Evaluation of growth hormone release and human growth hormone treatment in children with cranial irradiation-associated short stature

Romshe, Carolyn A.; Zipf, William B.; Miser, Angela W.; Miser, James S.; Sotos, Juan F.; Newton, William A.

doi:10.1016/s0022-3476(84)80988-9

Cited by 100 publications

(34 citation statements)

References 18 publications

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“…The reduction of height SDS during therapy has been described by several authors [2,3,10,[20][21][22][23]25] but not all [4,8,9,24,26]. We tried to clarify this by examining the influence of parameters of therapy such as duration of chemotherapy and irradiation dose on growth fail ure.…”

Section: Discussionmentioning

confidence: 96%

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Logghe

Bourguignon²,

Craen

et al. 1988

Horm Res

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Growth was studied in 88 long-term survivors of acute lymphoblastic leukemia who had been treated with three different regimens of therapy. The following time periods were evaluated: (1) during therapy; (2) between the end of therapy and the onset of puberty, and (3) between the onset of puberty and the most recent observation. We found: (1) a reduction of height SDS during therapy, related to the irradiation dose used; no significant effect of the duration of the therapy could be established; (2) a normal growth rate during the second time period studied for the total group, but a further decrease in height SDS for those found to be growth hormone deficient after therapy (47 %), and (3) a further decrease in height SDS during puberty. The timing of puberty in the female patients was normal. We conclude that in patients treated for acute lymphoblastic leukemia, growth impairment has several components, different in timing and mechanism.

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Section: Discussionmentioning

confidence: 96%

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Logghe

Bourguignon²,

Craen

et al. 1988

Horm Res

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“…The responsiveness of children who develop GH deficiency and growth failure after antineoplastic therapy represents such a clinical uncertainty. While some investi gators have found that these childhood cancer survivors respond well [13] and exhibit catch-up growth [14], other studies have suggested that growth after GH replacement Table 5. Response to GH therapy according to chronological age relative to children with idiopathic GH deficiency Table 6.…”

Section: Discussionmentioning

confidence: 99%

Efficacy of Growth Hormone Replacement Therapy in Children with Organic Growth Hormone Deficiency after Cranial Irradiation

Vassilopoulou‐Sellin

Klein

Moore³

et al. 1995

Horm Res

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We evaluated the growth response of 20 childhood cancer survivors who received growth hormone (GH) replacement therapy (0.3 mg/kg/week) for at least 12 months. In all subjects, GH deficiency was associated with cranial irradiation and was documented with growth charts, bone age, and somatomedin C levels; at least one GH stimulation test was available for 14 children. Pretreatment overall growth velocity was 3.3 ± 0.5 cm/year (mean ± SE)over a 3-year period. After GH replacement, growth velocity was 8.6 ± 0.6 cm/year during the first year (n = 20), 7.2 ± 0.5 cm/year during the second year (n = 17), 5.9 ± 0.6 cm/year during the third year (n = 11), and 6.1 ± 0.6 cm/year during the fourth year (n = 7). Growth response, tabulated by age at onset of GH replacement, was compared with the response in GH-naive children with idiopathic GH deficiency (data obtained through the Genentech Inc. National Cooperative Growth Study Summary, September 1991); the growth velocity fell within the range described for idiopathic GH deficiency adjusted for either chronological or bone age. We conclude that children with GH deficiency after cranial irradiation for neoplastic diseases respond to GH replacement therapy as well as children with idiopathic GH deficiency.

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“…Quantification of 24-h GH secretion, however, did demonstrate reduced spontaneous GH secretion and a reduction in GH pulse amplitude and frequency (Blatt et al 1984). GH response to insulininduced hypoglycaemia was, however, subnormal (Blatt et al 1984, Romshe et al 1984, Ahmed et al 1986). This combination of GH axis responses was also demonstrated in two monkeys cranially irradiated with 40 Gy that showed impaired spontaneous GH secretion and a reduced GH peak to insulin-induced hypoglycaemia but an adequate GH peak response with arginine (Chrousos et al 1982).…”

Section: The Impact Of Cranial Irradiation On the Gh Axismentioning

confidence: 96%

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-GH axis: the past 60 years

Murray¹,

Higham²,

Clayton³

2015

Journal of Endocrinology

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At the time of the publication of Geoffrey Harris's monograph on 'Neural control of the pituitary gland' 60 years ago, the pituitary was recognised to produce a growth factor, and extracts administered to children with hypopituitarism could accelerate growth. Since then our understanding of the neuroendocrinology of the GH axis has included identification of the key central components of the GH axis: GH-releasing hormone and somatostatin (SST) in the 1970s and 1980s and ghrelin in the 1990s. Characterisation of the physiological control of the axis was significantly advanced by frequent blood sampling studies in the 1980s and 1990s; the pulsatile pattern of GH secretion and the factors that influenced the frequency and amplitude of the pulses have been defined. Over the same time, spontaneously occurring and targeted mutations in the GH axis in rodents combined with the recognition of genetic causes of familial hypopituitarism demonstrated the key factors controlling pituitary development. As the understanding of the control of GH secretion advanced, developments of treatments for GH axis disorders have evolved. Administration of pituitary-derived human GH was followed by the introduction of recombinant human GH in the 1980s, and, more recently, by long-acting GH preparations. For GH excess disorders, dopamine agonists were used first followed by SST analogues, and in 2005 the GH receptor blocker pegvisomant was introduced. This review will cover the evolution of these discoveries and build a picture of our current understanding of the hypothalamo-GH axis.

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Evaluation of growth hormone release and human growth hormone treatment in children with cranial irradiation-associated short stature

Cited by 100 publications

References 18 publications

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Factors Contributing to the Impairment of Growth in Children with Acute Lymphoblastic Leukemia

Efficacy of Growth Hormone Replacement Therapy in Children with Organic Growth Hormone Deficiency after Cranial Irradiation

60 YEARS OF NEUROENDOCRINOLOGY: The hypothalamo-GH axis: the past 60 years

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