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dc.contributor.authorShalet, Stephen M
dc.date.accessioned2010-11-09T17:01:05Z
dc.date.available2010-11-09T17:01:05Z
dc.date.issued1986-08
dc.identifier.citationIrradiation-induced growth failure. 1986, 15 (3):591-606 Clin Endocrinol Metaben
dc.identifier.issn0300-595X
dc.identifier.pmid2429795
dc.identifier.urihttp://hdl.handle.net/10541/115187
dc.description.abstractShort stature may complicate the treatment during childhood of brain tumours and, to a lesser extent, ALL. A number of factors may be responsible, including spinal irradiation, malnutrition, recurrent tumour, chemotherapy, precocious puberty and radiation-induced GH deficiency. GH is always the first pituitary hormone to be affected by radiation damage to the hypothalamic-pituitary axis but larger radiation doses may result in panhypopituitarism. Some children retain normal GH responses to certain provocative stimuli, although physiological GH secretion is reduced. Nonetheless, in children suspected of radiation-induced GH deficiency, pharmacological tests of GH secretion remain useful, the ITT being the test of choice because of the marked radiation sensitivity of the GH response to hypoglycaemia. The hypothalamus is more radiosensitive than the pituitary. In many patients with radiation-induced GH deficiency, the damage appears to be at the hypothalamic level resulting in a deficiency of endogenous GRF. Treatment with synthetic GRF may provide an alternative to GH therapy in such children. Finally, there is no evidence to suggest that GH therapy given to a child with radiation-induced GH deficiency might induce a brain tumour recurrence or a relapse of ALL.
dc.language.isoenen
dc.subjectBrain Canceren
dc.subjectLymphoid Leukaemiaen
dc.subjectRadiation-Induced Leukaemiaen
dc.subjectRadiation-Induced Canceren
dc.subject.meshAdult
dc.subject.meshAnimals
dc.subject.meshBrain Neoplasms
dc.subject.meshChild
dc.subject.meshChild, Preschool
dc.subject.meshDevelopmental Disabilities
dc.subject.meshGrowth Disorders
dc.subject.meshGrowth Hormone
dc.subject.meshGrowth Hormone-Releasing Hormone
dc.subject.meshHumans
dc.subject.meshHypothalamo-Hypophyseal System
dc.subject.meshLeukemia, Lymphoid
dc.subject.meshLeukemia, Radiation-Induced
dc.subject.meshNeoplasms, Radiation-Induced
dc.subject.meshRadiation Injuries, Experimental
dc.subject.meshRadiotherapy
dc.subject.meshRetrospective Studies
dc.titleIrradiation-induced growth failure.en
dc.typeArticleen
dc.identifier.journalClinics in Endocrinology and Metabolismen
html.description.abstractShort stature may complicate the treatment during childhood of brain tumours and, to a lesser extent, ALL. A number of factors may be responsible, including spinal irradiation, malnutrition, recurrent tumour, chemotherapy, precocious puberty and radiation-induced GH deficiency. GH is always the first pituitary hormone to be affected by radiation damage to the hypothalamic-pituitary axis but larger radiation doses may result in panhypopituitarism. Some children retain normal GH responses to certain provocative stimuli, although physiological GH secretion is reduced. Nonetheless, in children suspected of radiation-induced GH deficiency, pharmacological tests of GH secretion remain useful, the ITT being the test of choice because of the marked radiation sensitivity of the GH response to hypoglycaemia. The hypothalamus is more radiosensitive than the pituitary. In many patients with radiation-induced GH deficiency, the damage appears to be at the hypothalamic level resulting in a deficiency of endogenous GRF. Treatment with synthetic GRF may provide an alternative to GH therapy in such children. Finally, there is no evidence to suggest that GH therapy given to a child with radiation-induced GH deficiency might induce a brain tumour recurrence or a relapse of ALL.


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