Affiliation
Department of Endocrinology, Christie Hospital NHS Trust, Manchester, United Kingdom.Issue Date
1996-10
Metadata
Show full item recordAbstract
GH deficiency in adult life is associated with a number of adverse biological changes including osteopenia, reduced exercise capacity, altered body composition, deleterious alterations in the lipid profile and insulin status, and reduced quality of life. Potentially, most of these changes can be reversed by GH replacement therapy. In an era of health rationing, however, GH replacement is unlikely to be offered to every GH-deficient adult. Therefore, we have proposed a strategy aimed at delineating which adults with GH deficiency might benefit most from GH therapy.Citation
Growth Hormone therapy for adult Growth Hormone deficiency. 1996, 7 (8):287-90 Trends Endocrinol. Metab.Journal
Trends in Endocrinology and MetabolismDOI
10.1016/S1043-2760(96)00130-0PubMed ID
18406761Type
ArticleLanguage
enISSN
1043-2760ae974a485f413a2113503eed53cd6c53
10.1016/S1043-2760(96)00130-0
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Growth hormone replacement in an adult with mild growth hormone deficiency and hereditary motor and sensory neuropathy: growth hormone restores independent mobility.Lissett, Catherine A; Toogood, Andy; Didi, Mohammed; Shalet, Stephen M; Department of Endocrinology, Christie Hospital, Withington, Manchester, UK. (1998)We present the case of an adult patient with growth hormone (GH) insufficiency and hereditary motor and sensory neuropathy type 1. Stopping GH replacement at the attainment of final height was associated with a marked reduction in power and mobility, resulting in the patient becoming wheelchair bound. GH replacement was assessed in a double-blind placebo-controlled trial. During the GH replacement arm of the trial, the patient's mobility and independence returned to previous levels. We suggest that the indications for GH replacement in adults should take account of other medical problems, in particular neuromuscular disorders, as well as the degree of GH deficiency.
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Pulsatile growth hormone secretion persists in genetic growth hormone-releasing hormone resistance.Maheshwari, Hiralal G; Pezzoli, Suzan S; Rahim, Asad; Shalet, Stephen M; Thorner, Michael O; Baumann, Gerhard; Center for Endocrinology, Metabolism and Molecular Medicine, Department of Medicine, Northwestern University Medical School, and Veterans Administration Chicago Health System, Lakeside Division, Chicago, Illinois 60611, USA. (2002-04)Growth hormone (GH) secretion is regulated by GH-releasing hormone (GHRH), somatostatin, and possibly ghrelin, but uncertainty remains about the relative contributions of these hypophysiotropic factors to GH pulsatility. Patients with genetic GHRH receptor (GHRH-R) deficiency present an opportunity to examine GH secretory dynamics in the selective absence of GHRH input. We studied circadian GH profiles in four young men homozygous for a null mutation in the GHRH-R gene by use of an ultrasensitive GH assay. Residual GH secretion was pulsatile, with normal pulse frequency, but severely reduced amplitude (<1% normal) and greater than normal process disorder (as assessed by approximate entropy). Nocturnal GH secretion, both basal and pulsatile, was enhanced compared with daytime. We conclude that rhythmic GH secretion persists in an amplitude-miniaturized version in the absence of a GHRH-R signal. The nocturnal enhancement of GH secretion is likely mediated by decreased somatostatin tone. Pulsatility of residual GH secretion may be caused by oscillations in somatostatin and/or ghrelin; it may also reflect intrinsic oscillations in somatotropes.