Journal ArticleDOI
The prevalence of severe growth hormone deficiency in adults who received growth hormone replacement in childhood [see comment].
TLDR
To determine how many patients who received GH replacement therapy in childhood until completion of growth have GH deficiency severe enough to be considered for GH Replacement therapy in adult life, this study surveys young adults treated with GH therapy for childhood GH deficiency.Abstract:
OBJECTIVE The few previous studies in which reassessment of GH status has been carried out in young adults treated with GH therapy for childhood GH deficiency concentrated on determining the incidence of 'transient GH deficiency'. As the benefits of GH replacement therapy in adults become increasingly appreciated, it is likely that GH therapy started in childhood for GH deficiency will be continued into adult life in many of those with severe GH deficiency. The aim of this study is to determine how many patients who received GH replacement therapy in childhood until completion of growth have GH deficiency severe enough to be considered for GH replacement therapy in adult life. DESIGN Retrospective analysis of the peak GH responses to provocative stimuli performed at the time of diagnosis of GH deficiency in childhood and at the completion of growth after GH replacement therapy had been stopped. PATIENTS Eighty-eight adults (49 male, 39 female) who had received GH therapy in childhood for a diagnosis of GH deficiency. The aetiology of the GH deficiency included craniopharyngioma, radiation induced associated with either a cerebral tumour or acute lymphoblastic leukaemia, histiocytosis-X and idiopathic. MEASUREMENTS In childhood the original diagnosis of GH deficiency was based biochemically on the failure of the peak GH response to reach 20 mU/l during two provocative tests in 59 of the 88 patients and to a single test in the remaining 29. A total of 147 tests were performed, the most common being an insulin tolerance test (ITT, n = 72) and an arginine stimulation test (AST, n = 53). At reassessment in young adult life 146 tests were performed (74 ITT, 64 AST). Severe GH deficiency was defined arbitrarily as a peak GH response of less than 9 mU/l to a single (n = 33) or to two (n = 55) pharmacological stimuli. RESULTS By definition all patients were considered GH deficient at the time of initial diagnosis. A peak GH response of less than 9 mU/l was seen in 64.8% at initial assessment and 60.2% at reassessment. Analysis in aetiological terms, however, showed that between assessments the incidence of severe GH deficiency increased in the group of radiation induced (48.8 vs. 55.8%) but decreased in the idiopathic group (78.1 vs. 53.1%). Out of the 55 patients who underwent two tests at reassessment, 47.3% of those with a GH peak less than 9 mU/l at one test had a GH peak greater than 9 mU/l at the second test. Fifteen of the 55 patients had additional pituitary hormone deficiencies and all 15 had a GH peak below 9 mU/l in both tests. CONCLUSIONS Our study suggests that all children who have received GH replacement therapy in childhood should undergo reassessment of GH status in young adult life. Between 40 and 60% of such patients merit consideration for GH therapy in adult life depending on the definition of severe GH deficiency in use. Patients with isolated GH deficiency should undergo two provocative tests of GH secretion, but those with additional anterior pituitary hormone deficiencies require only one test at reassessment.read more
Citations
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Journal ArticleDOI
Evaluation and Treatment of Adult Growth Hormone Deficiency: An Endocrine Society Clinical Practice Guideline
TL;DR: GH therapy offers benefits in body composition, exercise capacity, skeletal integrity, and quality of life measures and is most likely to benefit those patients who have more severe GHD, and the risks associated with GH treatment are low.
Journal ArticleDOI
The Diagnosis of Growth Hormone Deficiency in Children and Adults
TL;DR: A practical approach to the diagnosis of GHD in children and adults, and new strategies for assessment of GH status I.I.
Journal ArticleDOI
Guidelines for Growth Hormone and Insulin-Like Growth Factor-I Treatment in Children and Adolescents: Growth Hormone Deficiency, Idiopathic Short Stature, and Primary Insulin-Like Growth Factor-I Deficiency.
Adda Grimberg,Sara A. DiVall,Constantin Polychronakos,David B. Allen,Laurie E. Cohen,Jose Bernardo Quintos,Wilma C. Rossi,Chris Feudtner,Mohammad Hassan Murad +8 more
TL;DR: This guideline provides recommendations for the clinical management of children and adolescents with growth failure from GHD, ISS, or PIGFD using the best available evidence.
Journal ArticleDOI
CLINICAL PRACTICE GUIDELINE Evaluation and Treatment of Adult Growth Hormone Deficiency: An Endocrine Society Clinical Practice Guideline
Mark E. Molitch,David R. Clemmons,Saul Malozowski,George R. Merriam,Stephen M Shalet,Mary Lee Vance +5 more
TL;DR: This research highlights the need to understand more fully the role of Epstein-Barr virus in the development of type 2 diabetes and its role in the immune system.
Journal ArticleDOI
Growth hormone (GH) deficiency (GHD) of childhood onset: Reassessment of GH status and evaluation of the predictive criteria for permanent GHD in young adults
Mohamad Maghnie,Carolina Strigazzi,Carmine Tinelli,Michele Autelli,Mariangela Cisternino,Sandro Loche,Francesca Severi +6 more
TL;DR: It is suggested that patients with GHD and congenital hypothalamic-pituitary abnormalities do not require further investigation of GH secretion, whereas patients with IGHD and normal or small pituitary gland should be retested well before the attainment of adult height.
References
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Premature mortality due to cardiovascular disease in hypopituitarism.
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Journal ArticleDOI
Quality of life assessment before and after growth hormone treatment in adults with growth hormone deficiency
TL;DR: The quality of life assessment before and after growth hormone treatment in adults with growth hormone deficiency is compared to other children with similar medical conditions.
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Premature mortality due to cardiovascular disease in hypopituitarism.
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