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    Pathophysiology of radiation-induced growth hormone deficiency: efficacy and safety of GH replacement.

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    Authors
    Darzy, Ken H
    Shalet, Stephen M
    Affiliation
    Department of Endocrinology, Christie Hospital NHS Trust, Wilmslow Road, Withington, Manchester M20 4BX, United Kingdom.
    Issue Date
    2006-07
    
    Metadata
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    Abstract
    Radiation-induced growth hormone deficiency (GHD) is primarily due to hypothalamic damage. GH secretion by the pituitary may be affected either secondary to some degree of quantitative deprivation of hypothalamic input or, if the radiation dose is high enough, by direct pituitary damage. As a consequence, the neurosecretory profile of GH secretion in an irradiated patient remains pulsatile and qualitatively intact. The frequency of pulse generation is unaffected, but the amplitude of the GH pulses is markedly reduced. Over the last 25 years, the final heights achieved by children receiving GH replacement for radiation-induced GHD have improved; these improvements are attributable to refinements in GH dosing schedules, increased use of GnRH analogues for radiation-induced precocious puberty, and a reduced time interval between completion of irradiation and initiation of GH therapy. When retested at the completion of growth, 80-90% of these teenagers are likely to prove severely GH deficient and, therefore, will potentially benefit from GH replacement in adult life. Such long-term GH treatment in patients treated previously for a brain tumor means that critical and continuous surveillance must be devoted to the risk of tumor recurrence and the possibility of second neoplasms.
    Citation
    Pathophysiology of radiation-induced growth hormone deficiency: efficacy and safety of GH replacement. 2006, 16 Suppl A:S30-40 Growth Horm. IGF Res.
    Journal
    Growth Hormone & IGF Research
    URI
    http://hdl.handle.net/10541/72598
    DOI
    10.1016/j.ghir.2006.03.002
    PubMed ID
    16624606
    Type
    Article
    Language
    en
    ISSN
    1096-6374
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.ghir.2006.03.002
    Scopus Count
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