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AB1226 Leptin, adiponectin, resistin, visfatin serum levels and idiopathic recurrent pericarditis: A preliminary report
  1. L. Cantarini1,
  2. A. Brucato2,
  3. G. Simonini3,
  4. M. Imazio4,
  5. R. Cimaz5,
  6. D. Cumetti6,
  7. M.R. Bacarelli1,
  8. A. Vitale7,
  9. M.G. Brizi1,
  10. M. Galeazzi1,
  11. A. Fioravanti1
  1. 1Interdepartmental Research Center of Systemic Autoimmune and Autoinflammatory Diseases, Rheumatology Unit, Policlinico Le Scotte, University of Siena, Siena
  2. 2Internal Medicine, Ospedali Riuniti di Bergamo, Bergamo
  3. 3Department of Paediatrics, Rheumatology Unit, Anna Meyer Children’s Hospital and University of Florence, Florence
  4. 4Cardiology Department, Ospedale Maria Vittoria, Turin
  5. 5Department of Pediatrics, Rheumatology Unit, Anna Meyer Children’s Hospital, University of Florence, Florence
  6. 6Internal Medicine, Ospedali Riuniti di Bergamo, Bergamo
  7. 7Interdepartmental Research Center of Systemic Autoimmune and Autoinflammatory Diseases, Rheumatology Unit, Policlinico Le Scotte, University of Siena, Siena, Italy

Abstract

Background Idiopathic acute recurrent pericarditis (IRAP) represents the most troublesome complication of acute pericarditis and is an autoimmune process (1). White adipose tissue produces more than 50 adipokines that participate in inflammation and autoimmunity (2,3).

Objectives Our aims were to evaluate serum leptin, resistin, visfatin and adiponectin in IRAP patients versus healthy controls and to correlate their levels to parameters of disease activity.

Methods Serum leptin, resistin, visfatin and adiponectinlevels were assayed by enzyme-linked immunosorbent assay in 14 IRAP patients during recurrences(group 1), in 23 IRAP patients during symptom-free intervals (group 2) and in 18 healthy controls (group 3). Assessment parameters included demographic characteristics of patients and controls, clinical characteristics of patients and markers of inflammation. Comparisons between groups as well as reciprocal comparisons were evaluated.

Results group 1 showed serum leptin (p<0.008), visfatin (p<0.002), and adiponectin (p<0.04) significantly higher than group 2 and control group, whereas resistin serum levels did not significantly differ (p=0.69). Among IRAP patients, serum leptin significantly correlated with serum amyloid A (SAA) levels (rs=0.43, r2=0.27, p<0.02). Other than this correlation, none of the considered adipokines significantly correlated with the other considered variables in univariate analysis

Conclusions leptin, adiponectin and visfatin are increased in IRAP patients versus healthy controls. Our data suggest that these adipokines might be involved in IRAP pathogenesis and that a possible increased cardiovascular risk in these patients, through an early onset atherosclerosis, should be kept in mind. SAA might be a link between IRAP and increased cardiovascular diseases.

  1. Caforio AL, Brucato A, Doria A, Brambilla G, Angelini A, Ghirardello A, et al. Anti-heart and anti-intercalated disk autoantibodies: evidence for autoimmunity in idiopathic recurrent acute pericarditis.Heart 2010; 96:779-784.

  2. Lago F, Dieguez C, Gόmez-Reino J, Gualillo O. Adipokines as emerging mediators of immune response and inflammation. Nat Clin Pract Rheumatol 2007; 3:716-24.

  3. Lago F, Gόmez R, Conde J, Scotece M, Gόmez-Reino JJ, Gualillo O. Cardiometabolic comorbidities and rheumatic diseases: focus on the role of fat mass and adipokines. Arthritis Care Res (Hoboken) 2011; 63:1083-90.

Disclosure of Interest None Declared

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