title: A proinflammatory state is detectable in obese children and is accompanied by functional and morphological vascular changes.
abstract: BACKGROUND
  Obesity is generally accepted as a risk factor for premature atherosclerosis. Subclinical inflammation as quantified by blood levels of C-reactive protein (CRP) contributes to the development and progression of atherosclerosis. We hypothesized that inflammation in obese children is related to functional and early morphological vascular changes.
  
  
  RESULTS
  Blood levels of high sensitivity (hs) CRP, hsIL-6, the soluble intercellular adhesion molecule1 (ICAM-1), vascular cell adhesion molecule (VCAM)-1, and E-selectin were measured in 145 severely obese (body mass index [BMI], 32.2+/-5.8 kg/m2) and 54 lean (BMI, 18.9+/-3.2 kg/m2) children 12+/-4 years old. Flow-mediated dilation (FMD) of the brachial artery and carotid intima-media thickness (IMT) measured by high-resolution ultrasound as markers of early vascular changes were assessed in 92 (77 obese and 15 lean) and 59 (50 obese and 9 lean) children, respectively. Obese children had significantly higher levels of hsCRP, hsIL-6, and E-selectin than healthy controls (4.1+/-4.8 versus 0.9+/-1.5 mg/L, P<0.001 for hsCRP; 1.99+/-1.30 versus 1.42+/-1.01 pg/mL, P=0.05 for hsIL-6; and 78+/-38 versus 59+/-29 ng/mL, P=0.01 for E-selectin). There were no differences in the levels of ICAM-1 and VCAM-1 between groups. Obese children had lower peak FMD response (7.70+/-6.14 versus 11.06+/-3.07%, P=0.006) and increased IMT (0.37+/-0.04 versus 0.34+/-0.03 mm, P=0.03) compared with controls. Morbidly obese children (n=14, BMI 44.1+/-3.9 kg/m2) had highest levels of hsCRP (8.7+/-0.7 mg/L), hsIL-6 (3.32+/-1.1 pg/mL), and E-selectin (83+/-40 ng/mL).
  
  
  CONCLUSIONS
  A proinflammatory state is detectable in obese children, which is accompanied by impaired vascular endothelial function and early structural changes of arteries, even in young subjects at risk. It remains to be determined whether high hsCRP in obese children predicts cardiovascular events.
authors.affiliation: Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, Austria.
authors.forename: Stylianos
authors.initials: S
authors.lastname: Kapiotis
authors.forename: Gregor
authors.initials: G
authors.lastname: Holzer
authors.forename: Georg
authors.initials: G
authors.lastname: Schaller
authors.forename: Markus
authors.initials: M
authors.lastname: Haumer
authors.forename: Harald
authors.initials: H
authors.lastname: Widhalm
authors.forename: Daniel
authors.initials: D
authors.lastname: Weghuber
authors.forename: Bernd
authors.initials: B
authors.lastname: Jilma
authors.forename: Georg
authors.initials: G
authors.lastname: Röggla
authors.forename: Michael
authors.initials: M
authors.lastname: Wolzt
authors.forename: Kurt
authors.initials: K
authors.lastname: Widhalm
authors.forename: Oswald F
authors.initials: OF
authors.lastname: Wagner
mesh_terms: D000293:Adolescent; D015415:Biomarkers / Q000097:blood; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000000981:diagnostic imaging; D002648:Child; D003430:Cross-Sectional Studies; D019040:E-Selectin / Q000097:blood; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D009767:Obesity, Morbid / Q000097:blood; D012039:Regional Blood Flow; D017539:Tunica Intima / Q000000981:diagnostic imaging; D017540:Tunica Media / Q000000981:diagnostic imaging; D014463:Ultrasonography; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D019040:E-Selectin; D015850:Interleukin-6; D002097:C-Reactive Protein