No abstract available.
Growth Hormone*

No abstract available.
Diabetes Mellitus* ; Molecular Biology*

The McCune-Albright Syndrome is characterized by polyostotic fibrous dysplasia, cafe-au-lait colored patches of the skin and endocrinological abnormalities, including precocious puberty. Affected patients progress from GnRH-independent puberty to GnRH-dependent puberty. GnRH analogues are ineffective in GnRH-independent precocious puberty. Three year and 2 month old girl with breast development(SMR B3) and irregular vaginal bleeding were seen & diagnosed as incomplete sexual precocity. Decapeptyl treatment was started for the purpose of regression of breast development & vaginal bleeding with no effect. After 10 months, cafe-au-lait skin lesion & polyostotic fibrous dysplasia were noted and diagnosed as McCune-Albright syndrome. Breast development regressed to SMR B2 and vaginal bleeding was controlled with ketoconazole. As our experience, ketoconazole treatment might be effective to delay the progression of sexual development in patients with precocious puberty in McCune-Albright Syndrome.
Adolescent ; Breast ; Female ; Fibrous Dysplasia, Polyostotic* ; Gonadotropin-Releasing Hormone ; Humans ; Infant ; Ketoconazole* ; Puberty ; Puberty, Precocious ; Sexual Development ; Skin ; Triptorelin Pamoate ; Uterine Hemorrhage

PURPOSE:The recombinant human growth hormone is widely used to improve short stature but it was reported that GH therapy might accelerate sexual maturation especially short girl. We tried to find out the effects of GH on pubertal progression in female rat. METHODS:In animal experiment, forty female Sprague-Dawley rats were treated with rhGH(1U/kg). GH was given subcutaneously daily for 5weeks since 25day of life. We measured body weight and length twice a week, vaginal opening and epithelial change were observed daily. We checked the serum estrogen and insulin-like growth factor- I concentration weekly. The results were compared to 40 control female rats. RESULTS: 1) Body weight increased significantly in GH treated group(P<0.05). 2) Serum IGF- I concentration increased significantly after GH treatment(P<0.05). 3) Vaginal opening occurred on postnatal 34.3+/-1.9day in GH treated group and 35.4+/-2.2day in control group(p>0.1). First diestrous phase of puberty was noted on postnatal 36.8+/-1.9day and 38.3+/-3.0day, respectively(p>0.1). 4) The difference of serum E2 concentration of two group was insignificant. CONCLUSIONS:GH administration in female rats increased body weight and length without accelerating of pubertal maturation compared to control group. So GH treatment will give a good favor on final height.
Adolescent ; Animal Experimentation ; Animals ; Body Weight ; Estrogens ; Female ; Growth Hormone* ; Human Growth Hormone ; Humans ; Puberty ; Rats ; Rats, Sprague-Dawley ; Sexual Maturation

PURPOSE: Leptin is a hormone involved in the regulation of energy balance. Serum leptin levels are correlated with body fat. It provide information to hypothalamus on the amount of energy stored in the adipose tissue. Certain endocrine disease presents obesity in childhood, such as growth hormone deficiency, Prader- Willi syndrome and Turner syndrome. The purpose of this study is to evaluate leptin levels in obese children and to know whether it is a useful marker to differentiate the underlying cause of obesity. METHODS: One hundred sixty six obese children were included in this study. Height, weight, HTSDS, WTSDS, adjusted WTSDS to height age and BMI were measured. Serum leptin levels were measured. RESULTS :Leptin levels in simple obesity, growth hormone deficiency, Prader-Willi syndrome, Turner syndrome and control were 12.3+/-6.3ng/ml, 6.4+/-2.0ng/ml, 19.9+/-11.2ng/ml, 8.9+/-5.3ng/ml, 5.7+/-3.7ng/ml respectively. Leptin levels were significantly high in obese children, especially in Prader-Willi syndrome, simple obesity and Turner syndrome. Leptin concentration were correlated with BMI and WTSDS. CONCLUSION: Leptin can be used as an indicator of obesity but, not suitable as a differential diagnostic factor for obesity.
Adipose Tissue ; Child ; Endocrine System Diseases ; Growth Hormone ; Humans ; Hypothalamus ; Leptin* ; Obesity* ; Pediatric Obesity* ; Prader-Willi Syndrome ; Turner Syndrome

No abstract available.
Lip* ; Ulcer*

No abstract available.
Lip* ; Ulcer*

To demonstrate possible influences of general bone density on the mandible, histomorphometric analysis was carried out in mandibles and iliac bones and the correlation of the two bone densities was tested. Comparison of bony density in women and men over 60 years in the mandible was carried out too. Quantitative computed tomography (GCT) was taken in cross-section of mandibles at the same site where histomorphometric analysis was performed to evaluate the reliability of QCT. The analysis included 40 cadavers with no known disease affecting the bones. The subjects consisted of 15 females and 25 males with a mean age of 60.3 years. Spearman correlation analysis and Wilcoxon rank sum test was performed. The results were as follows. 1. There was statistically no correlation between the mandible and iliac bone in the walues of corrected cortical width (CCW), cortical porosity (POR) in cortex, and total bone volume(TBV), mean trabecular plate thickness (MTPT), mean trabecular plate density (MTPD), and mean trabecular plate separation (MTPS) in trabecular bone. 2. Comparison of women and men over 60 years, men had statistically higher bone density than women except for POR of buccal and lingual cortex, and MTPD of alveolar trabeculae in mandible. 3. There was statistically significant correlation between TBV of trabecular bone and CT NO., but not between POR and CT No. In mandible. According to the results above, there was no correlation between mandible and iliac bone density and between mandibular bony density and age. Further studies are required to support the results. A more noninvasive method to be able to measure the bone density of mandible should be developed and it is necessary to accumulate data on the normal values of bone density of mandible according to age and sex. Further study should be carried out about QCT to measure mandibular bony density using QCT.
Bone Density* ; Cadaver ; Female ; Humans ; Male ; Mandible* ; Porosity ; Reference Values

PURPOSE: Short stature is the most constant finding in Turner syndrome. Short stature in Turner syndrome has lately received considerable attention, mostly because of recent attemp to improve growth by hormonal treatments; growth hormone, oxandrolone, estrogen. The aim of this study was to find out whether growth promoting treatment would improve final height in girls with Turner syndrome. METHODS:Seventy-one girls with the clinical chracteristics Turner syndrome verified by karyotype analysis were entered into this study. The following selection criteria for final adult height were used; Chronological age of more than 14years old, bone age of more than 15years old and growth velocity of less than 0.5cm per 6months. Analysis was performed by means of multiple regression analysis between descriptive data; modality of treatment with oxandrolone and/or estrigen, parental height, karyotype and final adult height. RESULTS: 1) The final adult height of untreated Turner syndrome was 138.9+/-3.9cm. 2)The final adult height in 29 GH treated Turner girls was 143.9+/-6.5cm, significant higher value than 42 GH untreated Turner girls height, 139.8+/-5.2cm(p<0.01). 3) The final height in GH only group and combined group were 141.2+/-6.0cm, 146.2+/-6.2cm, respectively. The combined therapy was more effective than GH therapy(p<0.01). 4) The final height in 32 patients with karyotype of 45,X was 141.6+/-5.6cm, and that of 31 structural aberration group was 140.3+/-6.2cm. There was no significant difference between two groups. But in mosaicism, only numeric abnormalities, the final height 145.9+/-6.1cm was much more higher than other two groups(p<0.05). 5) The final adult height in Turner syndrome was in good correlation with target height. Final adult height(cm)= 1.01*Target height(cm)- 4.97 r=0.51, p<0.05. 6) There was positive correlation between final adult height and height SDS at start GH treatment and negative correlation with age at start GH treatment. The delta height (final height - height at start treatment) correlate with GH treatment duration. CONCLUSIONS:The final adult height in Turner syndrome in a given ethinic or national population varies in the same way as adult height in normal women. Growth hormone therapy may increase final height in Turner syndrome irrespective of ethinic or national difference. Further growth was observed in GH combined with estrogen or oxandrolone.
Adult* ; Estrogens ; Female ; Growth Hormone ; Humans ; Karyotype ; Mosaicism ; Oxandrolone ; Parents ; Patient Selection ; Turner Syndrome*

PURPOSE:Growth hormone stimulates longitudinal growth, and it also exerts various effects on the metabolism of carbohydrates, lipids and proteins, indirectly regulating fuel metabolism. A hallmark is the stimulation of lipolysis, suppression of glucose oxidation, and development of insulin resistance. These metabolic effects subsequently affect body composition and atherogenic risk factors. There have recently been numerous reports concerning the metabolic effects of growth hormone, but the results are conflicting and exact cellular mechanism of action is yet unknown. The aim of this study is to assess the effect of biosythetic growth hormone replacement on carbohydrate and lipid metabolism and its subsequent effect on atherogenic risk in growth hormone deficient and idiopathic short stature. METHODS:We studied 111 idiopathic short stature patients and 12 children diagnosed with growth hormone deficiency by growth hormone provocation tests. Subjects were divided into three groups on the basis of duration of treatment; those who had been receiving GH replacement for 6, 12 and 18 months. Growth hormone was adminstered in a subcutaneous dose of 0.1 units per kg 6 times a week, and levels of blood sugar, total cholesterol, triglycerides, HDL-cholesterol, free fatty acid were measured before and after treatment in each group and changes in the atherogenic index (calculated as total cholesterol/HDL-cholesterol) were compared. RESULTS: 1)Blood sugar levels showed no significant change after GH therapy in both idiopathic short stature and growth hormone deficient groups. 2)Levels of total cholesterol showed a signficant decrease 6, 12 and 18 months after GH therapy in the idiopathic short stature patients, but no signficant change was noted in the growth hormone deficient patients. 3)GrowthhormonetherapyshowednosignificanteffectoneitherHDL-cholesterol or atherogenic index in both idiopathic short stature and growth-hormone deficient children. 4)There was no significant change in triglyceride and free fatty levels in children with idiopathic short stature after growth hormone therapy. CONCLUSIONS:Growth hormone administration significantly lowered total cholesterol levels in idiopathic short stature children, but failed to have a significant effect on atherogenic risk. Despite the increasingly widespread use of growth hormone in the treatment of hypopituitarism and non-GHD short stature, data concerning the metabolic effects of growth hormone are conflicting and the precise underlying mechanism is yet to be revealed, making further research necessary to determine the long term consequences of growth hormone replacement.
Blood Glucose ; Body Composition ; Carbohydrates ; Child ; Cholesterol ; Glucose ; Growth Hormone* ; Humans ; Hypopituitarism ; Insulin Resistance ; Lipid Metabolism* ; Lipolysis ; Metabolism ; Risk Factors ; Triglycerides