ABSTRACT
Herpes simplex virus has rarely been identified as a cause of esophagitis in immunocompetent children. This virus affects predominantly males presenting with symptoms of fever, odynophagia, dysphagia, and retrosternal pain of acute onset. Esophagoscopy typically reveals exudative well-circumscribed ulcerations of the distal and/or mid-esophagus. Further investigations using biopsy, viral culture, polymerase chain reaction (PCR), and seroconversion of antibodies to Herpes simplex are recommended to assist with a definitive diagnosis. This esophagitis is often a self-limited infection in immunocompetent children. Nevertheless, antiviral treatment may expedite symptom relief with Herpes simplex virus infection. It is imperative to document herpes esophagitis in cases with subsequent severe odynophagia in immunocompetent children. Here we present the case of a 12-year-old immunocompetent boy with herpes esophagitis.
Subject(s)
Child , Humans , Male , Antibodies , Biopsy , Deglutition Disorders , Esophagitis , Esophagoscopy , Fever , Herpes Simplex , Methylmethacrylates , Polymerase Chain Reaction , Polystyrenes , Simplexvirus , Ulcer , VirusesABSTRACT
An unconscious 5-year-old girl was admitted to the Intensive Care Unit. She was neglected by her parents; she suffered from inadequate nutritional, medical and emotional care. The girl appeared to be emotionally detached, dehydrated and malnourished; she had edematous extremities, moderately bruised skin and brittle coarse hair. Laboratory testing showed electrolyte imbalance, anemia, pneumonia, copper deficiency, and liver dysfunction in addition to severe protein-energy malnutrition (PEM). Medical intervention was followed by improvement of most of the symptoms. During the rehabilitation phase, the patient showed a voracious appetite and gained weight too fast. The liver became enlarged and the patient developed a mild fever due to excessive nutrition. The microcytic anemia with severe PEM did not responded to iron supplementation possibly due to the copper deficiency. Addition of copper without zinc and iron helped to improve the anemia. The patient was discharged to a childcare center where she received cognitive and psychosocial therapy.
Subject(s)
Child , Child , Child, Preschool , Female , Humans , Anemia , Appetite , Child Abuse , Copper , Extremities , Fever , Hair , Intensive Care Units , Iron , Liver , Liver Diseases , Malnutrition , Parents , Pneumonia , Protein-Energy Malnutrition , Rehabilitation , Skin , ZincABSTRACT
PURPOSE: TATA box mutation/polymorphism in the promoter region of the bilirubin uridinediphosphoglucuronate glucuronosyltransferase 1A1 (UGT-1A1) gene is known to be an etiology of hyperbilirubinemia. This study examined if a TATA box mutation/polymorphism in UGT-1A1 gene promoter could be associated with the development of severe early neonatal jaundice in Korean infants. METHODS: Thirty-nine neonatal jaundice patients and 40 controlled infants were analyzed for UGT-1A1 promoter genotypes by using DNA sequencing. RESULTS: The homozygote for (TA)7TAA mutation was not found in this study. Comparison of the prevalence of UGT-1A1 promoter (TA)7TAA heterozygotes revealed no difference between the group with jaundice and the controlled group (15.4% vs. 10%). The peak bilirubin level was higher and the onset of jaundice was earlier in the jaundice group with (TA)7TAA heterozygote compared to the jaundice group without (TA)7TAA heterozygote (23.2+/-1.0 mg/dL vs. 19.7+/-2.4 mg/dL, P=0.004, 5.0+/-1.5 days vs. 8.3+/-4.1 days, P= 0.057). CONCLUSION: The results of this study showed that TATA box polymorphism in UGT-1A1 gene promoter did not increase the prevalence of severe early neonatal jaundice in Korean infants.
Subject(s)
Humans , Infant , Infant, Newborn , Bilirubin , Genotype , Glucuronosyltransferase , Heterozygote , Homozygote , Hyperbilirubinemia , Hyperbilirubinemia, Neonatal , Jaundice , Jaundice, Neonatal , Prevalence , Promoter Regions, Genetic , Sequence Analysis, DNA , TATA BoxABSTRACT
PURPOSE: Currently many studies have confirmed the relationship between serum adiponectin and its influence on insulin resistance in adults. But physiologic insulin resistance due to changes in sex hormones exists during puberty, which prohibits us from knowing the influence of adiponectin to insulin resistance in this population. In this study, we investigated the influence of adiponectin on insulin resistance in children and adolescents. METHODS: 18 obese children, from the OPD were selected. From All subjects, blood was sampled after overnight fasting, adiponectin, lipid profiles, AST, ALT, fasting glucose and insulin levels were measured to evaluate correlations with adiponectin. The group were divided into subgroups by BMI, sex and HOMA-IR values. All variables were compared for differences and relationships. RESULTS: Obese groups showed decrease in adiponectin and showed increased insulin. HOMA-IR values were increased in the obese group. In all study participants, adiponectin showed significant correlation with triglyceride and HDL. But adiponectin showed no significant correlation with HOMA-IR, insulin and glucose. In the obese group adiponectin showed no correlation with HOMA-IR, insulin and glucose. HOMA-IR showed significant correlation with BMI, body weight and age. There were no sexual differences in adiponectin, insulin and HOMA-IR values. Insulin resistant group showed decrease in adiponectin but had no statistical significance. CONCLUSION: Decreased adiponectin levels and increased insulin resistance were observed in obese children but adiponectin showed no correlation with insulin resistance in children and adolescence. Factors other than adiponectin may play a more significant role in insulin resistance in this age group.