title: Evidence of metabolic syndrome in lean children with premature pubarche at diagnosis.
abstract: We investigated for evidence of early metabolic syndrome irrespective of body mass index (BMI) in subjects with premature pubarche (PP). Ten children with PP were compared with controls matched for age, sex, ethnicity, and BMI. Congenital adrenal hyperplasia and other known causes of PP were excluded by standard methods. Anthropometry, blood pressure (BP), dual-energy x-ray absorptiometry body scan, fasting blood lipid profile, and cytokines were obtained. The children were divided into 2 groups: (1) the total group of children with PP, and their age-, sex-, ethnicity-, and BMI-matched controls and (2) those with PP and normal BMI (<19 kg/m(2)) and their matched controls selected from the original groups. The PP subjects with normal BMI (S(1)) showed significantly higher systolic BP (P = .028), diastolic BP (P = .028), and mean arterial pressure (P = .018) compared with matched controls (C(1)). Nevertheless, for both groups, all the above parameters were statistically not significant when corrected for height. Fat distribution in PP subjects indicated significantly higher android (P = .047) and android-gynoid ratio (P = .013). Normal-BMI PP children had significantly higher android-gynoid ratio fat distribution compared with their matched controls (P = .037). Trunk fat percentage (p: 0.04) and trunk fat (grams) (P = .007) were significantly elevated in PP children compared with matched controls. Again, for both groups, all the above parameters were not statistically significant when corrected for height. The PP subjects had significantly higher tumor necrosis factor (TNF)-alpha (P = .038) and interleukin-8 (picograms per milliliter) (P = .05) compared with matched controls. Normal-BMI PP children also had higher TNF-alpha (P = .028) compared with matched controls. When corrected for height, TNF-alpha was higher in the total (P = .037) and normal-BMI (P = .043) PP children. Premature pubarche can be linked to markers of the metabolic syndrome in lean children.
authors.affiliation: Department of Pediatrics, Vanderbilt University, Nashville, TN 37232, USA. revi.mathew@vanderbilt.edu
authors.forename: Revi P
authors.initials: RP
authors.lastname: Mathew
authors.forename: Daniel W
authors.initials: DW
authors.lastname: Byrne
authors.forename: MacRae F
authors.initials: MF
authors.lastname: Linton
authors.forename: Douglas E
authors.initials: DE
authors.lastname: Vaughan
authors.forename: Sergio
authors.initials: S
authors.lastname: Fazio
authors.forename: William E
authors.initials: WE
authors.lastname: Russell
mesh_terms: D015992:Body Mass Index; D002648:Child; D002784:Cholesterol / Q000097:blood; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D024821:Metabolic Syndrome / Q000209:etiology* / Q000378:metabolism; D011629:Puberty, Precocious / Q000150:complications* / Q000378:metabolism; D013851:Thinness / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D008075:Lipoproteins, HDL; D014409:Tumor Necrosis Factor-alpha; D019314:Dehydroepiandrosterone Sulfate; D002784:Cholesterol