OBJECTIVES: The purpose of this investigation was to determine whether women with unexplained elevations of maternal serum human chorionic gonadotropin(hCG) at 14-20weeks gestation are at incresed risk for poor pregnancy outcomes. METHODS: 661 pregnant women undergoing second trimester triple marker screening test for Down syndrome and neural tube defect and delivered at our hospital were reviewed. Of 656 pregnancies that did not have maternal serum alpha feto-protein> or =2.5 multiples of the median(MoM), risk for poor pregnancy outcomes include to preeclampsia, preterm delivery, preterm rupture of membrane(PROM), small for gestational age(SGA) and fetal distress was evaluated in women with elevated hCG(> or =2.0 MoM) compared with women without elevated hCG(<2.0 MoM). RESULTS: Pregnancies with elevated hCG levels were at increased risk for preeclampsia (risk ratio 3.4, 95% confidence interval 1.5-7.6) but elevated hCG levels were not significantly associated with preterm delivery, PROM, and SGA and fetal ditress independent with preeclampsia. CONCLUSION: Pregnancies with elevated second-trimester hCG appear to be at higher risk of subsequent preeclampsia and this finding supports the theory that placental vascular changes that ultimately lead to preeclampsia begin at least by the second trimester. But further studies must be to determine how such information can be used to improve pregnany outcome.
Chorion ; Chorionic Gonadotropin* ; Down Syndrome ; Female ; Fetal Distress ; Humans* ; Mass Screening ; Neural Tube Defects ; Pre-Eclampsia* ; Pregnancy ; Pregnancy Outcome ; Pregnancy Trimester, Second ; Pregnant Women ; Rupture

Acute generalized exanthematous pustulosis (AGEP) has symptoms of abrupt onset of a widespread pustular eruption on an erythematous. base. Most cases appear to be related to drug reactions, mainly antibiotics, but viral infections and hypersensitivity to mercury may cause AGEP. The essential features of AGEP include. (1) numerous (several dazen) small((5mm), mostly non follicular pustules arising on a widespread erythema:purpura and target-like lesions may be associated; (2) histology showing intraepidermal or subcorneal pustules associated with one or more of the following.clermal edema, vasculitis, perivascular eosinophils, or focal necrosis of keratinocytes; (3) fever (over 38C); (4) neutrophilia, and (5) acute evolution with spontaneous resulotion of pustules within 15 days. We report a case of AGEP which presented with widespread tiny pustules on the whole body except the face, palms and soles. There were petechia, purpura, and vesiculobullous lesions on the axilla, popliteal fossa and upper abdomen. A biopsy specimen from a pustule showed subcorneal pustules with perivascular polymorphous cellular infiltration, marked dermal edema and necrotic keratinocytes. There was complete resolution of the lesions within 10 days.
Abdomen ; Acute Generalized Exanthematous Pustulosis* ; Amoxicillin ; Anti-Bacterial Agents ; Axilla ; Biopsy ; Drug Eruptions ; Edema ; Eosinophils ; Fever ; Hypersensitivity ; Keratinocytes ; Necrosis ; Purpura ; Vasculitis

BACKGROUND/AIMS: In order to determine the relationship between the HBV precore mutant and the severity of liver disease in Korea, we performed liver biopsies in patients with HBV related chronic liver disease and compared the types of mutations and histologic findings in the same liver tissue simultaneously. METHODS: HBV DNA in liver tissues was amplified by polymerase chain reaction (PCR). The precore mutants were detected by PCR-SSCP(single strand conformation polymorphism), cloning the amplified PCR products and direct sequencing for them. RESULTS: 1. HBV DNA was detected in liver tissues of 28 cases among 30 patients with PCR. And with SSCP, the most cases were mixed type infections. 2. The HBV precore mutants were found in 12 cases among the total number of 28 cases(42.9%) and all mutations were G to A change at nucleotide 1896, creating a stop codon at codon 28. However, 10 cases among 12 mutants were associated with simultaneous another mutation at different positions or regions;9 cases at core gene region, 2 cases at nucleotide 1856(C to T change at codon 15), one case at core promoter, and one case with double mutations at nucleotide 1837 and 1846 respectively. Also, all HBV precore mutants were combined with wild type HBV sequence. 3. The relationship between HBV precore mutants and HBeAg status revealed that 4 cases from 13 HBeAg positive(30.8%) and 8 from 15 HBeAg negative or Anti-Hbe positive(53.3 %) were mutants. 4. In analysis of the types of mutants and histopathological findings of liver diseases, 6 among 15 chronic active hepatitis(40.0%), all 3 cases with hepatocellular carcinoma(100,0 %), 2 among 4 asymptomatic carriers with minimal histopathologic changes(50.0%) and a case with chronic lobular heaptitis(100.0%) showed precore region mutation. CONCLUSION: The patterns of HBV precore mutants in Korea could be summarized as followings. Firstly, most of the mutations are composed of G to A change at nucleotide 1896. Secondly, the most of the mutants at nuclmtide 1896 have been associated with simultaneous mutations at core promoter, core gene, and rarely at other positions, and manifested usua'ly mixed type viremic conditions. Thirdly, although precore mutation could be occurred in asymptomatic carrier, this type of mutation might be closely related with chronic or severe liver disease. However, it needs further investigations hereafter.
Biopsy ; Clone Cells ; Cloning, Organism ; Codon ; Codon, Terminator ; DNA ; Hepatitis B e Antigens ; Hepatitis B, Chronic* ; Hepatitis, Chronic* ; Humans ; Korea ; Liver Diseases ; Liver* ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational

No abstract available.
Spine* ; Zygapophyseal Joint*

No abstract available.
Diagnosis* ; Mycoplasma pneumoniae* ; Mycoplasma* ; Pneumonia* ; Pneumonia, Mycoplasma*

No abstract available.
Anemia, Neonatal* ; Fetal Blood* ; Infant, Newborn

No abstract available.
HIV-1* ; Humans* ; Tumor Necrosis Factor-alpha*

No abstract available.
Uterus*

No abstract available.
Acute Kidney Injury* ; Back Pain*

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