Abstract
Advances in transfusion and chelation therapy have significantly increased the life expetancy of patients with homozygous β-thalassemia. However, a variety of endocrine abnormalities frequently occur in such patients. A number of studies have shown that as thalassemic patients approach the age of puberty, a percentage develop growth retardation [1]. The growth failure of these patients has been attributed to hypothyroidism, delayed sexual maturation, hypogonadism, zinc deficit, and desferrioxamine toxicity. The aim of the present investigation was to evaluate a possible role of the GHRH-GH-IGF-I axis dysfunction in growth failure in homozygouys β-thalassemia.
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© 1995 Springer-Verlag Berlin Heidelberg
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Galati, M.C. et al. (1995). Growth in Homozygous β-Thalassemic Patients. In: Andò, S., Brancati, C. (eds) Endocrine Disorders in Thalassemia. Springer, Milano. https://doi.org/10.1007/978-88-470-2183-9_16
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DOI: https://doi.org/10.1007/978-88-470-2183-9_16
Publisher Name: Springer, Milano
Print ISBN: 978-88-470-2185-3
Online ISBN: 978-88-470-2183-9
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