Ketogenic diet is a high-fat, low-carbohydrate, low-protein diet used in the treatment of epilepsy since 1920's. Recently, it's use for intractable epilepsy in childhood has increased. Complications of ketogenic diet are known to include dehydration, vomiting, diarrhea, renal stones, metabolic derangement, hypercholesterolemia and refusal to eat. We experienced two cases of renal stones in children with intractable epilepsy during ketogenic diet.
Child ; Dehydration ; Diarrhea ; Diet, Protein-Restricted ; Disulfiram ; Epilepsy ; Humans ; Hypercholesterolemia ; Ketogenic Diet* ; Vomiting

PURPOSE: The gonadotropin-releasing hormone (GnRH) test results of girls with precocious puberty were analyzed to determine whether this test can efficiently and clearly differentiate between central precocious puberty (CPP) and other disorders. METHODS: Clinical and laboratory data of 54 girls with precocious pubertal signs were reviewed. Intravenous GnRH test was performed with blood samples obtained at 0, 30, 60, and 90 minutes. A peak luteinizing hormone (LH) level of > or =5.0 IU/L was indicative of CPP. RESULTS: Of the 40 girls with CPP, 36 (90.0%), 3 (7.5%), and 1 (2.5%) showed peak LH levels at 30, 60, and 90 minutes, respectively. A percentage of girls whose peak LH > or =5.0 IU/L up to 30, 60, and 90 minutes was 92.5%, 100%, and 100%, respectively. The peak LH/follicle stimulating hormone (FSH) ratio of girls with CPP was 0.89+/-0.49 and was <1 in 16 of the 40 girls (40.0%). Girls with peak LH/FSH ratio of >1.0 showed higher chronological age (CA) (8.3+/-0.6 vs. 7.7+/-1.0 years, P=0.033), bone age (BA) (10.9+/-0.8 vs. 9.7+/-1.1 years, P=0.001), and BA-CA difference (2.6+/-0.7 vs. 2.0+/-0.7 years, P=0.009) than those of girls with peak LH/FSH ratio of < or =1.0. Higher percentage of girls with peak LH/FSH ratio of >1.0 showed advanced breast development (> or =Tanner III) (93.7% vs. 41.7%, P=0.001). CONCLUSION: LH levels after 30 and 60 minutes of intravenous GnRH administration are the most useful for diagnosing CPP in girls.
Breast ; Gonadotropin-Releasing Hormone ; Luteinizing Hormone ; Piperazines ; Puberty, Precocious

OBJECTIVES: Repetitive and stereotyped behaviors are core symptoms in children with autism spectrum disorders (ASD). The purpose of our study was to investigate the frequency of motor stereotypes in ASD children and their clinical features. METHODS: Among 171 ASD children (age range, 3-15), the ASD group with motor stereotypes was defined according to two items in the Korean version of Autism Diagnostic Interview-Revised (K-ADI-R). We compared the clinical features, behavior problems and severity of other domains in the K-ADI-R and executive functions between the ASD group with motor stereotypes and the ASD group without motor stereotypes. RESULTS: Ninety (52.6%) of 171 ASD children had motor stereotypes. The ASD group with motor stereotypes had a lower intelligence quotient score (62.23 vs. 84.94, p<.001) compared to the ASD group without motor stereotypes. The ASD group with motor stereotypes had more impairments in the social interaction domain [adjusted odds ratio (AOR) 1.11, p=.001] and communication domain (AOR 1.15, p=.008). Thought problems and lethargy were more frequent in the ASD group with motor stereotypes than the ASD group without motor stereotypes (AOR 2.059, p=.034 ; adjusted OR 1.045, p=.046). However, no significant differences in executive function were observed between the ASD group with motor stereotypes and the ASD group without motor stereotypes. CONCLUSION: The ASD group with motor stereotypes showed more impairment in social interaction and communication domains, which are core symptoms of autism. Motor stereotypes may indicate greater severity of ASD.
Autistic Disorder ; Autism Spectrum Disorder* ; Child* ; Executive Function ; Humans ; Intelligence ; Interpersonal Relations ; Lethargy ; Odds Ratio ; Stereotyped Behavior

OBJECTIVE: Attention deficit hyperactivity disorder (ADHD) is frequently comorbid with a variety of psychiatric disorders. Among them, bipolar disorder (BPD) has especially attracted growing interest. This is partly due to the fact that early onset BPD has been frequently misdiagnosed as ADHD because of symptomatic overlap. The aim of the present study is to find the differences in demographic data and clinical features of ADHD+BPD and ADHD in children and adolescents. METHOD: Children and adolescents patients participating in the present study have been enrolled at the child psychiatric clinic since 2004. 14 patients meeting the DSM-IV criteria for ADHD+BPD and 19 patients meeting the criteria for ADHD and 15 healthy comparison subjects were recruited. All groups were evaluated through the Schedule for Affective disorders and Schizophrenia for School-Age Children-Present and Life Time version-Korean version (K-SADS-PL-K). Demographic data and clinical characteristics of the subjects were also collected. Parents were asked to complete the Child Behavior Check List (CBCL) and the Toddler Temperamental Scale (TTS) clinical ratings were obtained using the Young Mania Rating Scale (YMRS), the Children's Depression Iventory (CDI) and the Dupaul ADHD scale. Clinical variables between ADHD+BPD and ADHD were analyzed using the Mann-Whitney U test. YMRS, CDI, Dupaul ADHD scale (inattention and hyperactivity), CBCL, and TTS among the three groups were analyzed using the Kruskal-Wallis test with post-hoc Mann-Whitney U test. RESULTS: 1) ADHD+BPD group had an earlier onset age of ADHD than ADHD group 2) ADHD+BPD group had more co-morbid psychiatric disorders than ADHD group. 3) Compared to ADHD group, ADHD+BPD had more psychiatric family history, especially mood disorders. 4) ADHD+BPD group had prodromal symptoms such as irritability, anger dyscontrol and academic dysfunction, compared to ADHD group who rarely showed prodromal symptoms. 5) ADHD+BPD group had higher ADHD scores than the ADHD group in the Dupaul ADHD inattentive scale. 6) In global functions of CBCL, ADHD+BPD group showed more impaired functions at home and school than ADHD group. 7) In Attention diagnostic system (ADS), ADHD+BPD group had more omission and commission errors than ADHD group, especially in the visual system. 8) In the subtests of the IQ profile, ADHD+BPD group had lower arithmetic and block design scores than ADHD group. CONCLUSION: Clinicians have to rule out underlying bipolarity in children and adolescents with ADHD who show earlier age of onset and severe clinical features. Bipolarity should be explored intensively in ADHD children and adolescents who have early onset of symptoms and severe functional impairment.
Adolescent ; Age of Onset ; Anger ; Appointments and Schedules ; Attention Deficit Disorder with Hyperactivity ; Bipolar Disorder* ; Child ; Child Behavior ; Depression ; Diagnostic and Statistical Manual of Mental Disorders ; Humans ; Mood Disorders ; Parents ; Prodromal Symptoms ; Schizophrenia ; Temperament

AMP-activated protein kinase (AMPK), an enzyme involved in energy homeostasis, regulates inflammatory responses, but its precise mechanisms are not fully understood. Recent evidence has shown that resveratrol (RES), an AMPK activator, reduces prostaglandin E2 production in lipopolysaccharide (LPS)-treated microglia. Here, we examined the effect of RES on nuclear factor kappa B (NF-kappaB) dependent cyclooxygenase (COX)-2 activation in LPS-treated RWA 264.7 macrophages. We found that treatment with RES increased AMPK activation. AMPK and acetyl CoA carboxylase phosphorylation were attenuated in cells treated with LPS+RES, compared to cells treated with LPS alone. RES inhibited tumor necrosis factor (TNF)-alpha and TNF receptor 1 in LPS-treated cells. Finally, RES inhibited LPS-induced NF-kappaB translocation into the nucleus and COX-2 expression. Moreover, the effects of 5-aminoimidazole-4-carboxamide ribose and compound C were consistent with the effects of RES in LPS-treated cells. Taken together, these results suggest that the anti-inflammatory action of RES in RAW 264.7 macrophages is dependent on AMPK activation and is associated with inhibition of the LPS-stimulated NF-kappaB-dependent COX-2 signaling pathway.
Acetyl-CoA Carboxylase ; AMP-Activated Protein Kinases ; Dinoprostone ; Homeostasis ; Macrophages ; Microglia ; NF-kappa B ; Phosphorylation ; Prostaglandin-Endoperoxide Synthases ; Receptors, Tumor Necrosis Factor ; Ribose ; Stilbenes ; Tumor Necrosis Factor-alpha