The prevalence of severe growth hormone deficiency in adults who received growth hormone replacement in childhood

Nicolson, A; Toogood, Andy; Rahim, Asad; Shalet, Stephen M

doi:10.1046/j.1365-2265.1996.671492.x

Cited by 100 publications

(57 citation statements)

References 12 publications

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“…This evidence implies that in a large percentage of adult patients with GHD, the impairment of somatotrope function is partial and does not need replacement therapy. 44 Noteworthy, in agreement with other studies with classical provocative stimuli, 1,3±5 even when the maximal secretory capacity of somatotrope cells is evaluated by a potent and reproducible provocative test such as GHRH arginine, overweight has to be taken in a great account as the cause of severely impaired GH response in patients with suspected GH de®-ciency. In fact, our study demonstrates that the reduction of the GH reserve in obesity may be so marked that 50% of obese patients with otherwise normal pituitary function may have such an important impairment of the GH response to GHRH arginine that it overlaps with that seen in hypopituitaric patients with GH de®ciency.…”

Section: Discussionmentioning

confidence: 57%

Maximal secretory capacity of somatotrope cells in obesity: comparison with GH deficiency

et al. 1997

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OBJECTIVE: To evaluate the maximal secretory capacity of somatotrope cells in obesity and to compare it with that in hypopituitaric patients with GH de®ciency. DESIGN: Stimulation with GHRH. (1 mg/kg iv) combined with arginine (ARG, 0.5 g/kg iv), which strongly potentiates the GH response to the neurohormone, likely inhibiting hypothalamic somatostatin. The reproducibility of the GH response to GHRH ARG was evaluated in a second session. SUBJECTS: Forty-®ve patients with simple obesity (OB 11 male and 34 female, age 40.5 AE AE 1.8 y, BMI 38.8 AE AE 1.1 kg/m 2 ), 49 patients with hypopituitarism (GHD, 23 male and 26 female, 43.6 AE AE 2.4 y, 24.7 AE AE 0.7 kg/m 2 ) and 44 normal young volunteers (NS, 25 male and 19 female, 33.8 AE AE 1.0 y, 21.6 AE AE 0.3 kg/m 2 ) were studied. MEASUREMENTS: GH levels were assayed by IRMA method, basally at 7 60 and 0 min, and than every 15 min up to 120 min. Basal IGF±I levels were assayed by RIA method, after acid-ethanol extraction. RESULTS: IGF±I levels in OB were lower (P`0.005) than those in NS but higher (P`0.005) than those in GHD. Mean peak GH response to GHRH ARG in OB was clearly lower than that in NS (P`0.005) and higher (P`0.005) than that in GHD. Sixty±percent OB and 100% GHD showed peak GH responses lower than the minimum normal limit in NS (16.5 mg/l) while 4% OB and only 53% GHD with GH responses lower than 3 mg/l, the limit under which GH replacement therapy of severe de®ciency is allowed. Good intraindividual reproducibility of the GH response to GHRH arginine test was present in all groups (OB: r 0.78, P`0.0001; GHD: r 0.57, P`0.003; NS: r 0.74, P`0.0001;. CONCLUSIONS: The maximal secretory capacity of somatotrope cells is clearly less than normal in the obese but still more than is seen in GHD subjects. However, in about 50% of obese patients, the pituitary GH releasable pool overlaps with that of hypopituitaric patients with GH de®ciency. Thus, even when the maximal secretory capacity of somatotrope cells is evaluated by a potent and reproducible provocative tests such as GHRH arginine, overweight has to be taken in a great account as the cause of severely impaired GH response in patients with suspected GH de®ciency.

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Section: Discussionmentioning

confidence: 57%

Maximal secretory capacity of somatotrope cells in obesity: comparison with GH deficiency

et al. 1997

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“…In addition, the number of GH-D children cannot be automatically converted to adults with GH-D, since diagnosis was not confirmed when GH status was re-examined in adulthood in a number of patients previously treated for childhood idiopathic isolated GH-D (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

GH deficiency in adults: an epidemiological approach

Sassolas

Chazot

Jaquet

et al. 1999

European Journal of Endocrinology

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Objective: The prevalence of adult onset GH deficiency (GH-D) is poorly documented. Epidemiological data are now required to estimate the financial cost of GH treatment in adults. The aim of the present study was to estimate the prevalence of GH-D, from a cohort of 1652 adult patients with hypothalamo-pituitary diseases. Design: The hormonal status of all patients presenting with pituitary disease and observed during the year 1994 in 15 endocrine units was retrospectively analyzed, irrespective of the date of disease onset, of the nature and date of pituitary investigations, and whether or not they included specific testing of the GH axis. Of the whole population of 1652 patients, a selected group (RG2) was chosen after exclusion of patients with active acromegaly (n = 1414). Results: GH stimulation tests had been performed in 549 patients of the RG2 group and a documented GH-D was found in 301. A relationship between the value of the GH peak and the number of pituitary deficits was evaluated. For instance, it was shown that 93% of patients with three deficits had GH-D. These results constituted the basis for estimating the number of GH-D in the group of untested patients. The number of GH-D deduced from the number of established GH-D (n = 301) and from the number of GH-D hypothesized from other pituitary deficits (n = 406) was 707 cases. Prevalence and annual incidence were calculated from data recorded in a referral center with a well-defined catchment area, Marseilles (Bouches du Rhône department). We projected a prevalence of 2638 for France and an annual incidence of 12 GH-D per million of the adult population.

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“…Whether the pituitary size and/or the presence of morphological abnormalities could be useful in predicting permanent GHD, however, is not known. Furthermore, few data on retesting in patients with organic GHD have been reported (14).…”

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confidence: 99%

Growth Hormone (GH) Deficiency (GHD) of Childhood Onset: Reassessment of GH Status and Evaluation of the Predictive Criteria for Permanent GHD in Young Adults

Maghnie¹,

Strigazzi²,

Tinelli

et al. 1999

The Journal of Clinical Endocrinology &Amp; Metabolism

158

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GH secretion was reevaluated after completion of GH treatment at a mean age of 19.2 Ϯ 3.2 yr in 35 young adults with childhood-onset GH deficiency (GHD). The patients were subdivided into 4 groups according to their first pituitary magnetic resonance imaging (MRI) findings: group I, 11 patients with isolated GHD (IGHD) and normal pituitary volume (280 Ϯ 59.4 mm 3 ); group II, 7 patients with IGHD and small pituitary gland (163.1 Ϯ 24.4 mm 3 ; P ϭ 0.0009 vs. group I); group III, 13 patients (5 with IGHD and 8 with multiple pituitary hormone deficiency) with congenital hypothalamic-pituitary abnormalities such as pituitary hypoplasia (95.8 Ϯ 39.3 mm 3 ; P Ͻ 0.00001 vs. group I and P ϭ 0.003 vs. group II), pituitary stalk agenesis, and posterior pituitary ectopia; and group IV, 4 patients with multiple pituitary hormone deficiency secondary to craniopharyngioma. Pituitary MRI and GH secretory status were reevaluated after GH withdrawal using arginine, insulin induced-hypoglycemia, and sequential arginine-insulin tests. Serum insulin-like growth factor I (IGF-I) and IGF-binding protein-3 (IGFBP-3) were determined at the time of retesting and 6, 12, and 24 months after discontinuation of treatment in the patients with permanent GHD and after 6 months in those with normal GH responses to stimulation. The patients in groups I and II showed a normal response to stimulation after completion of GH treatment regardless of pituitary size, whereas all patients in groups III and IV still had a GH response of less than 3 g/L to any of the tests. Pituitary volume normalized in 6 of 7 patients in group II, whereas in all patients in group III MRI studies confirmed the initial findings. Mean IGF-I and IGFBP-3 concentrations at the time of retesting were significantly higher in groups I and II than in groups III and IV. In patients of groups III and IV, mean IGF-I was significantly decreased after 6 and 12 months, whereas IGFBP-3 was significantly decreased 12 months after treatment withdrawal. Our results confirm that a high proportion of children with IGHD and normal or small pituitary show normalization of GH secretion at the completion of GH treatment, whereas GHD is permanent in all patients with pituitary hypoplasia, pituitary stalk agenesis, and posterior pituitary ectopia. IGF-I and IGFBP-3 determinations shortly after GH withdrawal had limited value in the diagnosis of GHD of childhood onset associated with congenital hypothalamic-pituitary abnormalities, but became accurate after 6 -12 months. We suggest 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. (J Clin Endocrinol Metab 84: 1324 -1328, 1999

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The prevalence of severe growth hormone deficiency in adults who received growth hormone replacement in childhood

Cited by 100 publications

References 12 publications

Maximal secretory capacity of somatotrope cells in obesity: comparison with GH deficiency

Maximal secretory capacity of somatotrope cells in obesity: comparison with GH deficiency

GH deficiency in adults: an epidemiological approach

Growth Hormone (GH) Deficiency (GHD) of Childhood Onset: Reassessment of GH Status and Evaluation of the Predictive Criteria for Permanent GHD in Young Adults

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