2022 Clinical practice guidelines for central precocious puberty of Korean children and adolescents

The Committee of Central Precocious Puberty of Korean Pediatrics and Adolescents of the Korean Society of Pediatric Endocrinology has newly developed evidence-based 2022 clinical practice guidelines for central precocious puberty in Korean children and adolescents. These guidelines provide the grade of recommendations, which includes both the strength of recommendations and the level of evidence. In the absence of sufficient evidence, recommendations are based on expert opinion. These guidelines have been revised and supplement the previous guidelines "Clinical Guidelines for Precocious Puberty 2011," and are drawn from a comprehensive review of the latest domestic and international research and the grade of recommendation appropriate to the domestic situation. This review summarizes the newly revised guidelines into 8 key questions and 27 recommendations and consists of 4 sections: screening, diagnosis, treatment, and long-term outcome of central precocious puberty.

Changes in the Levels of Insulin Resistance after Growth Hormone Therapy and/or Sex Steroid Replacement in Turner Syndrome / 대한소아내분비학회지

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.

Changes in the Levels of Insulin Resistance after Growth Hormone Therapy and/or Sex Steroid Replacement in Turner Syndrome / 대한소아내분비학회지

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.

Determination of Serum Di-(2-ethylhexyl) Phthalate and Bisphenol A Level in Children with Idiopathic Central Precocious Puberty / 대한소아내분비학회지

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.

Cortical Dysplasia and Microdysgenesis; Correlations between Clinical Feaures, Neuroimaging and Electrophysiology after Lobectomy for Intractable Epilepsy in Children

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.

A Case Report of Acute Pancreatitis Caused by Mycoplasma Pneumoniae Infection / 대한소아소화기영양학회지

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.