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Pubertal Children (pubertal + child)
Selected AbstractsA Randomized Trial to Assess the Impact of Early Steroid Withdrawal on Growth in Pediatric Renal Transplantation: The TWIST StudyAMERICAN JOURNAL OF TRANSPLANTATION, Issue 4 2010R. Grenda Minimizing steroid exposure in pediatric renal transplant recipients can improve linear growth and reduce metabolic disorders. This randomized multicenter study investigated the impact of early steroid withdrawal on mean change in height standard deviation score (SDS) and the safety and efficacy of two immunosuppressive regimens during the first 6 months after transplantation. Children received tacrolimus, MMF, two doses of daclizumab and steroids until day 4 (TAC/MMF/DAC, n=98) or tacrolimus, MMF and standard-dose steroids (TAC/MMF/STR, n=98). Mean change in height SDS was 0.16 ± 0.32 with TAC/MMF/DAC and 0.03 ± 0.32 with TAC/MMF/STR. The mean treatment group difference was 0.13 (p < 0.005 [95% CI 0.04,0.22]), 0.21 in prepubertal (p = 0.009 [95% CI 0.05,0.36]) and 0.05 in pubertal children (p = ns). Frequency of biopsy-proven acute rejection was 10.2%, TAC/MMF/DAC, and 7.1%, TAC/MMF/STR. Patient and graft survival and renal function were similar. Significantly greater reductions in total cholesterol and triglycerides but significantly higher incidences of infection and anemia were found with TAC/MMF/DAC (p < 0.05 all comparisons). Early steroid withdrawal significantly aided growth at 6 months more so in prepubertal than pubertal children. This was accompanied by significantly better lipid and glucose metabolism profiles without increases in graft rejection or loss. [source] Influence of the leptin G-2548A polymorphism on leptin levels and anthropometric measurements in healthy Spanish adolescents,ANNALS OF HUMAN GENETICS, Issue 4 2010Pia Riestra Summary Polymorphisms in the leptin gene (LEP) have been associated with leptin levels and obesity in some studies in adults though this link has scarcely been investigated in children. In our study, we examined the relationship of the LEP G-2548A polymorphism with leptin levels, anthropometric variables and body composition in a population-based sample of pubescent children. Our study included 880 healthy schoolchildren (419 males and 461 females), 12,16 years of age. Plasma leptin levels were determined by ELISA. The LEP polymorphism was determined by allelic discrimination TaqMan® assay. Male carriers of the AA genotype had significantly lower plasma leptin levels than GA (p < 0.008) and GG (p < 0.001) carriers and significantly lower mean hip circumference (HC) values than GG carriers (p = 0.04). In girls, leptin levels were also lower in A-allele carriers than in GG carriers, and BMI and HC were significantly lower in AA carriers as compared with GG carriers. In addition, the frequency of the A allele was significantly lower (,2: 4.58, p = 0.032) in the OW-obese than in the NW group. In conclusion, the LEP G-2548A polymorphism is associated with variations in leptin levels, BMI and HC in Spanish pubertal children, and evidence suggests a link between the G allele and presence of overweight in girls. [source] Sex-specific association between leptin receptor polymorphisms and leptin levels and BMI in healthy adolescents,ACTA PAEDIATRICA, Issue 10 2010P Riestra Abstract Aim:, To examine the relationship of three common polymorphisms in the leptin receptor (LEPR) gene, implicated in the regulation of body weight, with leptin levels and obesity-related phenotypes in a population-based sample of healthy pubertal children in Spain. Methods:, The study included 806 boys and girls aged 12,16 whose anthropometrical data and body composition were recorded. Serum leptin levels were determined by ELISA. The LEPR Q223R, K109R and K656N polymorphisms were determined by TaqMan® allelic discrimination assays. Results:, When analysing the Q223R polymorphism, we observed that female carriers of the RR genotype had significantly higher plasma leptin levels (18.2 vs. 15.1 ng/mL p = 0.016) and significantly higher mean BMI values (22.5 vs. 21.3 Kg/m2 p = 0.032) than QR carriers. Furthermore, the frequency of the RR genotype in overweight-obese girls was significantly higher than that found in normal-weight girls. No significant differences were observed in boys. Neither boys nor girls showed significant differences when comparing leptin levels, anthropometric variables or body composition by K109R or K656N genotype. Conclusion:, The fact, that the Q223R polymorphism in the LEPR gene is significantly associated with leptin levels and BMI only in girls, suggests a sex-specific influence of this polymorphism on these variables. [source] Intrabdominal fat is related to metabolic risk factors in Hispanic Americans, African Americans and in girlsACTA PAEDIATRICA, Issue 12 2009K Casazza Abstract Aim:, This study aimed to test the association of individual adipose depots on cardiometabolic outcomes, whether the association varied by depot and if the associations differed by race/ethnicity or gender in early pubertal children. Methods:, Three hundred and twenty children (53% male) aged 7,12 years self-identified as African American (AA; n = 114), European American (EA; n = 120) or Hispanic American (HA; n = 86) participated. Insulin dynamics were assessed by intravenous glucose tolerance test; body composition with DXA; fat distribution with CT. Results:, AA had the least fat in each depot and HA had the most. Fat accumulation negatively impacted cardiometabolic outcomes independent of race/ethnicity or gender. AA and females were reproductively more mature. In AA and HA, each measure of adiposity influenced the insulin sensitivity index (SI), whereas intra-abdominal adipose tissue (IAAT) did not contribute to SI in EA. IAAT was positively associated with blood pressure in AA only. In females, adiposity adversely influenced cardiometabolic outcomes such that total fat mass, IAAT and/or SAAT was inversely associated with SI, and positively associated with blood pressure and fasting insulin. Conclusion:, IAAT is uniquely related to metabolic risk factors in Hispanic Americans, African Americans and girls, suggesting that either the threshold for adverse effects of IAAT is lower, or the IAAT metabolism differs in these groups. [source] Ghrelin does not regulate the GH response to insulin-induced hypoglycaemia in children but could be involved in the regulation of cortisol secretionCLINICAL ENDOCRINOLOGY, Issue 1 2007J. Huber Summary Objective, Ghrelin activates the growth hormone secretagogue receptor GHS-R. It strongly stimulates GH secretion and has a role in energy homeostasis. The relationship between plasma ghrelin and cortisol levels during insulin-induced hypoglycaemia in prepubertal and pubertal children has not yet been investigated. The aim of the present study was to establish whether insulin-induced hypoglycaemia stimulates ghrelin secretion and whether changes in ghrelin concentrations are related to changes in GH and cortisol in children. Design and patients, We studied a group of 20 children and adolescents (five girls, 15 boys, mean age 10·8 ± 3·7 years) undergoing insulin tolerance tests (ITTs) for clinical investigation of GH deficiency. Measurements, Stimulation tests were performed to investigate the relationship between ghrelin, GH, cortisol and glucose levels according to age and pubertal stage by determining the ghrelin profiles during insulin-induced hypoglycaemia (at 0, 60 and 120 min). Results, Ghrelin was significantly and inversely related to body weight, height, body mass index (BMI) and age of children (P < 0·05). Significant changes in ghrelin levels (P = 0·00013) were found after the insulin bolus, with a decline at 60 min and an increase to baseline values at 120 min. Changes in cortisol levels were negatively correlated with changes in ghrelin at 60 min (r = ,0·59, P = 0·004) and at 120 min (r = ,0·605, P = 0·003). Conclusions, This study shows that ghrelin might not regulate the GH response to insulin-induced hypoglycaemia in prepubertal and pubertal children. A role for ghrelin in the regulation of cortisol secretion can be hypothesized concerning the negative correlation between changes in ghrelin and cortisol. Furthermore, the results imply that ghrelin secretion is age dependent and is a function of growth. [source] Increased insulin sensitivity in young, growth hormone deficient childrenCLINICAL ENDOCRINOLOGY, Issue 1 2001Sandra Husbands OBJECTIVE Although growth hormone (GH) has well documented insulin antagonistic effects, GH deficient adults often demonstrate insulin resistance. In young GH deficient children, increased susceptibility to hypoglycaemia might indicate increased insulin sensitivity; however, this has not been documented. We therefore determined insulin sensitivity in GH deficient and GH sufficient children. DESIGN AND PATIENTS Prospective study of children undergoing insulin tolerance tests for clinical investigation of GH or cortisol secretion at a regional Paediatric Endocrine/Growth Clinic between October 1986 and December 1997. Ninety-one tests were performed in children with GH deficiency and 142 tests in children with normal GH response to insulin (peak GH , 20 IU/l). MEASUREMENTS The standard insulin tolerance test was modified to permit frequent measurements of glucose (0, 5, 10, 15, 20, 30, 45, 60 and 90 minutes). Rate of log glucose disappearance in the first 15 minutes was calculated as a direct measure of insulin sensitivity. RESULTS GH deficient children were more insulin sensitive than GH sufficient children (P = 0·004) and had lower glucose nadirs post-insulin (P = 0·005). Subgroup analysis revealed that these differences were greater in younger (< 12 years old) or pre/early pubertal children. In 14 prepubertal children, exogenous sex steroid priming resulted in lower insulin sensitivity (P < 0·05) compared to nonprimed tests. CONCLUSIONS Young GH deficient children were more insulin sensitive than children with normal GH secretion. This difference attenuated with age and puberty, possibly secondary to pubertal sex steroids; however, insulin resistance as reported in GH deficient adults, was not observed in adolescents. [source] | ||||||||||