title: Inflammatory activation in children with primary hypertension.
abstract: Low-grade inflammation plays a role in the pathogenesis of primary hypertension (PH) and target organ damage (TOD). We evaluated the profile of inflammatory mediators (CRP, RANTES, MIP-1beta, MIP-1alpha, MCP-1, IL-6, angiogenin, adiponectin) in 30 healthy children (12.7 +/- 3.3 years) and 44 patients with untreated PH (13.7 +/- 2.7 years; n.s). Patients had greater concentrations of CRP, MIP-1beta, and RANTES than controls (all p < 0.05). Children with metabolic syndrome (MS) had greater CRP than children without MS (p = 0.007) and CRP correlated with number of MS criteria, body mass index (BMI), visceral fat, deep subcutaneous fat assessed by magnetic resonance imaging, carotid intima-media thickness (cIMT), left ventricular mass index, and markers of oxidative stress. RANTES correlated with cholesterol, LDL cholesterol, ApoB, and ApoB/ApoA1. Angiogenin correlated with BMI, waist circumference, visceral fat, uric acid, and patients with cIMT>2SD had greater concentration of angiogenin than those with normal cIMT (p = 0.03). Adiponectin was lower in patients with cIMT>2SD than in those with normal cIMT (p = 0.02). No model explaining variability of TOD has been built. Elevated RANTES and MIP-1beta and normal IL-6 and TNF-alpha levels indicate a vascular inflammatory process. Lack of correlation between CRP and chemokines suggests that vascular inflammation in PH precedes the systemic inflammatory changes.
authors.affiliation: Department of Research, The Children's Memorial Health Institute, Warsaw, Poland. m.litwin@czd.pl
authors.forename: Mieczyslaw
authors.initials: M
authors.lastname: Litwin
authors.forename: Jacek
authors.initials: J
authors.lastname: Michałkiewicz
authors.forename: Anna
authors.initials: A
authors.lastname: Niemirska
authors.forename: Lidia
authors.initials: L
authors.lastname: Gackowska
authors.forename: Lidia
authors.initials: L
authors.lastname: Gockowska
authors.forename: Izabela
authors.initials: I
authors.lastname: Kubiszewska
authors.forename: Aldona
authors.initials: A
authors.lastname: Wierzbicka
authors.forename: Zbigniew T
authors.initials: ZT
authors.lastname: Wawer
authors.forename: Roman
authors.initials: R
authors.lastname: Janas
mesh_terms: D052242:Adiponectin / Q000097:blood; D000293:Adolescent; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D002318:Cardiovascular Diseases / Q000276:immunology; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000097:blood; D054405:Chemokine CCL3 / Q000097:blood; D054407:Chemokine CCL4 / Q000097:blood; D018946:Chemokine CCL5 / Q000097:blood; D002648:Child; D003430:Cross-Sectional Studies; D006801:Humans; D006973:Hypertension / Q000276:immunology*; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000097:blood*; D015850:Interleukin-6 / Q000097:blood; D024821:Metabolic Syndrome / Q000276:immunology; D009765:Obesity / Q000276:immunology; D011044:Poland; D012259:Ribonuclease, Pancreatic / Q000097:blood
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; C111835:CCL2 protein, human; C515429:CCL3 protein, human; C066507:CCL4 protein, human; C483024:CCL5 protein, human; D018932:Chemokine CCL2; D054405:Chemokine CCL3; D054407:Chemokine CCL4; D018946:Chemokine CCL5; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D002097:C-Reactive Protein; C046366:angiogenin; D012259:Ribonuclease, Pancreatic