The ICET-A Recommendations for the Diagnosis and Management of Disturbances of Glucose Homeostasis in Thalassemia Major Patients
De Sanctis, V; Soliman, AT; Yaarubi, SAL; Skordis, N; Khater, D; mohamed, elkholy; Stoeva, I; Fiscina, B; Angastiniotis, M; Daar, S; Kattamis, C; Elsedfy, Heba;
Abstract
Iron overload in patients with thalassemia major (TM) affects glucose regulation and is mediated by several mechanisms. The pathogenesis of glycaemic abnormalities in TM is complex and multifactorial. It has been predominantly attributed to a combination of reduced insulin secretory capacity and insulin resistance. The exact mechanisms responsible for progression from norm glycaemia to overt diabetes in these patients are still poorly understood but are attributed mainly to insulin deficiency resulting from the toxic effects of iron deposited in the pancreas and insulin resistance. A group of endocrinologists, haematologists and paediatricians, members of the International Network of Clinicians for Endocrinopathies in Thalassemia and Adolescence Medicine (ICET-A) convened to formulate recommendations for the diagnosis and management of abnormalities of glucose homeostasis in thalassemia major patients on the basis of available evidence from clinical and laboratory data and consensus practice. The results of their work and discussions are described in this article.
Other data
Title | The ICET-A Recommendations for the Diagnosis and Management of Disturbances of Glucose Homeostasis in Thalassemia Major Patients | Authors | De Sanctis, V; Soliman, AT; Yaarubi, SAL; Skordis, N; Khater, D; mohamed, elkholy ; Stoeva, I; Fiscina, B; Angastiniotis, M; Daar, S; Kattamis, C; Elsedfy, Heba | Keywords | BETA-CELL FUNCTION; IRON OVERLOAD; INSULIN-RESISTANCE; CHELATION-THERAPY; MONITORING-SYSTEM; CENTERED APPROACH; GRADING EVIDENCE; ADULT PATIENTS; TAXONOMY SORT; LIVER IRON | Issue Date | 2016 | Publisher | MATTIOLI 1885 | Journal | MEDITERRANEAN JOURNAL OF HEMATOLOGY AND INFECTIOUS DISEASES | DOI | 10.4084/MJHID.2016.058 | Scopus ID | 2-s2.0-85010904133 | Web of science ID | WOS:000388239500001 |
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