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dc.contributor.authorGhergherehchi, R|| Habibzadeh, A
dc.date.accessioned2018-08-26T07:45:22Z
dc.date.available2018-08-26T07:45:22Z
dc.date.issued2015
dc.identifier10.3109/03630269.2014.999081
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/48344
dc.description.abstractIron overload is a common finding in chronically transfused beta-thalassemia major (beta-TM) patients with possible effect on beta cell function and insulin resistance. In this study we aimed to evaluate glucose metabolism, insulin resistance and beta cell function in beta-TM patients. A total of 78 transfusion-dependant beta-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 beta cell function index (BFI) were also estimated. beta-Thalassemia major patients had significantly more abnormal OGTT than the control group. beta-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 beta-thalassemia (beta-thal) patients, with and without abnormal OGTT results, were also compared; beta-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 beta-TM patients with chelation therapy and multiple transfusions which are attributable to impaired b cells' function and increased insulin resistance.
dc.language.isoEnglish
dc.relation.ispartofHEMOGLOBIN
dc.subjectbeta Cell function index (BFI)|| beta-thalassemia (beta-thal)|| beta-thalassemia major (beta-TM)|| glucose intolerance|| insulin resistance
dc.titleInsulin Resistance and beta Cell Function in Patients with beta-Thalassemia Major
dc.typeArticle
dc.citation.volume39
dc.citation.issue1
dc.citation.spage69
dc.citation.epage73
dc.citation.indexWeb of science


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