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The Pancreatic changes affecting glucose homeostasis in transfusion dependent β- thalassemia (TDT): a short review

Quisisana Hospital, Ferrara. vdesanctis@libero.it. Department of Pediatrics, Division of Endocrinology, Hamad General Hospital, Doha, Qatar and Department of Pediatrics, Division of Endocrinology, Alexandria University Children's Hospital, Alexandria, Egypt. atsoliman56@gmail.com. Department of Diabetes and Endocrinology, Whittington Hospital, University College London, London, N19 5NF UK. ptzoulis@yahoo.co.uk. Department of Haematology, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Sultanate of Oman. sf.daar@gmail.com. Department of Pediatrics, NYU School of Medicine, New York, NY, USA. bfiscina@yahoo.com. First Department of Paediatrics, National Kapodistrian University of Athens 11527, Greece. christos.kattamis@gmail.com.

Acta bio-medica : Atenei Parmensis. 2021;92(3):e2021232
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Abstract
BACKGROUND The natural history of the glycometabolic state in transfusion-dependent β-thalassemia (TDT) patients is characterized by a deterioration of glucose tolerance over time. AIMS This review depicts our current knowledges on the complex and multifacet pathophysiologic mechanisms implicated in the development of alteration of glucose homeostasis in patients with TDT. SEARCH STRATEGY A systematic search was done on December 2020 including Web of Science (ISI), Scopus, PubMed, Embase, and Scholar for papers published in the last 20 years. Moreover, we checked the reference lists of the relevant articles and previously performed reviews for additional pertinent studies. The personal experience on the care of patients with thalassemias is also reported. CONCLUSION A regular packed red blood cells (PRBCs) transfusion program, optimization of chelation therapy, and prevention and treatment of liver infections are critical to achieve adequate glucometabolic control in TDT patients. Many exciting opportunities remain for further research and therapeutic development.
Study details
Study Design : Systematic Review
Language : eng
Credits : Bibliographic data from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine