PURPOSE:The purpose of this study was to assess the growth status and to evaluate the factors affecting the development of metabolic syndrome in children born with small for gestational age (SGA) at term gestation. METHODS:We retrospectively reviewed medical records of 73 (36 boys, 37 girls) children born with SGA at term gestation who were visited for short stature and metabolic problems at Seoul National University Children' Hospital between 1994 and 2003. We assessed several clinical parameters as follows:birth weight, height standard deviation score (SDS), weight SDS, weight for height, bone age (BA), chronologic age (CA), predicted adult height (PAH) and midparental height (MPH). We evaluated the factors affecting height SDS according to pubertal status. We also evaluated the factors affecting development of type 2 diabetes mellitus, dyslipidemia or obesity. RESULTS:Pubertal children had greater height SDS, weight SDS and difference between BA and CA than prepubertal children, respectively (P<0.05). Height SDS positively correlated with difference between BA and CA (r=0.43, P<0.01), but BA advancement (BA>CA) was not observed in prepubertal children. BA advancement was observed in all pubertal children except one. The children who had greater weight SDS than height SDS had significantly lower height SDS and delayed BA, respectively (P<0.05). The children who had metabolic problems had higher weight SDS (P<0.05). CONCLUSION: This study suggests that rapid skeletal maturation may develope during transition from prepuberty to puberty and catch-up growth may contribute to the development of metabolic syndrome in children born with SGA, but further study will be required.
Adolescent ; Adult ; Child* ; Diabetes Mellitus, Type 2 ; Dyslipidemias ; Gestational Age* ; Humans ; Medical Records ; Obesity ; Pregnancy* ; Puberty ; Retrospective Studies ; Seoul

This study was undertaken to investigate the response of non-immunologic contact urticaria(NICU) test before and after ingestion of cyclo-oxygenase inhibitors such as naproxene, ibuprofen and mefenamic acid. Forty patients who showed positive reaction to 5% benzoic acid (BA) in petrolatum by 20 minutes closed patch test were chosen and divided into 3 groups. Group I was consisted of 13 patients who were taken naproxene 250mg bid, group II, 14 patients, taken ibuprofen 600mg bid, and group III, 13 patients, taken mefenamic acid 500mg bid. All the patients were tested with 5%, 2.5%, 1%, 0.5% and 0.1% BA in petrolatum using Finn chamber on Scanpor tape on the right arm before medication and next day on the left arm after medication of each day. Mefenamic acid did not show any significant differences before and after ingestion of drug. Naproxene reduced reaction about half of patients. Ibuprofen reduced reaction in almost all patients and blocked reaction completely in 9 of 13 patients. This results suggested that there was no correlation between blocking effect to BA induced contact urticaria and so called anti-inflammatory potencies of naproxene and ibuprofen, and that NICU by BA is partly mediated by prostaglandins(PG) or mediated by other mediators, which were potentiated by PG, except histamin.
Arm ; Benzoic Acid ; Cyclooxygenase Inhibitors ; Eating ; Humans ; Ibuprofen ; Mefenamic Acid ; Naproxen ; Patch Tests ; Petrolatum ; Urticaria*

No abstract available.
Adolescent* ; Child* ; Cushing Syndrome* ; Humans

PURPOSE:We performed this study to compare correlation between the indices of insulin resistance using fasting insulin and glucose level and body mass index (BMI), and to determine the clinical usefulness of glucose/insulin ratio (G/I ratio), which is easily available in clinical base. METHODS:Total 119 children with simple obesity, whose BMI is over 95th percentile, were evaluated. We calculated G/I ratio, logInsulin, HOMA-IR, logHOMA-IR, and QUICKI and evaluated their relationship to BMI. RESULTS:Children with high-degree obesity had higher insulin resistance than children with mild to moderate-degree obesity (logInsulin, 1.13+/-.23 vs 1.27+/-.29; logHOMA-IR, 0.46+/-.24 vs 0.61+/-.30; QUICKI, 0.33+/-.03, 0.31+/-.03)(P<0.01), and pubertal children had higher insulin resistance than prepubertal children (G/I ratio, 7.39+/-.07 vs 4.85+/-.29; logInsulin, 1.14+/-.27 vs 1.31+/-.22; logHOMA-IR, 0.47+/-.28 vs 0.65+/-.22; QUICKI, 0.33+/-.03 vs 0.31+/-.02) (P<0.001). BMI had correlation coefficient as -0.436 for QUICKI, -0.432 for G/I ratio, 0.430 for logInsulin, and 0.425 for logHOMA-IR (P=0.000). G/I ratio was well correlated with QUICKI (r=0.901, P=0.000), logHOMA-IR (r=-0.865, P=0.000), and logInsulin (r=0.899, P=0.000). The changes of BMI were correlated with changes of G/I ratio (r=-0.547, P<0.01), QUICKI (r=-0.464, P=0.01), and logHOMA-IR (r=0.429, P<0.05). CONCLUSION: This study revealed that the degree of BMI had statistically significant correlation with insulin resistance, which can be reflected by G/I ratio, logHOMA-IR and QUICKI. G/I ratio was well correlated with logHOMA-IR and QUICKI, which suggests that G/I ratio could be used as an bedside index of insulin resistance. The changes of G/I ratio were more correlated with changes of BMI than those of logHOMA-IR and QUICKI.
Body Mass Index ; Child* ; Fasting ; Glucose ; Humans ; Insulin Resistance* ; Insulin* ; Obesity*

PURPOSE:There is a clear sexual dimorphism in circulating concentration of leptin in adulthood. However, we don' know when such dimorphism begins and how much pubertal development influences on it. So we examined body composition and circulating concentrations of leptin according to Tanner stage(TS). METHODS:We examined 112 children(M; 56, F; 56, Age; 8.5-17 yr) to evaluate the relationship of leptin and body composition. Body composition was determined by bioelectric impedence measurements(BIA) and by anthropometry. Leptin was measured by human specific RIA. Leptin level was analysed according to TS, body mass index(BMI), fat mass(FM), and lean body mass. RESULTS:BMI and free FM was correlated with TS in both sexes. FM was closely correlated with TS in girls but not in boys(M; r=0.08, P=0.54. F; r=0.73, P>0.001). Leptin levels increased in girls with advanced TS(r=0.355, P<0.01), but decreased in boys(r=-0.339, P<0.01). A strong exponential relationship was observed for leptin levels with BMI, FM, and percentage body fat as determined by BIA. There was significant sexual dimorphism of leptin level at TS VI/V. Because leptin level was significantly related FM, leptin level was normalized to FM(Leptin/FM). Leptin/FM of females(0.67+/-.27 ng/mL/kg) was also significantly higher then that of males(0.31+/-.15 ng/mL/kg)(P<0.001). CONCLUSION: These data suggest that plasma leptin levels increase in girls and decrease in boys after TS II as pubertal development proceeds; they show a significant gender difference, especially late puberty, even after adjustment for FM. Sexual dimorphism in leptin during puberty reflects not only differential changes in body composition but also different leptin resistance; reference ranges of leptin could be modified by TS and gender.
Adipose Tissue ; Adolescent* ; Anthropometry ; Body Composition* ; Child* ; Female ; Humans ; Leptin* ; Plasma ; Puberty ; Reference Values

PURPOSE:There is a clear sexual dimorphism in circulating concentration of leptin in adulthood. However, we don' know when such dimorphism begins and how much pubertal development influences on it. So we examined body composition and circulating concentrations of leptin according to Tanner stage(TS). METHODS:We examined 112 children(M; 56, F; 56, Age; 8.5-17 yr) to evaluate the relationship of leptin and body composition. Body composition was determined by bioelectric impedence measurements(BIA) and by anthropometry. Leptin was measured by human specific RIA. Leptin level was analysed according to TS, body mass index(BMI), fat mass(FM), and lean body mass. RESULTS:BMI and free FM was correlated with TS in both sexes. FM was closely correlated with TS in girls but not in boys(M; r=0.08, P=0.54. F; r=0.73, P>0.001). Leptin levels increased in girls with advanced TS(r=0.355, P<0.01), but decreased in boys(r=-0.339, P<0.01). A strong exponential relationship was observed for leptin levels with BMI, FM, and percentage body fat as determined by BIA. There was significant sexual dimorphism of leptin level at TS VI/V. Because leptin level was significantly related FM, leptin level was normalized to FM(Leptin/FM). Leptin/FM of females(0.67+/-.27 ng/mL/kg) was also significantly higher then that of males(0.31+/-.15 ng/mL/kg)(P<0.001). CONCLUSION: These data suggest that plasma leptin levels increase in girls and decrease in boys after TS II as pubertal development proceeds; they show a significant gender difference, especially late puberty, even after adjustment for FM. Sexual dimorphism in leptin during puberty reflects not only differential changes in body composition but also different leptin resistance; reference ranges of leptin could be modified by TS and gender.
Adipose Tissue ; Adolescent* ; Anthropometry ; Body Composition* ; Child* ; Female ; Humans ; Leptin* ; Plasma ; Puberty ; Reference Values

PURPOSE:Noonan syndrome(NS) is characterized by short stature, congenital heart disease, and typical facies. Recombinant human growth hormone(GH) has been reported to improve growth rate in a similar fashion to that seen in Turner syndrome. We investigated the clinical characteristics and growth reponses to GH therapy in children with NS. METHODS:The cases of sixty seven patients with NS were reviewed retrospectively. Ten of the 65 patients were assessed height, weight and pubertal stage every 3 months during GH therapy. RESULTS:Webbed neck(70%), delayed development(59.7%), low set posterior hairline(56.7%), eye abnormalities(56.7%) and mental retardation(55.2%) were the leading clinical characteristics. Short stature below the 3rd percentile was presented in 73.8 %. Growth patterns in NS children were variable and the evaluation of their growth must be individualized. The increments of height SDS were significant in children with GH therapy(height SDS:from -2.8+/-.6 to -2.3+/-.9, growth velocity:from 4.4+/-.8 cm to 9.2+/-.9 cm during first year, and 6.1+/-.1 cm during second year) (P<0.05). CONCLUSION: This study characterized the clinical profiles in Korean children with NS, which should be further extended with more children with NS. Additionally, the significant increase in final adult height after GH therapy in children with NS should be observed.
Adult ; Child* ; Facies ; Heart Defects, Congenital ; Humans ; Noonan Syndrome* ; Retrospective Studies ; Turner Syndrome

PURPOSE:Noonan syndrome(NS) is characterized by short stature, congenital heart disease, and typical facies. Recombinant human growth hormone(GH) has been reported to improve growth rate in a similar fashion to that seen in Turner syndrome. We investigated the clinical characteristics and growth reponses to GH therapy in children with NS. METHODS:The cases of sixty seven patients with NS were reviewed retrospectively. Ten of the 65 patients were assessed height, weight and pubertal stage every 3 months during GH therapy. RESULTS:Webbed neck(70%), delayed development(59.7%), low set posterior hairline(56.7%), eye abnormalities(56.7%) and mental retardation(55.2%) were the leading clinical characteristics. Short stature below the 3rd percentile was presented in 73.8 %. Growth patterns in NS children were variable and the evaluation of their growth must be individualized. The increments of height SDS were significant in children with GH therapy(height SDS:from -2.8+/-.6 to -2.3+/-.9, growth velocity:from 4.4+/-.8 cm to 9.2+/-.9 cm during first year, and 6.1+/-.1 cm during second year) (P<0.05). CONCLUSION: This study characterized the clinical profiles in Korean children with NS, which should be further extended with more children with NS. Additionally, the significant increase in final adult height after GH therapy in children with NS should be observed.
Adult ; Child* ; Facies ; Heart Defects, Congenital ; Humans ; Noonan Syndrome* ; Retrospective Studies ; Turner Syndrome

No abstract available.
Malformations of Cortical Development* ; Seizures*

No abstract available.
Malformations of Cortical Development* ; Seizures*