The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

The prevalence of childhood and adolescent obesity has increased and exacerbated during the coronavirus disease 2019 pandemic, both in Korea and globally. Childhood and adolescent obesity poses significant risks for premature morbidity and mortality. The development of serious comorbidities depends not only on the duration of obesity but also on the age of onset. Obesity in children and adolescents affects almost all organ systems, including the endocrine, cardiovascular, gastrointestinal, reproductive, nervous, and immune systems. Obesity in children and adolescents affects growth, cognitive function, and psychosocial interactions during development, in addition to aggravating known adult comorbidities such as type 2 diabetes mellitus, hypertension, dyslipidemia, nonalcoholic fatty liver disease, obstructive sleep apnea, and cancer. Childhood and adolescent obesity are highly associated with increased cardiometabolic risk factors and prevalence of metabolic syndrome. The risk of cardiovascular and metabolic diseases in later life can be considerably decreased by even a small weight loss before the onset of puberty. Childhood and adolescent obesity is a disease that requires treatment and is associated with many comorbidities and disease burdens. Therefore, early detection and therapeutic intervention are crucial.

PURPOSE: The aim of this study was to investigate the effects of growth hormone (GH) therapy and sex steroid replacement on glucose metabolism in Turner syndrome (TS). METHODS: We analyzed the clinical and laboratory data of 61 children and adults with TS. The results of oral glucose tolerance test or fasting glucose with insulin levels were obtained, and the changes in insulin resistance index determined using the homeostasis model of assessment (HOMA-IR) and insulin sensitivity (quantitative insulin sensitivity check index, QUICKI) were analyzed. Data were presented in median and range. RESULTS: With GH treatment (n = 21; median duration 38 months, range 5 to 96 months), the HOMA-IR increased to levels higher than that before treatment (2.48 vs. 1.18, P = 0.035), and QUICKI was decreased (0.33 vs. 0.37, P = 0.035). After estrogen was added (n = 13, median duration 11 months, range 2 to 55 months) to the therapy, the decrease in HOMA-IR tended to be greater and QUICKI tended to be higher (0.34 vs. 0.37, P = 0.046) than that during GH treatment alone (2.16 vs. 1.36, P = 0.055). However, there were no significant differences between GH with estrogen treatment and sex hormone cyclic replacement therapy (n = 7) in terms of changes in the HOMA-IR and QUICKI. With GH treatment, insulin resistance tended to increase and the insulin sensitivity was tended to decrease to a level lower than that before treatment, but recovered when estrogen was added to the treatment regimenon and maintained after GH therapy was discontinued and during cyclic treatment with sex steroids. CONCLUSION: The incidence of glucose intolerance or the levels of type 2 diabetes mellitus did not increased during or after GH treatment in patients with TS, but insulin resistance increased transiently; therefore, close monitoring of changes in glucose metabolism is essential during GH treatment. Early replacement of estrogen in addition to GH therapy when growth is nearly accomplished might prevent the aggravation of insulin resistance in TS patients.
Adult ; Child ; Diabetes Mellitus, Type 2 ; Estrogens ; Fasting ; Glucose ; Glucose Intolerance ; Glucose Tolerance Test ; Gonadal Steroid Hormones ; Growth Hormone ; Homeostasis ; Humans ; Incidence ; Insulin ; Insulin Resistance ; Steroids ; Turner Syndrome

PURPOSE: The aim of this study was to investigate the effects of growth hormone (GH) therapy and sex steroid replacement on glucose metabolism in Turner syndrome (TS). METHODS: We analyzed the clinical and laboratory data of 61 children and adults with TS. The results of oral glucose tolerance test or fasting glucose with insulin levels were obtained, and the changes in insulin resistance index determined using the homeostasis model of assessment (HOMA-IR) and insulin sensitivity (quantitative insulin sensitivity check index, QUICKI) were analyzed. Data were presented in median and range. RESULTS: With GH treatment (n = 21; median duration 38 months, range 5 to 96 months), the HOMA-IR increased to levels higher than that before treatment (2.48 vs. 1.18, P = 0.035), and QUICKI was decreased (0.33 vs. 0.37, P = 0.035). After estrogen was added (n = 13, median duration 11 months, range 2 to 55 months) to the therapy, the decrease in HOMA-IR tended to be greater and QUICKI tended to be higher (0.34 vs. 0.37, P = 0.046) than that during GH treatment alone (2.16 vs. 1.36, P = 0.055). However, there were no significant differences between GH with estrogen treatment and sex hormone cyclic replacement therapy (n = 7) in terms of changes in the HOMA-IR and QUICKI. With GH treatment, insulin resistance tended to increase and the insulin sensitivity was tended to decrease to a level lower than that before treatment, but recovered when estrogen was added to the treatment regimenon and maintained after GH therapy was discontinued and during cyclic treatment with sex steroids. CONCLUSION: The incidence of glucose intolerance or the levels of type 2 diabetes mellitus did not increased during or after GH treatment in patients with TS, but insulin resistance increased transiently; therefore, close monitoring of changes in glucose metabolism is essential during GH treatment. Early replacement of estrogen in addition to GH therapy when growth is nearly accomplished might prevent the aggravation of insulin resistance in TS patients.
Adult ; Child ; Diabetes Mellitus, Type 2 ; Estrogens ; Fasting ; Glucose ; Glucose Intolerance ; Glucose Tolerance Test ; Gonadal Steroid Hormones ; Growth Hormone ; Homeostasis ; Humans ; Incidence ; Insulin ; Insulin Resistance ; Steroids ; Turner Syndrome

Acute pancreatitis is associated with a wide variety of infectious agents including mumps, hepatitis B virus, Coxsackie virus, Mycoplasma, Legionella, Aspergillus and Toxoplasma. There are a few reports of acute pancreatitis caused by Mycoplasma pneumoniae infection abroad, but rare in Korea. We treated a case of acute pancreatitis in a 13-year-old girl who presented with nausea, vomiting, diarrhea and severe abdominal pain. The clinical and laboratory findings led to the diagnosis of acute pancreatitis; the cause was confirmed by serological evidence of mycoplasma pneumoniae infection. We report acute pancreatitis caused by mycoplasma pneumoniae infection and review the literature.
Abdominal Pain ; Adolescent ; Aspergillus ; Diagnosis ; Diarrhea ; Female ; Hepatitis B virus ; Humans ; Korea ; Legionella ; Mumps ; Mycoplasma pneumoniae* ; Mycoplasma* ; Nausea ; Pancreatitis* ; Pneumonia, Mycoplasma* ; Toxoplasma ; Vomiting

The steroid cell tumor, not otherwise specified, constitutes only 0.1% of ovarian malignancies and was asymptomatic in 3.3-25% In Korea, three reported cases of steroid cell tumors were endocrinologically symptomatic and were managed with laparotomy. However, there was no reports of such case without any endocrinologically symptoms. We present a 17 years old patient with huge pelvic mass that were managed with combined ultrasonographically guided drainage and laparoscopically excision and proven to be an asymptomatic steroid cell tumor of ovary, with brief review of literature.
Adolescent ; Drainage ; Female ; Humans ; Korea ; Laparoscopy ; Laparotomy ; Ovary

PURPOSE: Environmental endocrine disruptors may affect the endocrine system or sexual development in children. Several recent studies have focused on indoor and dietary pollutants such as di-(2-ethylhexyl) phthalate (DEHP), which is used as a plastic softener, and bisphenol A, which is used in food-packaging materials. Despite the accumulation of data and the substantial arguments implicatinf these pollutants in endocrinal disorders, no clear evidence has been established yet. Thus, we assessed the serum levels of DEHP and bisphenol A in patients diagnosed with idiopathic central precocious puberty (CPP) to estimate the possible environmental hazards associated with increasing number of cases of precocious puberty. METHODS: The study included 30 patients (29 girls and 1 boy) with idiopathic CPP and 30 normal control children who visited the pediatric endocrinology clinic. CPP was diagnosed on the basis of clinical & hormonal tests, including the gonadotropin-releasing hormone-stimulation test. The serum DEHP and bisphenol A levels were analyzed by gas chromatography/mass spectrometry. RESULTS: The mean chronological ages (CA) in the idiopathic CPP and control groups were similar (8.6+/-0.9 vs. 7.8+/-1.1 years). However, the overall growth stage in the CPP group was advanced. The CPP group had a significantly higher height SDS (1.3+/-1.0 vs. -0.4+/-1.1, P<0.005) and weight SDS (1.3+/-1.3 vs. -0.2+/-1.3, P<0.005) than the control group. Bone age was significantly more advanced in the CPP group than in the control group (BA-CA:14.6+/-9.4 months vs. 0.8+/-15.3 months, P<0.005). While the serum bisphenol A levels were not significantly different between the groups (11.2+/-10.3 vs.16.2+/-12.5 ng/mL), the DEHP levels were significantly higher in the CPP group than in the control group (159.01+/-92.78 vs. 103.55+/-92.98 ng/mL, P<0.05). CONCLUSION: This study suggests that DEHP, one of most commonly used plasticizers, may be an etiologic factor for precocious puberty.
Benzhydryl Compounds ; Child ; Diethylhexyl Phthalate ; Endocrine Disruptors ; Endocrine System ; Endocrinology ; Hazardous Substances ; Humans ; Phenols ; Phthalic Acids ; Piperazines ; Plasticizers ; Plastics ; Puberty, Precocious ; Sexual Development

PURPOSE: The diagnosis of cortical dysplasia(CD) and microdysgenesis(MD) is valuable because they often cause childhood intractable epilepsy. This study is to analyze clinical manifestations, EEG findings, and imaging features based on the pathologic diagnosis(cortical dysplasia and microdysgenesis) in childhood intractable epilepsy with surgical treatment. METHODS: We performed retrospective studies and analyzed 27 patients with MCD diagnosed by pathologic findings after brain lobectomy for intractable epilepsy from October 2003 to September 2006 in our hospital. We compared their clinical characteristics, EEGs, neuroimaging studies including MRI, and FDG-PET. We analyzed the locations of malformations of cortical development(MCD). The surgical outcomes were reviewed. RESULTS: There were no pathognomonic seizure types or EEG findings for microdysgenesis. The clinical and EEG features of microdysgenesis were similar to those of cortical dysplasia. Only 6(37 percent) out of 16 microdysgenesis patients showed normal MRI findings and also 2(18 percent) out of 10 cortical dysplasia patients showed normal MRI findings. The most common location of MCD was frontal lobe in both of the groups, followed by temporal lobe. 10(63%) out of 16 microdysgenesis patients and 9 (90%) out of 10 cortical dysplasia patients became seizure free. The locations of MCD was not related to the prognosis of the outcomes. All the patients who had had developmental delay showed improvement in development after the surgery. CONCLUSION: There were no significant differences in gender, seizure onset age, duration of seizures, seizure types, EEG findings, and MCD locations between CD and MD. The seizure outcomes were better in CD than in MD. All the patients whose pre- and post-oprative developmental status were compared showed developmental improvement.
Age of Onset ; Brain ; Child* ; Diagnosis ; Electroencephalography ; Electrophysiology* ; Epilepsy* ; Frontal Lobe ; Humans ; Magnetic Resonance Imaging ; Malformations of Cortical Development* ; Neuroimaging* ; Prognosis ; Retrospective Studies ; Seizures ; Temporal Lobe