Impact of obesity on functional and laboratory parameters in patients with rheumatoid arthritis
Tóm tắt
Overweight patients with rheumatoid arthritis (RA) have more disease activity, lower rates of remission, and twice as likely to require a tumor necrosis factor inhibitor. Provided that the prevalence of obesity is increasing, this may significantly affect RA incidence. An association between obesity and RA is logic, as biologic mechanisms of inflammation are present in fatty tissue, and it may be a trigger to chronic systemic inflammation. Human obesity is characterized by increased plasma leptin levels, which if elevated in morbidly obese patients may enhance constitutive immunological stimuli and increased levels of inflammatory marker. The aim of this study was to assess the impact of obesity and serum leptin level on disease activity and functional outcome in RA patients. This study was carried out at Minia University Hospital, Egypt. Patients were recruited from Rheumatology Outpatient Clinic from October 2012 to June 2013. It included 36 RA patients, fulfilling the 2010 ACR/EULAR classification criteria. They were divided into two groups: obese patients with a BMI of 25 or greater and nonobese patients (BMI ≤ 25). A total of 12 healthy individuals were included as controls. All patients were subjected to history taking and clinical examination; patient’s functional status and disease activity were assessed using the Health Assessment Questionnaire (HAQ) disability index and DAS-28, respectively. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and rheumatoid factor (RF) were determined. Serum level of leptin was measured using enzyme-linked immunosorbent assay. Data were analyzed using SPSS for Windows, version 16.0. RA obese patients showed a higher duration of morning stiffness (P = 0.02), HAQ index (P = 0.001), DAS-28 (P = 0.0001), visual analogue scale (VAS) of pain (P = 0.0001), and articular index (P = 0.001) compared with nonobese ones. They showed higher ESR (P = 0.003), serum leptin (P = 0.008), CRP (P = 0.0001), and RF (P = 0.002). There was a positive correlation between BMI and each of ESR (P = 0.003), CRP (P = 0.0001), and RF (P = 0.01). There was a positive correlation between waist circumference and each of ESR (P = 0.03), serum leptin (P = 0.03), CRP (P = 0.0001), and RF (P = 0.04). There was a positive correlation between BMI and HAQ index (P = 0.0001), DAS-28 (P = 0.001), articular index (P = 0.003), and VAS of pain (P = 0.0001). There was a positive correlation between waist circumference and HAQ index (P = 0.001), DAS-28 (P = 0.03), and VAS of pain (P = 0.0001). Moreover, there was a positive correlation between VAS of pain and serum leptin (P = 0.04). Serum leptin was correlated with CRP (P= 0.01). Linear regression analysis showed that the VAS was the first and most significant risk factor (β = 0.73; P = 0.01) and that HAQ was the second (β = –0.53; P = 0.04) to affect serum leptin levels. Obese RA patients had higher disease activity parameters, clinical scores and laboratory indices, and worse functional outcomes compared with nonobese patients. Higher serum leptin levels were associated with higher disease activity scores.
Tài liệu tham khảo
Haslam D, James W. Obesity. Lancet 2005; 366:1197–1209.
Kushner RF. Treatment of the obese patient (Contemporary endocrinology). ISBN1-59745-400-1. Totowa, NJ: Humana Press; 2009.
Crowson CS, Matteson EL, Davis JM, Gabriel SE. Contribution of obesity to the rise in incidence of rheumatoid arthritis. Arthritis Care Res (Hoboken) 2013; 65:71–77.
Matteson E. The role of fat cells in inflammatory process in rheumatoid arthritis; in the Mayo Clinic (2012).
Myasoedova E, Crowson CS, Kremers HM, Therneau TM, Gabriel SE. Is the incidence of rheumatoid arthritis rising? Results from Olmsted County, Minnesota, 1955–2007. Arthritis Rheum 2010; 62:1576–1582.
Flegal KM, Carroll MD, Ogden CL, Curtin LR. Prevalence and trends in obesity among US adults, 1999–2008. JAMA 2010; 303:235–241.
Samad F, Uysal KT, Wiesbrock SM, Pandey M, Hotamisligil GS, Loskutoff DJ. Tumor necrosis factor is a key component in the obesitylinked elevation of plasminogen activator inhibitor-1. Proc Natl Acad Sci USA 1999; 96:6902–6907.
Schols AM, Creutzberg EC, Buurman WA, Campfield LA, Saris WH, Wouters EF. Plasma leptin is related to proinflammatory status and dietary intake in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1999; 160:1220–1226.
Fraser DA, Thoen J, Reseland JE, Førre O, Kjeldsen-Kragh J. Decreased CD4+ lymphocyte activation and increased interleukin-4 production in peripheral blood of rheumatoid arthritis patients after acute starvation. Clin Rheumatol 1999; 18:394–401.
Emery P, Foster W, Suarez-Almazor M. Rheumatoid arthritis. Clin Evid. 2002; 7:1101-21
Funovits J, Aletaha D, Bykerk V, Combe B, Dougados M, Emery P. The American College of Rheumatology/European League Against Rheumatism classification criteria for rheumatoid arthritis: methodological report phase 1. Ann Rheum Dis 2010; 69:1589–1595.
Bruce B, Fries J. The Stanford health assessment questionnaire (HAQ): a review of its history, issues, progress, and documentation. J Rheumatol 2003; 30:167–178.
Fransen J, van Riel P. The Disease Activity Score and the EULAR response criteria. Clin Exp Rheumatol 2005; 23:S93–S99.
Westergren A. Diagnostic tests: the erythrocyte sedimentation rate range and limitations of the technique. Triangle 1957; 3:20–25.
Shaffer J, Goldin M. In: I Davidsohn and J.B. Henry (editors) Todd-Sanford clinical diagnosis by laboratory methods. 15th ed. W.B. Saunders Co., Philadelphia, PA.; 1974.
Cheng C, Persellin R. Interference by Clq in slide latex tests for rheumatoid factor. Ann Intern Med 1971; 75:683–686. 7
Artiss J, Zak B. Measurement of cholesterol concentration. In Rifai N, Warnick GR, Dominiczak MH, (editors) Handbook of lipoprotein testing. Washington: AACC Press 1997; 99–114.
Fransson EI, Batty GD, Tabak AG, Brunner EJ, Kumari M, Shipley MJ, et al. Association between change in body composition and change in inflammatory markers: an 11-year follow-up in the Whitehall II Study. J Clin Endocrinol Metab 2010; 95:5370–5374.
Derdemezis CS, Voulgari PV, Drosos AA, Kiortsis DN. Obesity, adipose tissue and rheumatoid arthritis: coincidence or more complex relationship?. Clin Exp Rheumatol 2011; 29:712–727.
Stavropoulos-Kalinoglou A, Metsios GS, Panoulas VF, Nevill AM, Jamurtas AZ, Koutedakis Y et al. Underweight and obese states both associate with worse disease activity and physical function in patients with established rheumatoid arthritis. Clin Rheumatol 2009; 28: 439–444.
Solus J, Sokka T, Oeser A. Adipocytokines are associated with radiographic joint damage in rheumatoid arthritis. Arthritis Rheum 2009; 60:1906–1914.
Park YJ, Cho CS, Emery P, Kim WU. LDL cholesterolemia as a novel risk factor for radiographic progression of rheumatoid arthritis: a single-center prospective study. PLoS One. 2013; 8:e68975.
Allam A, Radwan A. The relationship of serum leptin levels with disease activity in Egyptian patients with rheumatoid arthritis. Egypt Rheumatol 2012; 34:185–190.
Park YW, Zhu S, Palaniappan L, Heshka S, Carnethon MR, Heymsfield SB. The metabolic syndrome: Prevalence and associated risk factors: Findings in the US population from The Third National Health and Nutrition Examination Survey, 1988–1994. Arch Intern Med 2003; 163:42-36.
Trayhurn P, Wood IS. Signaling role of adipose tissue: adipokines and inflammation in obesity. Biochem Soc Trans 2005; 33:1078–1081.
Targońska-Stepniak B, Dryglewska M, Majdan M. Adiponectin and leptin serum concentrations in patients with rheumatoid arthritis. Rheumatol Int 2010; 30:731–737.
Popa C, Netea MG, Radstake TR. Markers of inflammation are negatively correlated with serum leptin in rheumatoid arthritis. Ann Rheum Dis 2005; 64:1195–1198.