title: Inflammatory and prothrombotic states in obese children of European descent.
abstract: Adipose tissue may release mediators that induce a chronic inflammatory state and alterations in coagulation, which contribute to insulin resistance, atherosclerosis, and thrombosis. We investigated whether inflammatory and/or prothrombotic states exist in obese children and assessed their interrelationship. Sixty-one subjects were recruited, aged between 6 and 16 years, to participate in a cross-sectional study at Children's University Hospital of Geneva. Selected pro/anti-inflammatory cytokines/chemokines and hemostasis parameters were measured in obese children and lean controls. Cardiovascular risk factors in the family were indexed. Fasting glucose level, insulin, prothrombin time (PT), fibrinogen, activated partial thromboplastin time (aPTT), D-dimer, endogenous thrombin potential (ETP), C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon-γ-inducible-protein (IP-10), monocyte chemoattractant protein 1 (MCP-1), and interleukin-1 receptor antagonist (IL-1Ra) were measured. We estimated insulin resistance by homeostatic model assessment (HOMA). Anti- (IL-1Ra) and proinflammatory cytokines (MCP-1, IL-6) were significantly increased in obese children in comparison to the control group, even before puberty. Hemostasis was also altered in obese children with a significantly increased fibrinogen level, increased D-dimer, a shortened PT, as well as an increased ETP. No correlation was found between cytokine levels and hemostasis parameters, except for IL-6 and fibrinogen. Obese children present with inflammatory and prothrombotic states as early as 6 years of age and these states are similar in prepubertal and pubertal obese children. The cytokines IL-1Ra and MCP-1 were most significantly increased in obese children. Further investigation is necessary to determine if these cytokines, together with ETP, can reliably predict the development of diabetes and atherosclerosis.
authors.affiliation: Pediatric Endocrine and Diabetes Unit, Children's Hospital, University Hospitals and Faculty of Medicine, Geneva, Switzerland.
authors.forename: Sophie
authors.initials: S
authors.lastname: Stoppa-Vaucher
authors.forename: Mirjam A
authors.initials: MA
authors.lastname: Dirlewanger
authors.forename: Christoph A
authors.initials: CA
authors.lastname: Meier
authors.forename: Philippe
authors.initials: P
authors.lastname: de Moerloose
authors.forename: Guido
authors.initials: G
authors.lastname: Reber
authors.forename: Pascale
authors.initials: P
authors.lastname: Roux-Lombard
authors.forename: Christoph
authors.initials: C
authors.lastname: Combescure
authors.forename: Sonja
authors.initials: S
authors.lastname: Saudan
authors.forename: Valerie M
authors.initials: VM
authors.lastname: Schwitzgebel
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000293:Adolescent; D050197:Atherosclerosis / Q000097:blood / Q000209:etiology; D001778:Blood Coagulation Disorders / Q000097:blood / Q000209:etiology*; D002648:Child; D003430:Cross-Sectional Studies; D016207:Cytokines / Q000097:blood*; D005060:Europe; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005340:Fibrinogen / Q000378:metabolism; D006487:Hemostasis; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D018836:Inflammation Mediators / Q000378:metabolism*; D007333:Insulin Resistance; D015848:Interleukin-5 / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications*; D011517:Prothrombin Time; D013557:Switzerland; D013917:Thrombin / Q000378:metabolism*; D013927:Thrombosis / Q000097:blood / Q000209:etiology; D044465:White People
chemical_list: D016207:Cytokines; D005338:Fibrin Fibrinogen Degradation Products; D018836:Inflammation Mediators; D015848:Interleukin-5; C036309:fibrin fragment D; D005340:Fibrinogen; D013917:Thrombin