Evaluation Of Glucose Metabolism Disorder: Insulin Resistance And Insulin Receptors In Hyperthyroidism Children

Objective: Hyperthyroidism may cause abnormal glucose metabolism with impaired glucose tolerance,even secondary diabetes mellitus.The purpose of this study was to evaluate features and underlying pathogenesis of glucose metabolism disorder in pediatric patients with hyperthyroidism in order to provid great help to comprehensive diagnosis and treatment of hyperthyroidism.Methods: Fasting, post-prandial 60 minute and post-prandial 120 minute blood glucose were measured using SUPER GLUCOCARD?glucose meter.The levels of insulin,c-peptide,glucagon,cortisol in fasting and post-prandial 60 minute and T3,T4,TSH, anti-thyroglobulin antibody(TGA), anti-microsomal antibody(TMA) in fasting were measured using radio-immunity assay(RIA) in 29 patients with hyperthyroidism were divied into two groups :group one included 10 cases impaired glucose tolerance and group two consisted of 19 cases with normal glucose tolerance. 20 nomal age-matched children served as controls.In addition, erythrocyte fasting andpost-prandial 60 minute insulin receptor of 14 with hyperthyroidism and 7 normal age-matched controls were measured using insulin radioreceptor assay. Results:1.Abnormal glucose metabolism were found in 10 of 29 patients with hyperthyroidism.Incidence of glycometabolic disorder was 50% in patients with more than one year course compared with 9% in cases with less than one year disease course(p<0.05) 2.1n hyperthyroidism with glycometabolic disorder(groupl).Levels of glucose, insulin, insulin/glucose, insulin/glucagon in post-prandial 60 minute were significantly increasing; Post-prandial 60 minute glucose was correlated with glucagon;Numbers of fasting insulin receptor of tall and low affinity in erythrocyte membrane were lower than post-prandial insulin receptor (p<0.05); Avidity of post-prandial insulin receptor of low affinity in erythrocyte membrane are lower than it of fasting insulin receptor (p<0.05); Post-prandial insulin receptor of low affinity was positively correlated with insulin andc-peptide(rl=0.9054,r2=0.9002,p<0.05)3.In TGA and TMA, normal matched control group are lower than in patients with hyperthyroidism (p<0.01).Conclusions:1. Glycometabolic disorder with impaired glucose tolerance and insulin resistance are present in patients with hyperthyroidism. The longer was course of the disease,the higher was incidence of glycometabolism.2. Glycometabolic disorder is possibl correlated with autoimmunity.The impaired B-islet cells, decreased the numbers and altered affinity of insulin receptor on Target cells might play important roles in themechanisms of glycometabolic disorder and insulin resistance in children with hyperthyroidism 3. Close monitering of glycometabolic status will be very important in the treatment of hyperthyroidism in childhood. The appropriate disposal is necessary, once glycometabolic abnormality appears.