No abstract available.
Hand ; Hyperplasia

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*

It has been clarified that myoepithelial cells contain S-100 protein which is known to be a marker protein of neural tissue. To evaluate the participation of myoepithelial cells in the histogenesis of the salivary gland tumors, normal salivary glands and various salivary gland tumors were stained by immuno-peroxidase method. PAP kits (DAKO Co, USA) for the S-100 protein and the Cytokeratin were used and the following resulting were obtained. Acinic cells of the normal salivery gland were negative for both cytokeratin and S-100 protein. The intercalated duct cells were weakly positive for cytokeratin and S-100 protein. The normal myoepithelial cells scattered around the acini and the intercalated ducts were positive only S-100 protein. In contrast, the striated duct were positive only for cytokeratin. In plemorphic adenoma, the S-100 protein positive cells were found in solid sheets of tumor cells, in chondromyxoid areas and in areas of spindle-cell stroma as well as in the outer layer of the tubular structures. Only the inner lining of the tubules were positive for cytokeratin. In basal cell adenoma, the stromal spindle cells were strongly positive for S-100 protein and the epithelial cells weakly positive. When tubules were present within the epithelial sheets, the inner most lining cells were positive for cytokeratin. The peripheral palisaded tumor cells were negative for both substances. By immunostaining of the adenoid cystic carcinoma, S-100 protein containing cells were found focally scattered independently on the variety of histologies. The lining cells of true cystic structure were positive for cytokeratin. Immunostaining of the mucoepidermoid carcinoma demostrated that the squamous cells and the tubular epithelial cells contained cytokeraitn, whereas only a few intermediate cells were positive for S-100 protein. In Warthin's tumor there were no S-100 protein positive cells, although basally located epithelial cells of the papillae were positive for cytokeratin. These findings suggest that salivary gland tumors other than the Warthin's tumor arise from myoepithelial cells or reserve cells having dual potentiality differentating into myoepithelial and intercalcated duct cells.

PURPOSE: A number of studies have been published on the effect of growth hormone therapy over 1-3 years in children with growth hormone deficiency(GHD) & Familial short stature(FSS). So far final height data are seldomly available. Final heights of GH treated children with GHD & FSS were evaluated. METHODS: 10 Children with GHD and 69 children with with FSS were enrolled for the study. They were treated with GH 0.1IU/kg/daily in 10 GHD and 20 children with FSS. They were grown up and reached adult height. 49 children with FSS were not treated at all. Facors influencing final height were investigated. RESULTS: 1) All patients with GHD(Idiopathic 8 cases, Organic 2 cases) had additional gonadotropin deficiency and had multiple pituitary hormone deficiency. 2) At start of GH treatment boys of idiopathic GHD were 9.8 years old and 12.4 years old in girls and their mean height was 114.8cm(-2.8SDS), 123.0cm(-2.9 SDS)in boys and girls respectively. Boy with orgnaic GHD was 11.1 years and 6.7 years old in girl. Their height were 126.0cm(-1.5SDS) and 104cm(-1.2SDS) respectively. 3) Mean final height of idiopathic GHD was 167.6cm(-0.5SDS) in male and 161.0 cm(0.7SDS) and that of organic GHD was 173.0cm(0.5SDS) in male and 157cm (0SDS) in girl. 4) Mean Final height in untreated children with FSS was 159.8+/-.2cm(-1.6 SDS)in male and 149.6+/-.3cm(-1.4SDS) in female. Mean final height of GH treated in FSS was 162.5+/-.1cm(-1.5SDS) in male and 152.0+/-.4cm(-1.2SDS) in female But there was no statiscally difference between untreated and treated children in final height. 5) The age of onset of menarche was 12.74+/-.78 years old in GH treated group (n=12) and 12.45+/-.16 years old in untreated group(n=34). CONCLUSION: The GH administration in patients with GHD has been confirmed for growth promotion. but in case of FSS there was no significant difference between treated and untreated group. More further studies are needed for the confirmation of the efficacy of GH therapy in patients with FSS.
Adult ; Age of Onset ; Child* ; Female ; Gonadotropins ; Growth Hormone* ; Humans ; Male ; Menarche

It has been proven that the newborn screening programs for congenital hypothyroidism are very important for its early detection and the early treatment of congenital It has been proven that the newborn screening programs for congenital hypothyroidism are very important for its early detection and the early treatment of congenital hypothyroidism can ameliorate and possibly reverse its consequences. Treatment with L-thyroxine is started in case of suspicious hypothyroidism at the first visit. Serum concentration of total and free thyroxine become normal within 1week after start of therapy but TSH values become normal from 2 months to 6 months after L-thyroxine therapy. The possible explanations for prolonged TSH elevation in congenital hypothyroidism are poor compliance for therapy, an inadequate dose of L-thyroxine, elevated threshold for thyrotropin suppression and two novel mutations in the thyrotropin (TSH) receptor gene in a child with resistance to TSH. Authors have experienced two cases of prolonged TSH elevation with normal T3 and T4 levels till 18months and 27 months of age after optimal L-thyroxine therapy and literature were reviewed.
Child ; Compliance ; Congenital Hypothyroidism* ; Humans ; Hypothyroidism ; Infant, Newborn ; Mass Screening ; Thyrotropin ; Thyroxine

No abstract available.
Scalp*

No abstract available.
Cellulitis* ; Child* ; Eosinophils* ; Humans

No abstract available.
Nevus*

Cyclosporine is one of the main therapeutic agents for psoriasis. It is known that psoriasis relapses 2∼3 months after discontinuation of cyclosporine, and exacerbation due to abrupt discontinuation of cyclosporine is uncommon. We report a case of psoriasis that was aggravated by cyclosporine cessation for guselkumab treatment, but improved with continuous administration of guselkumab. A 55-year-old man with a history of psoriasis presented with erythematous scaly plaques on the whole body. He had been treated with cyclosporine for 18 months and had received a subcutaneous injection of guselkumab 1 month previously. Two weeks after the first injection, the patient experienced exacerbation of the lesions. Considering the aggravation caused by abrupt discontinuation of cyclosporine, guselkumab administration was continued. The aggravated psoriatic lesions improved after additional guselkumab injections. At 16 weeks, the Psoriasis Area and Severity Index score was 0, which remained constant thereafter.