Relation of serum leptin and insulin-like growth factor-1 levels to intima-media thickness and functions of common carotid artery in children and adolescents with type 1 diabetes

BACKGROUND AND AIM: Leptin and insulin-like growth factor-1 (IGF-1) have been suggested to be involved in the pathogenesis of atherosclerosis. The aim of this study was to evaluate the relationship between serum leptin, IGF-1 and intima-media thickness (IMT) and functions of common carotid artery (CCA) in children and adolescent patients with type 1 diabetes. MATERIAL AND METHODS: Serum leptin and IGF-1 levels were measured in 45 diabetic patients (23 girls and 22 boys). Age, diabetes duration as well as major cardiovascular risk factors, including anthropometric and metabolic parameters, were matched between girls and boys. The relation of serum leptin and IGF-1 levels to CCA structure and functions were measured by ultrasonography as IMT, cross-sectional compliance (CSC), cross-sectional distensibility (CSD), diastolic wall stress (DWS) and incremental elastic modulus (IEM). RESULTS: Serum leptin levels of diabetic girls were higher than those in the boys (21.8 +/- 14.5 microg/l vs 8.9 +/- 10.6 micro/l, p = 0.002). However, the difference for serum IGF-I levels was not significant between diabetic girls and boys (240.7 +/- 96.8 ng/ml vs 234.7 +/- 93.2 ng/ml; p > 0.05). In all subjects, leptin levels were correlated with CSC (p = 0.04), CSD (p = 0.04) and IEM (p = 0.01), and IGF-1 levels were only correlated with CSC (p = 0.01). Leptin did not show any correlation with ultrasonographic measurements in both girls and boys separately. IGF-1 was correlated with CSC (p = 0.001), CSD (p = 0.002) and IEM (p < 0.001) in boys but not in girls. In a multivariate regression model, IGF-1 emerged as independent correlates for mean CSD and IEM in boys but not in girls. CONCLUSION: Serum leptin and IGF-1 levels in children and adolescent patients with type 1 diabetes are associated with functions of common carotid artery, and the association of IGF-1 levels is influenced by sex.     

Serum leptin concentrations in relation to pubertal development

OBJECTIVES: The amount of adipose tissue influences pubertal development and fertility in girls. A candidate for mediating this is the hormone leptin, derived from adipocytes. This work was carried out to determine whether the leptin concentration in serum is regulated during pubertal development. SUBJECTS AND METHODS: Serum concentrations of leptin were determined by radioimmunoassay in a sample of 252 healthy children representing all pubertal stages. RESULTS: Serum leptin concentrations correlated directly with age (r = 0.53), body mass index (BMI) (r = 0.71), and weight for height SD score (r = 0.44) in girls and with BMI (r = 0.33) and weight for height SD score in boys (r = 0.36). Leptin concentrations increased with pubertal development in girls, resulting in significantly higher concentrations at pubertal stages 4 and 5 than at the prepubertal stage, whereas there was no change in the boys. CONCLUSIONS: Serum leptin concentrations increased during pubertal development in the girls, but remained constant in the boys. Whether the increase in serum leptin concentrations in girls is of importance for, or a consequence of, pubertal development is still to be determined.     

Diurnal leptin rhythms in children treated with prednisolone once daily in the morning or in the evening

Serum leptin levels exhibit a marked diurnal variation in children. The aim of the present study was to investigate whether the timing of administration of exogenous glucocorticoids, which have been found to increase serum leptin, affects the diurnal rhythm. Four girls and four boys aged 10.6 to 15.8 (mean 13.2) years with asthma were studied. The design was an open 2-period cross-over trial with a 1-day run in, two 4-day periods of prednisolone 5 mg in the morning or in the evening, with a 3-week washout in between treatment periods. During run in and on the last day of the prednisolone periods a fasting blood sample was drawn at 08.00 h, and thereafter samples were obtained every 2 h throughout the day until 08.00 h the next morning. Serum leptin was measured by a specific radioimmunoassay. During all periods, leptin levels were low during the day with a nadir at 10.00 h (run-in [mean +/- SEM]: 3.9+/-1.28; morning prednisolone: 5.2+/-1.58; evening prednisolone: 5.7+/-2.02 microg/l). Increases in leptin levels were detected from 20.00 h with zeniths at 24.00 h (run in: 7.2+/-1.86; evening prednisolone: 9.2+/-2.36 microg/l) and 02.00 h (morning prednisolone: 9.4+/-1.78 microg/l) (F = 115.5; p <0.01). As compared to run in, leptin levels were increased at all time points during prednisolone treatment in the morning (F = 16.0, p = 0.01) and in the evening (F = 12.6, p = 0.01). No statistically significant differences were found in leptin levels during prednisolone in the morning or in the evening (F = 0.44, p = 0.53). Therefore, the timing of administration of exogenous glucocorticoids does not affect diurnal leptin rhythms in children.     

Changes in leptin, insulin and body composition in obese children during a weight reduction program

BACKGROUND: Girls have higher leptin concentrations than boys at all stages of biological development and this is also seen in the state of obesity. Little is known about whether gender and biological development of obese children influence changes in leptin associated with a short-term weight reduction program. OBJECTIVE: To study whether leptin concentration, body composition and insulin levels in obese children were influenced by a 3-week intervention program including diet and sports. STUDY DESIGN: Sixty-two obese children (32 boys and 30 girls) were examined before and after the intervention program. Body composition was measured by bioelectrical impedance and BMI-SDS was calculated. Serum leptin and serum insulin were determined by RIA. RESULTS: Girls had higher leptin levels than boys, before and after the weight reduction program. Body mass, fat mass (FM), leptin and insulin were decreased after the intervention in both sexes. We found a greater change in serum leptin in girls but the change in FM was of greater magnitude in boys. However, percentage changes in leptin were not significantly different between the sexes. Before the intervention, leptin concentrations were correlated with %FM, FM and moderately with BMI-SDS in all children. Only in pubertal boys did correlation of leptin with %FM increase after the intervention (from r=0.57 to r=0.75, p<0.01). Changes in leptin were found to be associated with initial leptin values in boys (r=0.95, p<0.01) and in girls (r=0.93, p<0.01), independent of Tanner stages. CONCLUSION: Serum leptin levels were positively correlated with adiposity in obese children and a diet and sports intervention program decreased serum leptin, insulin and body fat in all children. Changes in leptin were best described by the initial leptin concentration. The increase in correlation of leptin with %FM in obese pubertal boys after the intervention could have its underlying mechanism in an increased sensitivity to leptin and anabolic hormones.     

Pubertal changes in serum leptin levels in adolescents with type 1 diabetes mellitus: a controlled longitudinal study

The mechanism of the pubertal delay seen in some adolescents with type 1 diabetes mellitus is not entirely clear. Since leptin has been implicated as a neuroendocrine modulator of puberty, we measured serum leptin levels longitudinally in 24 post-'honeymoon' patients with diabetes mellitus (M/F = 15/9) with a mean (+/- SD) age of 10.5 +/- 0.9 years and 26 controls (M/F = 15/11) with a mean age of 10.0 +/- 1.1 years. Physical examinations; serum leptin, IGF-I, IGFBP-3 and IGFBP-1 levels; and bone age X-rays were performed annually for up to 48 months. Glycosylated hemoglobin (HbA1c) was measured 2-4 times a year in patients with diabetes mellitus. Serum leptin levels strongly correlated with the body mass index z-scores (BMI-Z) in both controls (r = 0.666, p <0.00001) and diabetic patients (r = 0.577, p <0.00001). Girls had increased serum leptin levels for a given BMI compared to boys (p <0.005). There were no significant differences in serum leptin levels of patients with diabetes mellitus compared to controls, nor were differences seen when the groups were stratified by age, Tanner stage, or gender. There were also no significant correlations between serum leptin levels and degree of metabolic control (i.e. HbA1c) or insulin dose standardized for body weight. Although there was no significant diabetes-related or metabolic control-related delay in bone age z-score or pubertal development, there was a significant negative correlation between HbA1c and growth velocity z-score, indicating that children with poor diabetes control had modest but significant slowing of growth. It is concluded that neither pubertal development nor serum leptin levels are significantly altered in adolescents with diabetes mellitus managed with standard therapy. The potential role of leptin in initiation of pubertal development is not easily demonstrable in observational studies.     

Serum leptin levels in premature pubarche and prepubertal girls with and without obesity

Leptin can be regarded as a marker of the nutritional status of the body. This study was performed to determine the correlation of leptin levels with insulin (I) and androgens in girls with premature pubarche (PP) and prepubertal controls (C) with (OB) or without (nOB) obesity. We studied 25 girls with PP and 14 C; girls were dived into two subgroups according to body mass index (BMI): OB (18 PP and 8 C) and nOB (7 PP and 6 C). Obesity was defined as BMI >95th percentile for chronological age. Serum levels of leptin, I, glucose (G), DHEAS, testosterone, androstenedione (A), cortisol, SHBG, IGFBP-1 and lipid profile were measured. The fasting G to I ratio (FGIR) was calculated and FGIR <7 was considered as suggestive of I resistance (IR). Data were analyzed comparing PP vs C and OB vs nOB. Serum DHEAS (0.60 +/- 0.45 vs 0.18 +/- 0.22 microg/ml) and A (895.5 +/- 420.4 vs 457.0 +/- 352.1 pg/ml) levels were significantly higher in PP than C. Other hormonal and metabolic parameters were similar. Serum leptin (30.8 +/- 18.3 vs 8.1 +/- 5.9 ng/ml), A (841.8 +/- 471.1 vs 522.5 +/- 317.2 pg/ml), DHEAS (0.53 +/- 0.44 vs 0.31 +/- 0.39 microg/ml), G (88.4 +/- 8.8 vs 80.2 +/- 8.1 mg/dl), I (13.5 +/- 7.7 vs 5.1 +/- 3.7 microU/ml) and total cholesterol (TC) (180.5 +/- 30.9 vs 161.8 +/- 29.5 mg/dl) levels were greater in the OB than in the nOB group. IR was observed in 10 girls with OB and in one with nOB. Leptin was correlated with BMI (r = 0.83), SHBG (r = -0.44), IGFBP-1 (r = -0.47), I (r = 0.37), A (r = 0.48) and TC (r = 0.36), but in multiple regression analysis only with BMI (r2 = 0.72, p < 0.001). Girls with PP and prepubertal OB girls showed elevated leptin levels independent of I and androgen levels. Girls with OB had a greater degree of hyperandrogenism and IR. As obesity, IR and hyperandrogenism are common findings in polycystic ovary syndrome (PCOS), which is more prevalent in young women with a history of PP, a role of leptin in PCOS can be suggested. In addition, girls with PP could be considered a population at risk for plurimetabolic syndrome.     

Leptin is closely related to body fat in prepubertal children aged 8-11 years

BACKGROUND: In adults and obese children, serum leptin concentrations are closely related to body fat. AIM: To investigate whether such a relationship between leptin concentrations and body fat is also evident in children with a relatively normal body composition. METHODS: The study was a cross-sectional population study in 170 Caucasian children (91 boys and 79 girls), with a mean age of 9.9+/-0.6 y (range 8.5-10.9 y) and a mean BMI of 17.4+/-2.6 (range 12.8-28.1). Serum leptin was measured and compared to total body fat as determined by dual-energy X-ray absorptiometry. RESULTS: In the whole population, serum leptin concentrations were highly correlated with total body fat (r=0.83, p<0.001). A stepwise forward multi-regression analysis revealed that the inclusion of other anthropometrical data did not add any significance to the model. Leptin concentrations were significantly higher in girls (5.2 ng/ml) than in boys (3.2 mg/ml; p=0.003). Gender differences still prevailed (p=0.007) after adjusting for number of kilograms of fat tissue. CONCLUSION: This study shows that, already at the young age of 9-11 y, an adult-like pattern of regulation of leptin exists. This indicates similar risk factor dependency of leptin across all age groups.     

Circulating leptin levels and bone mineral density in children with biliary atresia

AIM: To investigate circulating leptin levels in biliary atresia (BA) patients and the association of leptin with bone mineral density (BMD) and the severity of BA. METHODS: We have examined 50 patients with BA and 15 matched healthy controls. Serum leptin, osteocalcin and C-terminal telopeptide of type I collagen (CTX) levels were measured by sandwich enzyme-linked immunosorbent assay (ELISA). BMD of the lumbar spine was measured by dual energy X-ray absorptiometry. RESULTS: Serum leptin levels of BA patients were lower than those of healthy controls (2.7 +/- 0.3 vs. 7.1 +/- 1.7 ng/mL, p = 0.0001). Among the BA patients, serum leptin levels were significantly lower in patients with jaundice than patients without jaundice (1.7 +/- 0.2 vs. 3.4 +/- 0.4 ng/mL, p = 0.001). BMD of BA patients was correlated (p < 0.001) with leptin levels, age and BMI (r = 0.55, r = 0.75 and r = 0.58, respectively). The serum CTX levels were significantly higher in jaundice patients compared with jaundice-free patients and the healthy controls (0.6 +/- 0.2 vs. 0.2 +/- 0.1 ng/mL, p = 0.01), whereas the serum osteocalcin levels in BA patients were not different from those in the controls. CONCLUSION: Circulating leptin levels are correlated with BMD and the presence of jaundice in BA, suggesting that the leptin may play a physiological role in maintaining bone mass of BA patients with jaundice.     

Thyroid gland volume and urinary iodine excretion in children 6-11 years old in an endemic area

Goiter prevalence and urinary iodine excretion levels were assessed in 605 schoolchildren (301 males and 304 females), aged 6-11 years, living in the Antalya region, a well known endemic goiter area in Turkey. Goiter prevalence was evaluated by clinical examination and ultrasound of the thyroid gland. Urinary iodine levels were expressed as microg/g creatinine. Goiter by inspection and palpation was found in 35% (n = 212) of all subjects, in 37.5% (n = 114) of girls and 32.5% (n = 98) of boys. Iodine deficiency of moderate degree was detected from the point of goiter prevalence. With regard to the upper limits of reference thyroid volumes reported by WHO and ICCIDD, goiter by ultrasonography was found in 34% (n = 206) of all subjects, in 36.8% (n = 112) of girls and 31% (n = 94) of boys. Median iodine/creatinine ratios of all subjects, and goitrous and non-goitrous subjects, were 64.1+/-20.1, 62.8+/-21.8 and 64.9+/-19.1 microg/g, respectively. Urinary iodine excretion levels revealed mild iodine deficiency in the region. No significant correlation was observed between urinary iodine excretion levels and thyroid volumes (r = 0.12, p>0.05). Iodine deficiency of mild to moderate degree in schoolchildren aged 6-11 years was detected in Antalya. It was concluded that urgent measures must be undertaken to eradicate iodine deficiency in the region.     

Diurnal rhythm in serum leptin

AIM: To assess 24-hour serum leptin levels in children. SUBJECTS AND METHODS: Five girls and two boys aged 10.4-13.6 (mean 12.2) years with pubertal stages I to III were studied. All children were healthy. A fasting blood sample was drawn at 08.00 hours, and thereafter samples were obtained every 2 hours throughout 24 hours until 08.00 hours the next morning. Serum leptin was measured by a specific radioimmunoassay. RESULTS: A statistically significant circadian variation was found in mean leptin profile expressed as a percentage of overall day mean (F-ratio =10.4; P<0.001) with trough and peak levels (+/- SEM) at 10.00 (6.55+/-1.52 mg/l) and 24.00 hours (10.99+/-2.34 mg/l), respectively. CONCLUSIONS: In normal children serum leptin levels exhibit a nocturnal increase and a decrease during the morning. The nocturnal rise may represent a time lagged stimulating effect of insulin. The diurnal rhythm needs to be considered when serum leptin is assessed in clinical studies.     

No evidence for leptin as an independent associate of blood pressure in childhood and juvenile obesity

We studied whether leptin is an independent associate of blood pressure in obese children and adolescence. 102 obese children (48 girls, age: 11.6 +/- 2.22 yr; body mass index [BMI]: 27.45 +/- 4.4; blood pressure: 122.5 +/- 11.1/64.7 +/- 10.6 mm Hg and 54 boys, age: 11.5 +/- 2.4 yr; BMI: 27.6 +/- 4.4; blood pressure: 122.5 +/- 13.2/60.9 +/- 8.1 mm Hg [mean +/- SD]) were investigated. Serum leptin and insulin were measured by RIA; glucose was determined enzymatically. Fat mass (FM) was calculated by bioelectrical impedance. Leptin was higher in girls than in boys (p=0.018) but no significant gender differences were found with respect to indices of adiposity and systolic blood pressure (SBP). Children were divided into three groups, according to pubertal stage (Group 1: prepubertal, 32 boys/13 girls; Group 2: pubertal, 17 boys/25 girls; Group 3: late/postpubertal, 5 boys/10 girls). SBP and DBP correlated with body weight in the whole group (r=0.49, p<0.0001, and r=0.27, p=0.004). In Group 1, BMI showed the highest correlation to SBP; in Group 3 no indices of adiposity were related to SBP. In no case was leptin significantly associated with SBP after adjustment for adiposity. In Group 2, glucose was significantly associated with SBP after adjustment for body weight. In Group 3, however, no correlations were found between SBP, DBP and metabolic characteristics, perhaps due to small sample size. Stepwise multiple regression revealed that body weight and glucose contributed to the variation in SBP in the whole group (R2=0.31, p<0.0001). Insulin accounted for almost 8% of the variation in DBP (R2=0.08, p=0.0034). Body weight contributed significantly to SBP in boys (R2=0.39, p<0.0001) and girls (R2=0.24, p< 0.001). The results imply that body weight contributes independently to the variation in blood pressure. Glucose and insulin contribute to mean blood pressure to some extent, but our data do not support the assumption that leptin per se serves as an independent predictor of blood pressure in obese children and adolescents.     

肾病综合征患儿血清铁与转铁蛋白的变化

目的：肾病综合征(NS)患儿尿中丢失白蛋白的同时也伴有转铁蛋白的丢失,测定血清铁及转铁蛋白等铁代谢相关指标以及尿转铁蛋白,了解其变化及其相互关系。方法：NS患儿37例,测定其治疗前和恢复期铁代谢相关指标(血清铁、铁蛋白、转铁蛋白、转铁蛋白饱和度、总铁结合力以及外周血红细胞参数)及尿转铁蛋白,并与正常对照组比较。结果：①在NS治疗前血清铁为18.8±3.8μmol/L,分别与恢复期的21.0±3.5μmol/L,及对照组的22.2±3.8μmol/L比较,差异有显著性(P<0.01);转铁蛋白为1.9±0.3g/L,分别与恢复期的2.9±0.6g/L和对照组的3.1±0.5g/L比较,差异有显著性(P<0.01);总铁结合力为56.4±9.2μmol/L,分别与恢复期的51.9±7.7μmol/L和对照组的50.7±6.8μmol/L比较,差异亦有显著性(均P<0.01);转铁蛋白饱和度为(55.7±9.2)%,与NS恢复期及对照组的(47.4±13.3)%,(46.4±8.2)%比较,差异有显著性(P<0.01)。②血清白蛋白与转铁蛋白呈正相关(r=0.609,P<0.01)。③血清转铁蛋白浓度与尿转铁蛋白呈负相关(r=-0.550,P<0.01)。结论：NS患儿血清铁及转铁蛋白明显降低,可能与转铁蛋白从尿中丢失有关。     

女童性早熟与血清瘦素、类胰岛素样生长因子-1水平及脑电图关系的研究

目的 探讨特发性中枢性性早熟(ICPP)与单纯性乳房发育(SPT)女童血清瘦素、类胰岛素样生长因子-1(IGF-1)水平、脑电图异常率及这些指标对真性性早熟的诊断价值。方法 乳房早发育为主患儿中特发性中枢性早熟18例,单纯性乳房发育12例,用放射免疫法和酶标免疫法测定两组血清瘦素、IGF-1及行脑电图检查。结果 ICPP组血清瘦素、IGF-1水平明显高于SPT组(P均<0.001)。其脑电图异常率明显高于SPT组(P<0.01)。血清瘦素与IGF-1之间呈明显正相关(r=0.668 P<0.001)。血清瘦素与黄体生成素(LH)或LH/卵泡刺激素(FSH)间无相关性。结论 血清瘦素、IGF-1、脑电图可作为真性性早熟的早期诊断指标之一。     

Plasma homocysteine levels in children and adolescents with type 1 diabetes

OBJECTIVE: Hyperhomocysteinemia has been established as a risk factor for cardiovascular disease. The objective was to investigate total plasma homocysteine concentrations in children and adolescents with type 1 diabetes and a control group. METHOD: Twenty-seven children with type 1 diabetes and 27 subjects of an age- and sex-matched control group were recruited. Fasting samples were collected for plasma total homocysteine, serum vitamin B12, folate, and creatinine. RESULTS: Fasting total homocysteine concentrations showed no difference between patients and controls (5.6 +/- 2.9 micromol/L vs 5.7 +/- 2.2 micromol/L; p greater than 0.05). The diabetic patients had significantly higher serum folate than the healthy controls (11.4 +/- 3.3 ng/mL vs 9.4 +/- 4.1 ng/mL; P = 0.02 and higher serum B12 than the control group (282.8 +/- 119 pg/mL vs 228.5 +/- 50.9 pg/mL; P = 0.03). Total plasma homocysteine concentration correlated with age (r = 0.44, P = 0.02), weight (r = 0.56, P = 0.002), body mass index (r = 0.57, P = 0.002), folate (r = -0.48, P = 0.01), and creatinine (r = 0.41, P = 0.03) in diabetic patients. In stepwise multivariate regression model for diabetics, the independent correlates for total plasma homocysteine concentration was folate (P = 0.002). CONCLUSION: We concluded that fasting plasma total homocysteine concentrations were within normal limits in children and adolescents with type 1 diabetes who were without any clinical evidence of microvascular and macrovascular complications.     

Three-Year Follow-up Study on Serum Leptin Levels in GH Deficient Children with GH Replacement Therapy

Interactions between GH and leptin have been extensively studied. However, results of long-term GH therapy on serum leptin levels in GH-deficient children were not consistent. Moreover, no such reports were available in Japanese children with this disease. We studied 35 Japanese patients with GH deficiency (26 boys and 9 girls, mean age: 9.8 ± 6.2 yr old), of whom 6 patients with complete and 29 with incomplete GH deficiency were identified by GH provocation test. Serum leptin levels, percent of ideal body weight (%IBW) and percent fat (%fat) were determined at 0, 1, 3, 6, 12, 18, 24, and 36 mo after beginning GH therapy. Baseline levels of %fat and leptin were significantly higher in girls than boys (P<0.05), though serum leptin did not change throughout the study period in either group. Further, %IBW did not change significantly, whereas %fat exhibited significant changes after 6 mo in boys and remained virtually constant thereafter for up to 3 yr. In summary, serum leptin levels did not change in GH-deficient boys and girls during the 3-yr period after the start of GH replacement therapy, despite a decrease in %fat after 6 mo of therapy in the boys. Thus, it is conceivable that long-term GH replacement therapy can be employed without an effect on normal leptin secretion.     

经济不发达地区3～9岁儿童血清瘦素水平的变化

目的：了解经济不发达地区3～9岁儿童在营养状况相对较差时血清瘦素的水平及与相关生长发育指标的关系。方法：根据年龄和性别将研究对象分为<6岁女孩组(F36组)、<6岁男孩组(M36)、≥6岁女孩组(F69组)和≥6岁男孩组(M69组)共4组,调查其年龄、体重、身高并计算体重指数(BMI)、体脂百分量(BF%),使用双抗体夹心ELISA法检测瘦素浓度,比较各组间瘦素浓度的差异,同时在各组分析瘦素与各指标间的相关性。结果：①瘦素浓度在同性别比较中,差异无显著性(P>0.05),在同年龄比较中,女孩明显高于男孩(P<0.05);②无论是男孩还是女孩,在3～6岁儿童瘦素与BMI和BF无明显相关(P>0.05),而在6～9岁儿童瘦素浓度与BMI和BF显著相关(P<0.05)。结论：在经济不发达地区3～9岁儿童中瘦素存在性别差异,6～9岁儿童中瘦素与BMI和BF密切相关。     

激素敏感型肾病综合征患儿甲基泼尼松龙冲击前后白介素13的表达

目的：观察白介素13（IL-13）在小儿类固醇敏感肾病综合征（SRNS）中的变化及甲基泼尼松龙冲击治疗（MPT）对IL-13表达的影响,探讨其在SRNS发病中的作用。方法：分别采用ELISA法及RT-PCR法测定20例正常儿童及28例SRNS患儿MPT前、结束后2 d、5 d、尿蛋白转阴后2周血清IL-13水平及外周血单个核细胞(PBMC) IL-13 mRNA水平。采用双缩脲法对SRNS患儿检测24 h尿蛋白量。结果：血清IL-13蛋白水平及PBMC IL-13 mRNA表达MPT前明显高于MPT结束后5 d组、尿蛋白转阴后2周组及正常对照组,差异有显著性（均P＜0.01）;MPT结束后5 d组较正常对照组高,差异有显著性（P＜0.05）; MPT前与结束后2 d比较差异无显著性（P＞0.05）。尿蛋白转阴后2周组血清IL-13蛋白水平及PBMC IL-13 mRNA表达与正常对照组比较无统计学意义。SRNS患儿血清中IL-13水平与24 h尿蛋白量呈正相关。结论：SRNS患儿血清IL-13及其基因表达异常,MPT对SRNS患儿IL-13在蛋白合成和基因转录两个水平上可能有抑制作用。［中国当代儿科杂志,2007,9（6）：533-536］     

Serum leptin level in children with atopic dermatitis-treated topical steroids

Leptin, the obese gene product, is a 16-kDa peptide hormone secreted by adiposities. Systemic administration of exogenous glucocorticoids has been found to increase circulating leptin levels. In this study, we aimed to assess serum leptin in children with atopic dermatitis (AD)-treated with local steroids. Twenty children with AD were included during the 2001-2002 time period. The study was conducted prospectively. Atopy was defined as the presence of at least one aeroallergen-specific immunoglobulin E (IgE) antibody. Serum leptin was determined using a commercially available radioimmunoassay kit with 3.4-8.3% intra-assay and 3.0-6.2% interassay coefficients of variation, and 0.5 ng/ml sensitivity. Fourteen boys and six girls with AD, the mean age of the patients was 3.1 +/- 2.2. Forty-three percentage of the family histories for atopy were positive, 60% of the cases passive smoking histories were positive. In seven patients the aeroallergen-specific IgE were positive. All 20 patients treated clobetasone 17-butirate (0.05%). There was no significant difference in serum leptin between patients (mean +/- s.d.: 4.6 +/- 3.8), and controls (mean +/- s.d.: 6.2 +/- 3.6) (p > 0.05). Local steroid does not influence circulating leptin levels, suggesting that regulation of body weight is unaffected.     

Are adolescent boys with Klinefelter syndrome androgen deficient? A longitudinal study of Finnish 47,XXY boys

Testosterone (T)-substitution therapy is widely used in adult patients with Klinefelter syndrome (KS) to prevent symptoms and sequels of androgen deficiency, but it is currently unknown if adolescent boys with KS benefit from early T therapy. To evaluate the optimal age to start T substitution, we searched for signs of androgen deficiency in pubertal boys with KS. 14 nonmosaic 47,XXY boys, aged 10-13.9 y, were followed up for 4-37 mo with staging of puberty and frequent reproductive hormone measurements. Furthermore, indices reflecting androgen action (serum SHBG, leptin, and prostate-specific antigen (PSA) levels) were studied. Both onset and progression of puberty according to Tanner stages were normal in boys with KS. Consistently, serum T concentrations increased as expected and remained normal throughout follow-up. Changes in the indices of androgen action (decreases in serum SHBG and leptin, and increase in serum PSA concentrations) occurred normally, except that average leptin levels were higher in the boys with KS (KS boys 11.8 +/- 7.0 microg/L; controls 7.6 +/- 4.7 microg/L; p = 0.033). Despite normal T concentrations, the KS boys displayed from the age of 13 y elevated serum FSH and LH levels, and exaggerated gonadotropin responses to gonadotropin-releasing hormone. These data do not demonstrate an unequivocal androgen deficiency in adolescent boys with KS that would necessitate androgen supplementation therapy during early puberty.     

Apolipoproteins and Lipoproteins in Children with Type I Diabetes: Relation to Glycosylated Serum Protein and HbA1

ABSTRACT. Serum levels of cholesterol (C), triglycerides (TG), lipoprotein-C and apolipoproteins (apo) A-I, A-II and B were measured in 30 children with type I diabetes mellitus (16 boys, 14 girls, aged 11–14 years) and in 26 healthy controls (15 boys, 11 girls, aged 10–13 years). For 19 diabetics controls matched for age, sex and relative body weight were selected. The diabetic patients were considered to be in fair metabolic control according to HbA₁ levels and glycosylated serum protein concentrations. Mean serum apo A-I, A-II and B, C, TG, low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) did not differ significantly between diabetic and nondiabetic children. Very low density lipoprotein cholesterol (VLDL-C) was significantly higher in diabetic children than in controls. Serum C and LDL-C levels showed close univariate linear correlations with glycosylated serum protein (LDL-C: r =0.53, p <0.01, C: r =0.58, p <0.01) in diabetics. The ratio LDL/HDL-C was significantly correlated to HbA₁ levels ( r =0.47, p <0.01). By canonical and multiple linear correlation analysis significant relations of a selected set of variables concerning the control and therapy of diabetes (serum glucose, HbA₁, glycosylated serum protein, insulin dose) with a set of lipoprotein variables (C, TG, VLDL-C, HDL-C, LDL-C, apo A-I, A-II, B) could be demonstrated. From these data we conclude that significant relations between atherogenic serum lipids and lipoproteins (C, LDL-C) and the degree of metabolic control exist in diabetic children, even in the absence of marked dyslipoproteinemia. The close relation of LDL-C and total C with glycosylated serum protein in the diabetics might be due to glycosylation of LDL .