatment of choice for ankylosing spondylitis due to the reduction of inflammation of the axial skeleton and joints through tumor necrosis factor blockade, have multiple therapeutic and adverse side effects. Out of all the side effects reported, one of the underexplored potential therapeutic side effects is remission of diabetes. We report a case of a diabetic Caucasian woman who developed continued glycemic control after treatment with a tumor necrosis factor-alpha inhibitor, etanercept. Additionally, we present a graphical account of fluctuations of glycosylated Hemoglobin (HbA1c) and C-reactive protein associated with etanercept treatment, and we provide a detailed discussion of the implications of this therapeutic side effect. Health care professionals need to be aware of the potentially therapeutic side effect of tumor necrosis factor-alpha inhibitors and should exercise caution when using it in conjunction with exogenous insulin and or oral hypoglycemic drugs. Randomized double blind controlled studies need to assess the efficacy of biologic agents as a potential treatment against type 2 diabetes especially in those individuals with inflammatory arthritis.
Keywords
Ankylosing Spondylitis, Etanercept, Tumor Necrosis Factor-Alpha Inhibitor, Diabetes, Rheumatic Diseases, Inflammatory
Reference
[1]
Keystone E, Breedveld F, Kavanaugh A, et al. Longterm Effect of Delaying Combination Therapy with Tumor Necrosis Factor Inhibitor in Patients with Aggressive Early Rheumatoid Arthritis: 10-year Efficacy and Safety of Adalimumab from the Randomized Controlled PREMIER Trial with Open-label Extension. Journal of Rheumatology. 2014; 41(1):5-14.
[2]
Beisswenger P, Brown W, Tan M, et al. Meal-induced increases in C-reactive protein, interleukin-6 and tumour necrosis factor α are attenuated by prandial + basal insulin in patients with Type 2 diabetes. Diabetic Medicine: A Journal of the British Diabetic Association. 2011; 28(9):1088-1095.
[3]
Fénix-Caballero S, Alegre-del Rey E, Castaño-Lara R, Puigventós-Latorre F, Borrero-Rubio J, López-Vallejo J. Direct and indirect comparison of the efficacy and safety of adalimumab, etanercept, infliximab and golimumab in psoriatic arthritis. Journal of Clinical Pharmacy & Therapeutics. 2013; 38(4):286-293.
[4]
Wiedmann M, Mössner J, Baerwald C, Pierer M. TNF alpha inhibition as treatment modality for certain rheumatologic and gastrointestinal diseases. Endocrine, Metabolic & Immune Disorders Drug Targets [serial online]. September 2009; 9(3): 295-314.
[5]
Scott L. Etanercept: A Review of Its Use in Autoimmune Inflammatory Diseases. Drugs. 2014; 74(12):1379-1410.
[6]
Mease P, Goffe B, Metz J, VanderStoep A, Finck B, Burge D. Etanercept in the treatment of psoriatic arthritis and psoriasis: a randomised trial. Lancet. 2000; 356(9227):385-390.
[7]
Deepak P, Sifuentes H, Sherid M, Stobaugh D, Sadozai Y, Ehrenpreis E. T-cell non-Hodgkin's lymphomas reported to the FDA AERS with tumor necrosis factor-alpha (TNF-α) inhibitors: results of the REFURBISH study. The American Journal of Gastroenterology. January 2013; 108(1):99-105.
[8]
Yoo I, Choung R, Jeen Y, et al. Incidences of serious infections and tuberculosis among patients receiving anti-tumor necrosis factor-α therapy. Yonsei Medical Journal [serial online]. March 2014; 55(2): 442-448.
[9]
Goren I, Muller E, Pfeilschifter J, Frank S: Severely impaired insulin signaling in chronic wounds of diabetic ob/ob mice: a potential role of tumor necrosis factor-alpha. American Journal of Pathology. 2006, 168:765-777.
[10]
Dogrul A, Gul H, Yesilyurt O, Ulas U, Yildiz O. Systemic and spinal administration of etanercept, a tumor necrosis factor alpha inhibitor, blocks tactile allodynia in diabetic mice. Acta Diabetologica. 2011; 48(2):135-142.
[11]
Czajkowska J, Shutty B, Zito S. Development of low blood glucose readings in nine non-diabetic patients treated with tumor necrosis factor-alpha inhibitors: a case series. Journal of Medical Case Reports. 2012; 6: 5.
[12]
Mastrandrea L, Yu J, Behrens T, Buchlis J, Albini C, Fourtner S, Quattrin T: Etanercept treatment in children with new-onset type 1 diabetes: pilot randomized, placebo-controlled, double-blind study. Diabetes Care. 2009; 32:1244-1249.
[13]
Yazdani-Biuki B, Stelzl H, Brezinschek HP, Hermann J, Mueller T, Krippl P, Graninger W, Wascher TC: Improvement of insulin sensitivity in insulin resistant subjects during prolonged treatment with the anti-TNF alpha antibody infliximab. European Journal of Clinical Investigation. 2004, 34:641-642.
[14]
Bonilla E, Lee YY, Phillips PE, Perl A: Hypoglycemia after initiation of treatment with etanercept in a patient with type 2 diabetes mellitus. Annals of Rheumatic Diseases. 2001; 66:1688.
[15]
Hotamisligil GS, Peraldi P, Budavari A, Ellis R, White MF, Spiegelman BM. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance. Science. 1996; 271: 665–668.
[16]
Emanuelli B, Peraldi P, Filloux C, Chavey C, Freidinger K, Hilton DJ, Hotamisligil GS, Van Obberghen E. SOCS-3 inhibits insulin signaling and is up-regulated in response to tumor necrosis factor-alpha in the adipose tissue of obese mice. J Biol Chem. 2001; 276: 47944–47949.
[17]
Hussey S, McGee S, Garnham A, McConell G, Hargreaves M. Exercise increases skeletal muscle GLUT4 gene expression in patients with type 2 diabetes. Diabetes, Obesity & Metabolism [serial online]. August 2012; 14(8):768-771.
[18]
Roher N, Samokhvalov V, Díaz M, MacKenzie S, Klip A, Planas J. The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. Endocrinology [serial online]. April 2008; 149(4):1880-1889.
[19]
Ladefoged M, Buschard K, Hansen A. Increased expression of toll-like receptor 4 and inflammatory cytokines, interleukin-6 in particular, in islets from a mouse model of obesity and type 2 diabetes. APMIS: Acta Pathologica, Microbiologica, Et Immunologica Scandinavica [serial online]. June 2013; 121(6):531-538.
[20]
Dixon WG, Watson KD, Lunt M, Hyrich KL, Silman AJ, Symmons DP, British Society for Rheumatology Biologics Register Control Centre Consortium. British Society for Rheumatology Biologics Register Reduction in the incidence of myocardial infarction in patients with rheumatoid arthritis who respond to anti-tumor necrosis factor alpha therapy: results from the British Society for Rheumatology Biologics Register. Arthritis Rheum. 2007 Sep;56(9):2905–12.
[21]
Popa C, Netea MG, Radstake T, et al. Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patients with active rheumatoid arthritis. Annals of Rheumatologic Diseases. 2005 Feb; 64(2):303–5.
[22]
Irace C, Mancuso G, Fiaschi E, Madia A, Sesti G, Gnasso A. Effect of anti TNF-alpha therapy on arterial diameter and wall shear stress and HDL cholesterol. Atherosclerosis. 2004 Nov; 177(1):113–8.
[23]
Angel K, Provan SA, Gulseth HL, Mowinckel P, Kvien TK, Atar D. Tumor necrosis factor-alpha antagonists improve aortic stiffness in patients with inflammatory arthropathies: a controlled study. Hypertension. 2010 Feb;55(2):333–8.
[24]
Greenberg JD, Kremer JM, Curtis JR, et al. CORRONA Investigators Tumour necrosis factor antagonist use and associated risk reduction of cardiovascular events among patients with rheumatoid arthritis. Ann Rheum Dis. 2011 Apr; 70(4):576–82.
[25]
Ryan C, Leonardi CL, Krueger JG, et al. Association between biologic therapies for chronic plaque psoriasis and cardiovascular events: a meta-analysis of randomized controlled trials. JAMA. 2011 Aug 24; 306(8):864–71.
[26]
Tzellos T, Kyrgidis A, Zouboulis CC. Re-evaluation of the risk for major adverse cardiovascular events in patients treated with anti-IL-12/23 biological agents for chronic plaque psoriasis: a meta-analysis of randomized controlled trials. Journal of European Academy of Dermatology Venereology. 2013 May; 27(5):622–7.
Open Science Scholarly Journals
Open Science is a peer-reviewed platform, the journals of which cover a wide range of academic disciplines and serve the world's research and scholarly communities. Upon acceptance, Open Science Journals will be immediately and permanently free for everyone to read and download.
CONTACT US
Office Address:
228 Park Ave., S#45956, New York, NY 10003
Phone: +(001)(347)535 0661
E-mail:
LET'S GET IN TOUCH
Name
E-mail
Subject
Message
SEND MASSAGE
Copyright © 2013-, Open Science Publishers - All Rights Reserved