Evidence of metabolic syndrome in lean children with premature pubarche at diagnosis

Revi P. Mathew, Daniel W. Byrne, MacRae F. Linton, Douglas E. Vaughan, Sergio Fazio, William E. Russell

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 (2) and their matched controls selected from the original groups. The PP subjects with normal BMI (S1) showed significantly higher systolic BP (P = .028), diastolic BP (P = .028), and mean arterial pressure (P = .018) compared with matched controls (C1). 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)-α (P = .038) and interleukin-8 (picograms per milliliter) (P = .05) compared with matched controls. Normal-BMI PP children also had higher TNF-α (P = .028) compared with matched controls. When corrected for height, TNF-α 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.

Original languageEnglish (US)
Pages (from-to)733-740
Number of pages8
JournalMetabolism: Clinical and Experimental
Volume57
Issue number6
DOIs
StatePublished - Jun 2008
Externally publishedYes

Fingerprint

Body Mass Index
Fats
Blood Pressure
Tumor Necrosis Factor-alpha
Congenital Adrenal Hyperplasia
Anthropometry
Interleukin-8
Fasting
Arterial Pressure
X-Rays
Cytokines
Hypertension
Lipids

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Evidence of metabolic syndrome in lean children with premature pubarche at diagnosis. / Mathew, Revi P.; Byrne, Daniel W.; Linton, MacRae F.; Vaughan, Douglas E.; Fazio, Sergio; Russell, William E.

In: Metabolism: Clinical and Experimental, Vol. 57, No. 6, 06.2008, p. 733-740.

Research output: Contribution to journalArticle

Mathew, Revi P. ; Byrne, Daniel W. ; Linton, MacRae F. ; Vaughan, Douglas E. ; Fazio, Sergio ; Russell, William E. / Evidence of metabolic syndrome in lean children with premature pubarche at diagnosis. In: Metabolism: Clinical and Experimental. 2008 ; Vol. 57, No. 6. pp. 733-740.
@article{41938ffad6aa400eabfb92b2680541d8,
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 (2) and their matched controls selected from the original groups. The PP subjects with normal BMI (S1) showed significantly higher systolic BP (P = .028), diastolic BP (P = .028), and mean arterial pressure (P = .018) compared with matched controls (C1). 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)-α (P = .038) and interleukin-8 (picograms per milliliter) (P = .05) compared with matched controls. Normal-BMI PP children also had higher TNF-α (P = .028) compared with matched controls. When corrected for height, TNF-α 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.",
author = "Mathew, {Revi P.} and Byrne, {Daniel W.} and Linton, {MacRae F.} and Vaughan, {Douglas E.} and Sergio Fazio and Russell, {William E.}",
year = "2008",
month = "6",
doi = "10.1016/j.metabol.2008.01.010",
language = "English (US)",
volume = "57",
pages = "733--740",
journal = "Metabolism: Clinical and Experimental",
issn = "0026-0495",
publisher = "W.B. Saunders Ltd",
number = "6",

}

TY - JOUR

T1 - Evidence of metabolic syndrome in lean children with premature pubarche at diagnosis

AU - Mathew, Revi P.

AU - Byrne, Daniel W.

AU - Linton, MacRae F.

AU - Vaughan, Douglas E.

AU - Fazio, Sergio

AU - Russell, William E.

PY - 2008/6

Y1 - 2008/6

N2 - 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 (2) and their matched controls selected from the original groups. The PP subjects with normal BMI (S1) showed significantly higher systolic BP (P = .028), diastolic BP (P = .028), and mean arterial pressure (P = .018) compared with matched controls (C1). 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)-α (P = .038) and interleukin-8 (picograms per milliliter) (P = .05) compared with matched controls. Normal-BMI PP children also had higher TNF-α (P = .028) compared with matched controls. When corrected for height, TNF-α 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.

AB - 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 (2) and their matched controls selected from the original groups. The PP subjects with normal BMI (S1) showed significantly higher systolic BP (P = .028), diastolic BP (P = .028), and mean arterial pressure (P = .018) compared with matched controls (C1). 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)-α (P = .038) and interleukin-8 (picograms per milliliter) (P = .05) compared with matched controls. Normal-BMI PP children also had higher TNF-α (P = .028) compared with matched controls. When corrected for height, TNF-α 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.

UR - http://www.scopus.com/inward/record.url?scp=43849107760&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=43849107760&partnerID=8YFLogxK

U2 - 10.1016/j.metabol.2008.01.010

DO - 10.1016/j.metabol.2008.01.010

M3 - Article

VL - 57

SP - 733

EP - 740

JO - Metabolism: Clinical and Experimental

JF - Metabolism: Clinical and Experimental

SN - 0026-0495

IS - 6

ER -