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Thèse de Doctorat
DOI
10.11606/T.5.2011.tde-17062011-163644
Document
Auteur
Nom complet
Carlos Ewerton Maia Rodrigues
Adresse Mail
Unité de l'USP
Domain de Connaissance
Date de Soutenance
Editeur
São Paulo, 2011
Directeur
Jury
Carvalho, Jozélio Freire de (Président)
Appenzeller, Simone
Pereira, Rosa Maria Rodrigues
Silva, Clovis Artur Almeida da
Souza, Alexandre Wagner Silva de
Titre en portugais
Adipocitocinas na síndrome antifosfolípide primária: potenciais marcadores de inflamação, resistência insulínica e síndrome metabólica
Mots-clés en portugais
Adipocitocinas
Inflamação
Resistência à insulina
Síndrome antifosfolipídica
Síndrome X metabólica
Resumé en portugais
INTRODUÇÃO: Síndrome antifosfolípide está associada com aterosclerose acelerada. Embora adipocitocinas exerçam um papel fundamental na interface entre obesidade, inflamação, resistência insulínica e aterosclerose, a exata natureza e relativa contribuição das adipocitocinas, como potenciais marcadores, requer investigação na síndrome antifosfolípide primária (SAFP). OBJETIVO: Este estudo foi desenvolvido para avaliar a possível associação das adipocitocinas com síndrome metabólica (SM), inflamação e outros fatores de risco cardiovascular na SAFP. MÉTODOS: 56 pacientes com SAFP e 72 controles saudáveis pareados por sexo e idade foram incluídos. Adiponectina, leptina, visfatina, resistina, inibidor do ativador de plasminogênio-1 (PAI-1), lipoproteina (a), glicemia, insulina, VHS, PCR, ácido úrico e perfil lipídico foram dosados. SM foi definida de acordo com os critérios da Federação Internacional de Diabetes (IDF) e resistência insulínica foi estabelecida pelo índice de homeostasis model assessment (HOMA). RESULTADOS: Leptina [21,5 (12,9- 45,7) vs 12,1 (6,9-26,8) ng/mL, P=0.001] foi maior em SAFP do que em controles. Adiponectina (P=0,10), resistina (P=0,23), visfatina (P=0,68) and PAI-1 (P=0,77) não diferiu entre os grupos. Em SAFP, leptina e PAI-1 foram positivamente correlacionada com IMC (r=0,61 and 0,29), HOMA-IR (r=O,71 and 0,28) and CRP (r=0,32 and 0,36). Adiponectina foi negativamente correlacionada com IMC (r=-0,28), triglicérides (r=-0,43), HOMA-IR (r=-0,36) e positivamente correlacionada com HDL (r=0,37), aCL IgG (r=0,41), anti- 2GPI IgG (r=0,31) e anti- 2GPI IgM (r=0,38). A análise de pacientes com e sem SM revelou uma associação positiva com leptina (P=0,002) e PAI-1 (P=0,03) e uma associação negativa com adiponectina (P=0,042). No modelo de regressão linear múltipla, observamos que as variáveis que independentemente influenciam a adiponectina foram triglicérides (P<0,001), VLDL-c (P=0,002) e anti-2GPI IgG (P=0,042), leptina foram IMC (P<0,001), glicemia (P=0,046), HOMA-IR (P<0,001) e VHS (P=0,006) e PAI-1 foram PCR (P=0,013) e SM (P=0,048). CONCLUSÕES: O presente estudo demonstra que as adipocitocinas podem estar envolvidas com inflamação, resistência insulínica e SM em pacientes com SAFP
Titre en anglais
Adipocytokines in primary antiphospholipid syndrome: potential markers of inflammation, insulin resistance and metabolic syndrome
Mots-clés en anglais
Adipocytokines
Antiphospholipid syndrome
Inflammation
Insulin resistance
Metabolic X syndrome
Resumé en anglais
INTRODUCTION: Antiphospholipid syndrome is associated with accelerated atherosclerosis. Although adipocytokines play a key role in the interface between obesity, inflammation, insulin resistance and atherosclerosis, the exact nature and relative contribution of adipocytokines as potential markers warrant further investigation in primary antiphospholipid syndrome (PAPS). OBJECTIVE: This study was undertaken to evaluate a possible association of adipocytokines with metabolic syndrome (MetS), inflammation and other cardiovascular risk factors in PAPS. METHODS: Fifty-six PAPS patients and 72 age- and gender-matched healthy controls were included. Sera samples were tested for adiponectin, leptin, visfatin, resistin, plasminogen activator inhibitor-1 (PAI-1), lipoprotein (a), glucose, insulin, ESR, CRP, uric acid and lipid profiles. MetS was defined according to the guidelines of the International Diabetes Federation (IDF) and insulin resistance was established using the homeostasis model assessment (HOMA) index. RESULTS: Concentrations of leptin [21.5 (12.1-45.7) vs 12.1 (6.9-26.8) ng/mL, P=0.001] were higher in PAPS than in controls. Concentrations of adiponectin (P=0.10), resistin (P=0.23), visfatin (P=0.68) and PAI-1 (P=0.77) did not differ between patients and controls. In PAPS, leptin and PAI-1 levels were positively correlated with BMI (r=0.61 and 0.29), HOMA-IR (r=0.71 and 0.28) and CRP (r=0.32 and 0.36). Adiponectin was negatively correlated with BMI (r=-0.28), triglycerides (r=-0.43) and HOMA-IR index (r=-0.36) and positively correlated with HDL (r=0.37), aCL IgG (r=0.41), anti- 2GPI IgG (r=0.31) and anti- 2GPI IgM (r=0.38). Further analysis of patients with and without MetS revealed a positive association of the syndrome with leptin (P=0.002) and PAI-1 (P=0.03) and a negative association with adiponectin (P=0.042). In the multiple linear regression model, we observed that the variables that independently influence the adiponectin were triglycerides (P<0.001), VLDL-C (P=0.002) and anti-2GPI IgG (P=0.042), leptin were BMI (P<0.001), glucose (P=0.046), HOMA-IR (P <0.001) and ESR (P=0.006) and PAI-1 were CRP (P=0.013) and MetS (P=0.048). CONCLUSION: The findings of the present study provide evidence that adipocytokines may be involved in inflammation, insulin resistance and metabolic syndrome of PAPS patients
 
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Date de Publication
2011-06-21
 
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