Background: It is presumed that free T4 and thyroid-stimulating hormone (TSH) levels are related to obesity, but the findings are inconsistent. In this study we evaluated T4 and TSH concentrations between normal children and those with obesity and possible correlations between body mass index (BMI) and these markers. Methods: In this prospective study, 190 children who were overweight and obese and 133 children without obesity of the same age and sex were evaluated. Thyroid function tests (TSH, total T4, free T4 and free T3) were measured in all subjects in both groups. Thyroid antibodies (thyroid peroxidase and thyroglobulin) were determined among those with elevated TSH levels. Results: Levels of TSH and total T4 were significantly higher in children with obesity compared with the control group. Subclinical hypothyroidism was significantly higher in children with obesity (14.7%) compared with normal subjects (6.8%, p = 0.02). Among children with obesity and increased TSH levels, 10.7% had positive thyroid peroxidase and thyroglobulin antibodies. There was significantly positive correlation between BMI z score and TSH level (r = 0.198, p < 0.001) and T4 level (r = 0.18, p = 0.001). Conclusion: TSH and total T4 levels are increased in children who are overweight or obese and are a common finding in these children, but the incidence of thyroid antibodies is low in these patients and so could not be accounted for by thyroid autoimmunity. Due to these findings it is possible that increased TSH and total T4 levels are a consequence of obesity and could be reduced by decreasing BMI.
Iron overload is a common finding in chronically transfused β-thalassemia major (β-TM) patients with possible effect on β cell function and insulin resistance. In this study we aimed to evaluate glucose metabolism, insulin resistance and β cell function in β-TM patients. A total of 78 transfusion-dependent β-TM patients and 40 age and sex matched normal children were included. Oral glucose tolerance tests (OGTT) were performed in all subjects. Fasting plasma insulin level, insulin resistance index (IRI) and β cell function index (BFI) were also estimated. β-Thalassemia major patients had significantly more abnormal OGTT than the control group. β-Thalassemia major patients had significantly higher levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) fasting blood sugar and IRI than the control group. Findings between β-thalassemia (β-thal) patients, with and without abnormal OGTT results, were also compared; β-thal patients with abnormal OGTT had significantly higher duration of chelation therapy, serum ferritin levels, AST, ALT and increased IRI and decreased BFI in comparison to patients with normal OGTT. Abnormal glucose metabolism is common in β-TM patients with chelation therapy and multiple transfusions which are attributable to impaired β cells' function and increased insulin resistance.
AbstractsAim of the work To determine the extent and severity of the aforementioned obesity-related atherosclerotic risk factors among school aged children and adolescents. Subjects and methods The sample has included 98 obese (nonsyndromic) and 36 non obese control subjects aged 6-16 years. A questionnaire was filled to evaluate the daily and weekly PA calculated in hours, anthropometry was done and blood pressure was measured, together with assessment of serum lipid profile and levels of fasting blood sugar, ALT, UA, E-selectin and hs CRP. Results 55% of obese group have shown 4 or 5 atherosclerotic RFs. One or more features of abnormal lipid profile were found in 94% of obese group with 73% showing high cholesterol level. ALT and UA were significantly higher in the obese group, similarly E-selectin that was elevated in71% of obese and hs CRP were significantly higher among obese. FBS did not show similar significant elevations. Positive correlations were found between cholesterol, E-selectin and hs CRP with BMI and waist/hip ratio. Conclusion Most of obese children and adolescents do suffer from some risk factors that can lead to an earlier and greater risk for developing atherosclerosis.
A B S T R A C TBackground: Nonalcoholic fatty liver disease (NAFLD) is a very common chronic disorder and obesity is thought to be the most common etiology of fatty infiltration of the liver. Objectives: The objective of this study is to compare the effect of lifestyle intervention alone or in combination with vitamin E therapy in obese pediatric nonalcoholic fatty liver disease (NAFLD). Patients and Methods:In the double-blind placebo study, 33 obese children with NAFLD from 2008 to 2009 were included. Lifestyle intervention (balanced calorie diet, 1300-1800 kcal/d and physical activity) was prescribed to all. The patients were concurrently randomized to receive vitamin E 400 mg/d (n = 17)] or placebo (n = 16). Results: At the end of six months of therapy there was significant change in body mass index, serum aminotransferases, triglycerides, total cholesterol and low density lipoprotein-cholesterol levels in both groups (P <0.001), but the improvement in all these factors was only marginally different between the two groups. Alanine aminotransferase decreased to normal levels in 8 of 17 patients (47.05%) in the lifestyle and vitamin E group, and 7 of 16 patients (43.75%) in lifestyle and placebo group. Similarly, the improvement in the grade of steatosis on ultrasonography after intervention was the same in both groups. Conclusions: lifestyle intervention with diet and physical exercise in obese children with NAFLD were induced weight loss and was associated with a significant improvement in liver function. Vitamin E did not seem to increase the efficacy of lifestyle intervention.
Glycogen storage diseases (GSDs) are caused by abnormalities in enzymes that are involved in the regulation of gluconeogenesis and glycogenolysis. GSD I, an autosomal recessive metabolic disorder, is the most common GSD and has four subtypes. Here, we examined GSD Ia caused by the defective glucose-6-phosphatase catalytic (G6PC) gene. We investigated the frequency of GSD Ia and clarified its molecular aspect in patients with the main clinical and biochemical characteristics of GSD, including 37 unrelated patients with a mean age of three years at the time of diagnosis. All patients belonged to the Azeri Turkish population. Hypoglycaemia and hypertriglyceridaemia were the most frequent laboratory findings. Mutations were detected by performing direct sequencing. Mutation analysis of the G6PC gene revealed that GSD Ia accounted for 11% in GSD patients with involvement of liver. Three patients were homozygous for R83C mutation. In addition, a novel stop mutation, Y85X, was identified in a patient with the typical features of GSD Ia.
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