Syndrome In Prepubertal Children Research Articles

Persistent sleep-disordered breathing independently contributes to metabolic syndrome in prepubertal children.

Obstructive sleep apnea (OSA) is a risk factor for metabolic syndrome (MetS) in adults, but its association in prepubertal children is still questionable due to the relatively limited cardiometabolic data available and the phenotypic heterogeneity. To identify the role of OSA as a potential mediator of MetS in prepubertal children. A total of 255 prepubertal children from the Childhood Adenotonsillectomy Trial were included, with standardized measurements taken before OSA treatment and 7 months later. MetS was defined if three or more of the following criteria were present: adiposity, high blood pressure, elevated glycemia, and dyslipidemia. A causal mediation analysis was conducted to assess the effect of OSA treatment on MetS. OSA treatment significantly impacted MetS, with the apnea-hypopnea index emerging as mediator (p = .02). This mediation role was not detected for any of the individual risk factors that define MetS. We further found that the relationship between MetS and OSA is ascribable to respiratory disturbance caused by the apnea episodes, while systemic inflammation as measured by C-reactive protein, is mediated by desaturation events and fragmented sleep. In terms of evolution, patients with MetS were significantly more likely to recover after OSA treatment (odds ratio = 2.56, 95% confidence interval [CI] 1.20-5.46; risk ratio = 2.06, 95%CI 1.19-3.54) than the opposite, patients without MetS to develop it. The findings point to a causal role of OSA in the development of metabolic dysfunction, suggesting that persistent OSA may increase the risk of MetS in prepubertal children. This mediation role implies a need for developing screening for MetS in children presenting OSA symptoms.

Gut Hormones Secretion across Clusters of Metabolic Syndrome in Prepubertal Children with Obesity.

Metabolic Syndrome (MetS) represents a common dysmetabolic state in children with obesity. Although data in youth show a role of gut hormones (GH) in the risk of developing MetS, no data are available during the prepubertal age, especially across clusters of MetS. We characterized components of MetS and changes in GH concentrations in 90 prepubertal children with obesity compared to 30 healthy age- and gender-matched peers. Children with obesity were divided into three groups according to the number of the components of MetS (group 1: 30 obese without components of MetS; group 2: 30 obese with 1 component of MetS; group 3: 30 obese with 2 or more components of MetS). Anthropometric parameters, blood pressure (BP), fasting insulin and glycemia, lipid profile, transaminases, and GH concentration were determined. Differences across the groups were evaluated by the Kruskal-Wallis test and post hoc analysis by Mann-Whitney test. Fasting glycemia and insulin, HOMA-IR, triglycerides, and BP progressively increased and high-density lipoprotein progressively decreased across the groups of children with obesity compared to controls, showing worse values in group 3. GLP-1 and ghrelin values progressively decreased and obestatin progressively increased. The more components of the MetS were present, the further GH concentrations deviated from standard values. Components of MetS and GH concentrations are impaired in prepubertal children with obesity compared to controls. The close association between progressive alterations in GH levels and increasing number of components of the MetS might indicate a role of these hormones in the determination of metabolic risk.

Predictive Ability of the Estimate of Fat Mass to Detect Early-Onset Metabolic Syndrome in Prepubertal Children with Obesity.

Body mass index (BMI), usually used as a body fatness marker, does not accurately discriminate between amounts of lean and fat mass, crucial factors in determining metabolic syndrome (MS) risk. We assessed the predictive ability of the estimate of FM (eFM) calculated using the following formula: FM = weight − exp(0.3073 × height2 − 10.0155 ×d-growth-standards/standards/body-mass-index-for-age-bmi-for-age weight− 1 + 0.004571 × weight − 0.9180 × ln(age) + 0.6488 × age0.5 + 0.04723×male + 2.8055) (exp = exponential function, score 1 if child was of black (BA), south Asian (SA), other Asian (AO), or other (other) ethnic origin and score 0 if not, ln = natural logarithmic transformation, male = 1, female = 0), to detect MS in 185 prepubertal obese children compared to other adiposity parameters. The eFM, BMI, waist circumference (WC), body shape index (ABSI), tri-ponderal mass index, and conicity index (C-Index) were calculated. Patients were classified as having MS if they met ≥ 3/5 of the following criteria: WC ≥ 95th percentile; triglycerides ≥ 95th percentile; HDL-cholesterol ≤ 5th percentile; blood pressure ≥ 95th percentile; fasting blood glucose ≥ 100 mg/dL; and/or HOMA-IR ≥ 97.5th percentile. MS occurred in 18.9% of obese subjects (p < 0.001), with a higher prevalence in females vs. males (p = 0.005). The eFM was correlated with BMI, WC, ABSI, and Con-I (p < 0.001). Higher eFM values were present in the MS vs. non-MS group (p < 0.001); the eFM was higher in patients with hypertension and insulin resistance (p < 0.01). The eFM shows a good predictive ability for MS. Additional to BMI, the identification of new parameters determinable with simple anthropometric measures and with a good ability for the early detection of MS, such as the eFM, may be useful in clinical practice, particularly when instrumentation to estimate the body composition is not available.

Long-Term Follow-up of Pseudotumor Cerebri Syndrome in Prepubertal Children, Adolescents, and Adults

PurposePseudotumor cerebri syndrome can have a recurrent course. We compared the long-term disease course, recurrences, and final visual outcomes in prepubertal children, adolescents, and adults. MethodsIn this retrospective observational study, patients were divided into prepubertal children (group A) adolescents (group B), and adults (group C). ResultsSixty-five patients (56 females, nine males) were included, 26.2% in group A, 24.6% in group B, and 49.2% in group C. Age at diagnosis was 8.6 ± 2.0 years, 14.3 ± 1.5 years, and 31.9 ± 9.7 years for the prepubertal children, adolescents, and adults, respectively. Medical treatment duration was similar (2.4 to 3.3 years, P > 0.05). Recurrences were observed in 23.5% of prepubertal children, 50% of adolescents, and 28.1% of adults. Recurrences occurred within 1.3 ± 0.6 years from treatment cessation in the prepubertal group compared with 3.8 ± 5.1 years in adolescents and 2.7 ± 2.0 years in adults (P = 0.267). Optic neuropathy was evident in 41% of group A, 31% of group B, and 87.5% of group C (P < 0.001). Obesity and cerebrospinal fluid opening pressures were unassociated with either relapsing rates or final visual outcomes in all groups. ConclusionsPseudotumor cerebri syndrome exhibits a relapsing course in a third of cases. Recurrences tend to occur within one year after treatment cessation in prepubertal children, and within three years in older patients, revealing the importance of longer follow-up, especially in adults. Optic neuropathy was more common in adults along with a tendency for visual decline. Longer treatment times were associated with fewer recurrences.

Irisin is a biomarker for metabolic syndrome in prepubertal children.

The aim of the present study was to evaluate the association of irisin with obesity and metabolic syndrome (MetS) in Korean prepubertal children. A total of 96 children and adolescents aged 6 to 10 years (56 males) were included in this study. Subjects were divided into 3 groups: normal weight (n = 54), overweight (n = 16), and obese (n = 26). In the subgroup analyses, overweight/obese children were further divided based on their MetS status (with MetS vs. without MetS). Children with obesity tended to exhibit a lower mean irisin concentration compared to those with normal weight (p = 0.028). Using Pearson's correlation coefficient to compare all the children in the study, there was a significant inverse correlation between irisin and body mass index (BMI) standard deviation scores (SDS) (r = -0.210, p = 0.041), waist circumference SDS (r = -0.203, p = 0.049), and glucose (r = -0.296, p = 0.004). In the subgroup analyses of overweight/obese children, irisin exhibited a significant inverse correlation with glucose (r = -0.507, p = 0.001) and triglycerides (r = -0.331, p = 0.033). Children with MetS exhibited lower irisin concentrations than those without MetS (14.70 ng/mL vs. 22.02 ng/mL, p = 0.001), and these associations were significant after adjusting for age, gender, and BMI SDS (14.51 ng/mL vs. 22.06 ng/mL, p = 0.002). The irisin level of 15.43 ng/mL was determined to be a possible cutoff to distinguish children with metabolic syndrome from overweight/obese children, with a sensitivity of 75% and a specificity of 94% (p < 0.001). Our results suggest that decreased irisin levels may be associated with MetS in prepubertal children and that irisin might be a biomarker for MetS in prepubertal children.

Leptin as a predictor of metabolic syndrome in prepubertal children.

Leptin has been suggested as a potential biomarker of cardiovascular risk. This paper aims to ascertain, based on a sample of prepubertal children, which serum leptin value best suited to identify metabolic syndrome (MS). This observational, cross-sectional study recruited children from the outpatient pediatrics clinic, with the purpose of validating serum leptin level cutoffs to identify MS. All obese and overweight children who met eligibility criteria were included in the study, as was a sample of normal-weight children. The sample underwent clinical assessment and blood fasting glucose, lipid profile, insulin, and leptin were measured. Sensitivity and specificity were estimated for each leptin measurement, using MS as the outcome. These values were used to construct a receiver operating characteristic (ROC) curve. The association between MS and leptin was assessed using logistic models to predict MS. A total of 65 normal weight, 46 overweight, and 164 obese children were analyzed (160 boys, 115 girls; age: 93.7 ± 17.8 months). The most appropriate leptin cutoff was 13.4 ng/mL (sensitivity 67.6%; specificity 68.9%; accuracy 72.1%). The logistic model indicated that leptin levels above 13.4 ng/dL were significantly associated with MS and that, for every 1 ng/dL increase in leptin levels, the odds of MS increase by 3% (p = 0.002; OR 1.03; 95% CI 1.01-1.05). Leptin may be a useful biomarker of cardiovascular risk in prepubertal children, with an optimal cutoff of 13.4 ng/mL. Identification of potential new risk markers for cardiovascular disease in children could contribute to the development of preventive strategies.

Relationship of serum 25-Hydroxyvitamin D (25[OH]D) levels and components of metabolic syndrome in prepubertal children

ObjectiveThe relationship between 25-hydroxyvitamin D (25[OH]D) levels and the lipid and metabolic levels of the prepubertal normal population is unclear. Our goals were to investigate the association of serum 25(OH)D concentrations with lipid and metabolic levels in Korean prepubertal children ages 7–9 y. MethodsWe followed 205 children, ages 7–9 y in the Ewha Birth and Growth Cohort study, a prospective cohort sample established in 2001–2006, from July to August 2011. We studied the association of serum 25-hydroxyvitamin D (25[OH]D) levels with components of metabolic syndrome and insulin resistance indices using multivariate regression analysis adjusted for body mass index (BMI) z-scores. ResultsThe mean age of the 205 subjects was 7.89 ± 0.85 y, and the sample included 109 boys (53.2%). The average 25(OH)D levels of all participants was 25.0 ± 5.4 ng/mL. After adjustment for age and sex, triacylglycerol levels were significantly associated with 25(OH)D (β = –0.02, P = 0.02) concentrations even after adjustment for BMI z-scores (β = −0.02, P = 0.04). However, other metabolic components were not correlated with 25(OH)D status. Those with the lowest quartile of 25(OH)D levels had the highest serum triacylglycerol levels (P = 0.04, Ptrend = 0.01). ConclusionsWe found that serum 25(OH)D levels were negatively associated with serum triacylglycerol levels, even independently of adiposity, in prepubertal children. This study suggests that 25(OH)D insufficiency is related to metabolic syndrome via the derangement of triacylglycerol metabolism.

The ApoB/A-I Ratio and Metabolic Syndrome in Prepubertal Children

Studies about the relationship of apolipoproteins (apo) and metabolic syndrome in children are scarce. In this study, we analyze apo levels and determine the best cutoff point of the apoB/A-I ratio to diagnose dyslipidemia in prepubertal children with metabolic syndrome. A community-based, cross-sectional study that enrolled 337 children with Tanner stage 1 and average age and body mass index of 9.7±1.6 years and 19.2±3.8 kg/m(2) was carried out. Diagnosis of acute or chronic illnesses constituted the exclusion criteria; in addition, children undergoing medical treatment or receiving vitamins and/or oral supplements were not included. Metabolic syndrome was identified in 42 (12.5%) children (19 girls and 23 boys). The mean apoB/A-I ratio in the children with metabolic syndrome was 0.67±0.18. The best cutoff point of the apoB/A-I ratio for recognizing dyslipidemia was 0.60 (area under the receiver operating characteristic curve, 0.778; sensitivity 80%, specificity 55%). A total of 102 children exhibited apoB/A-I ratio ≥0.60. Diagnosis of metabolic syndrome was performed in 42 (41.2%) children. Among children with metabolic syndrome, 38 (90.5%) had hypertriglyceridemia, 34 (81.0%) low high-density lipoprotein cholesterol (HDL-C), 32 (76.2%) hypertriglyceridemia+low HDL-C, and 40 (95.2%) an apoB/A-I ratio ≥0.60. Our results show that the best cutoff point of the apoB/A-I ratio for recognizing dyslipidemia in prepubertal children is 0.60 and that among children with metabolic syndrome, an apoB/A-I ratio ≥0.60 is the marker of dyslipidemia with the highest frequency.

Presence of early risk markers of metabolic syndrome in prepubertal children with a history of intrauterine growth restriction

Studies on people with low birth weight found metabolic syndrome associated with intrauterine growth restriction (IUGR). To study the presence of early risk markers of metabolic syndrome in a prepubertal population with IUGR. We studied 45 prepubertal children with a history of IUGR, without apparent disease, and 47 children in a control group. BMI, weight, height, and BMI Z score, and body fat mass were calculated. Basal glycemia, insulin, proinsulin, cortisol, serum lipids and uric acid levels were analyzed. Insulin sensitivity was calculated by QUICKI and insulin resistance by HOMA-IR. Basal insulin levels were higher in the IUGR group compared with the controls (6.6 microU/ml vs. 4.4 microU/ml; p= 0.008). Similar results were found for the basal cortisol levels (18.8 ug/dl vs. 13.1 ug/dl; p= 0.006) and uric acid (4.2 mg/dl vs. 2.7 mg/dl; p= 0.0008). QUICKI index was lower in the IUGR group (2.06 vs. 2.86, p= 0.001). The IUGR children who developed obesity presented higher levels of proinsulin (26.04 ug/dl vs. 13.3 ug/dl; p= 0.05), insulin (11 microU/ml vs. 5.5 microU/ml, p= 0.005), and HOMA-IR (2.06 vs. 0.9, p= 0.004), and lower QUICKI (1.71 vs. 2.16, p= 0.01) than in the case of the IUGR children with appropriate weight; these differences weren't observed among the control group. Children with IUGR, without apparent disease, showed metabolic changes that were expressed through risk markers of metabolic syndrome in childhood.

The possible role of liver steatosis in defining metabolic syndrome in prepubertal children

Insulin resistance is a key component of the metabolic syndrome (MS) and is strongly associated with liver steatosis. Our aim was to evaluate whether MS should be diagnosed already in obese prepubertal children and whether its prevalence is influenced by the inclusion of hepatic steatosis as a diagnostic criterion. Eighty-nine obese children (43 boys; age median [range], 8.5 [6-10] years) were enrolled. Metabolic syndrome was diagnosed according to a classic definition: presence of 3 or more of the following criteria—body mass index greater than 2 standard deviation score, triglycerides greater than the 95th percentile, high-density lipoprotein cholesterol less than the fifth percentile, blood pressure greater than the 95th percentile, and impaired glucose tolerance. Afterward, liver steatosis was included as an additional criterion to this definition. Metabolic syndrome was diagnosed in 12 children (13.5%) according to the first definition and in 18 children (20.2%) when liver steatosis was included. The prevalence of MS increased across homeostasis model assessment of insulin resistance tertiles ( P for trend = .01). The prevalence of the single components of the MS was as follows: obesity, 100%; hypertriglyceridemia, 27%; low high-density lipoprotein cholesterol, 2.2%; hypertension, 34.8%; impaired glucose tolerance, 4.5%; and nonalcoholic fatty liver disease, 21.3%. In conclusion, MS is common already among prepubertal obese children, particularly when liver steatosis is included among the diagnostic criteria. Therefore, screening for the MS should be performed in this age group; and hepatic steatosis should be considered as an additional diagnostic criterion.

Sequelae of Syndrome X in Children Born Small for Gestational Age

Objective: Low birth weight is associated with the presence of syndrome X in adults. We studied the components of this syndrome in prepubertal children born SGA (small for gestational age) and children born AGA (appropriate for gestational age). Methods: Twenty-nine SGA children, age (mean ± SD) 9.1 ± 1.1 years and 24 AGA children, age 9.0 ± 1.1 years were studied. Fasting serum lipid concentrations were determined. A hyperinsulinemic euglycemic clamp was performed to measure insulin sensitivity. Ambulatory monitoring was performed to obtain 24-hour recordings of blood pressure. Results: Prepubertal SGA children are less insulin sensitive and have a higher nighttime systolic blood pressure (SBP) after correction for BMI than children born AGA. No differences were found in lipid concentrations between the 2 groups. Conclusions: Not all components of syndrome X can yet be found in 9-year-old children born SGA; follow-up of this cohort is required.