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Abstract Number: 2933

Metabolic Syndrome, Adipocytokines and Inflammation in Sjögren’s Syndrome

Kristopherson Lustosa Augusto1, Eloisa Bonfá2, Rosa M. R. Pereira1, Cleonice Bueno3, Vilma S. T. Viana4 and Sandra G. Pasoto5, 1Rheumatology Division, Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil, 2Rheumatology Division, University of Sao Paulo, Sao Paulo, Brazil, 3Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil, 4Rheumatology, Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil, 5Rheumatology, Faculdade de Medicina da Universidade de São Paulo, Sao Paulo, Brazil

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Adipocytokines, Inflammation, interleukins (IL) and metabolic syndrome, Sjogren's syndrome

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Session Information

Title: Sjogren's Syndrome I: Clinical Perspectives

Session Type: Abstract Submissions (ACR)

Background/Purpose

Systemic inflammation has been linked to increased frequency of metabolic syndrome (MetS) in autoimmune diseases. However, there are no studies concerning the frequency of this complication and adipocytokine sera profile in Primary Sjögren’s syndrome (SS).

The aim of this study was to evaluate the frequency of MetS and serum levels of inflammatory cytokines, B-cell activating factor (BAFF) and adipocytokines in SS patients

Methods

Seventy-one female SS patients (American-European Consensus Group Criteria), aged 18-65 years and 71 healthy women matched for age and race were enrolled in this case-control study. Clinical data were collected by a standardized questionnaire and physical examination at inclusion. Serum levels of glucose, total cholesterol, low density lipoprotein (LDL), high density lipoprotein (HDL), triglycerides, interleukin-1 beta (IL-1b), IL-6, BAFF, insulin, leptin, adiponectin, visfatin, resistin, ghrelin and plasminogen activator inhibitor-1 (PAI-1) were determined for all patients and controls. MetS (International Diabetes Federation) and disease activity [(EULAR Sjögren’s Syndrome Disease Activity Index (ESSDAI)] were also determined.

Results Patients and controls were comparable regarding mean age (47.6 ± 10.3 vs. 47.2 ± 10.3 years, p=0.833), ethnicity (white: 77.5 vs. 77.5 %, p=1.000), body mass index (BMI) (27.6 ± 6.4 vs. 26.7 ± 3.6 kg/m2, p=0.783), smoking (p=0.538), sedentary lifestyle (p=0.847) and menopause (p=0.502). In contrast, MetS (39.4 vs. 16.9%, p=0.005), hypertension (32.4 vs. 11.3%, p=0.004) and dyslipidemia (22.5 vs. 4.2%, p=0.002) were more frequent in patients than controls in spite of similar abdominal and hip circumferences (p>0.05). No differences were observed regarding glucose (p=0.062), insulin (p=0.271) and HOMA-IR (p=0.662). Serum levels of IL-1b (p=0.008), IL-6 (p<0.0001), BAFF (p<0.0001), resistin (p<0.0001) and adiponectin (p=0.001) were higher in patients than in controls. Further analysis showed that SS patients with (n=28) and without (n=43) MetS were similar regarding age (p=0.111) and race (p=0,773). In contrast, the first group had higher BMI, abdominal circumference, cholesterol/LDL/VLDL, triglycerides, insulin and leptin levels, HOMA-IR score, and higher frequencies of hypertension and diabetes (p<0.05). ESSDAI (p=0.240), prednisone use (35.7 vs. 23.3%, p=0.289), current (3.0 ± 4.5 vs. 1.6 ± 3.2 mg/day, p=0.299) and cumulative dose (p=0.495) were similar in both groups. Otherwise, IL-1b levels were higher in SS patients with MetS than those without MetS (83.1 ± 187.6 vs. 8.4 ± 27.7 pg/mL, p=0.046). Multivariate analysis with adjustment for age, ethnicity, current and cumulative prednisone doses and usage time revealed that MetS group had higher values of hypertension (p=0.010), HOMA-IR (p=0.001), LDL (p=0.041), VLDL (p=0.001), triglycerides (p=0.001), glucose (p=0.045), insulin (p=0.006), leptin (p=0.008) and IL-1b (p=0.048).

Conclusion

This study identified a high frequency of MetS and an abnormal adipocytokine profile in SS patients. The interesting association of MetS with elevated IL-1b suggests that inflammation plays an important role in its pathogenesis in SS.


Disclosure:

K. L. Augusto,
None;

E. Bonfá,
None;

R. M. R. Pereira,
None;

C. Bueno,
None;

V. S. T. Viana,
None;

S. G. Pasoto,
None.

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