Growth hormone release after glucagon as a reliable test of growth hormone assessment in adults

Gómez, José Manuel; Espadero, R.; Escobar-Jiménez, Fernándo; Hawkins, Federico; Picó, Antonio; Herrera-Pombo, J L; Vilardell, E; Durán, Alejandra; Mesa, Jordi; Faure, Eduardo; Sanmartı́, Anna

doi:10.1046/j.1365-2265.2002.01472.x

Cited by 123 publications

(109 citation statements)

References 28 publications

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“…Gomez et al, who evaluated the GST in healthy controls, found that none of their 46 volunteers failed to achieve a GH response !3 mg/l; however, the population used was lean. They did, however, note a significant correlation between BMI and peak GH response (30). We have demonstrated a negative correlation between peak GH and BMI in both healthy controls and in SAH patients; patients and healthy controls with a BMI O30 kg/m 2 frequently failed to achieve a peak GH level O3 mg/l.…”

Section: Discussionmentioning

confidence: 86%

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Gardner

Javadpour

Stoneley

et al. 2013

European Journal of Endocrinology

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Objective: Hypopituitarism following subarachnoid haemorrhage (SAH) has been reported to be a frequent occurrence. However, there is considerable heterogeneity between studies with differing patient populations and treatment modalities and most importantly employing differing endocrine protocols and (normal) reference ranges of GH. We aimed to examine prospectively a cohort of SAH survivors for development of hypopituitarism post-SAH using rigorous endocrine testing and compare GH response to glucagon stimulation with a cohort of healthy controls of a similar BMI. Design and methods: Sixty-four patients were investigated for evidence of hypopituitarism 3 months post-SAH with 50 patients tested again at 12 months. Glucagon stimulation testing (GST), with confirmation of deficiencies by GHRH/arginine testing for GH deficiency (GHD) and short synacthen testing for ACTH deficiency, was used. Basal testing of other hormonal axes was undertaken. Results: Mean age of patients was 53G11.7 years and mean BMI was 27.5G5.7 kg/m 2 . After confirmatory testing, the prevalence of hypopituitarism was 12% (GHD 10%, asymptomatic hypocortisolaemia 2%). There was no association between hypopituitarism and post-SAH vasospasm, presence of cerebral infarction, Fisher grade, or clinical grading at presentation. There was a significant correlation between BMI and peak GH to glucagon stimulation in both patients and controls. Conclusions: Identification of 'true' GHD after SAH requires confirmatory testing with an alternative stimulation test and application of BMI-specific cut-offs. Using such stringent criteria, we found a prevalence of hypopituitarism of 12% in our population.

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Section: Discussionmentioning

confidence: 86%

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Gardner

Javadpour

Stoneley

et al. 2013

European Journal of Endocrinology

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“…Among classical provocative tests, while the diagnostic reliability of ITT has been confirmed by many studies, the glucagon test has been validated more recently showing quite good sensitivity (Se) and specificity (Sp) (16,17). On the other hand, it has been demonstrated that testing with ARG alone should not be considered a reliable alternative test (18).…”

Section: How To Testmentioning

confidence: 99%

Retesting the childhood-onset GH-deficient patient

Gasco¹,

Corneli

Beccuti³

et al. 2008

European Journal of Endocrinology

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GH deficiency (GHD) in adults has to be shown by a single provocative test, provided that it is validated. Insulin tolerance test (ITT) has been indicated as the test of choice; now also glucagon test is validated and represents an alternative. The GHRH plus arginine (ARG) test and testing with GHRH plus a GH secretagogue are equally reliable diagnostic tools, and are now considered as 'golden' standards as ITT. Childhood-onset (CO) GHD needs retesting in late adolescence or young adulthood; this is a major clinical challenge and raises questions about the most appropriate method and cut-off value. Appropriate re-evaluation of GH status is represented by simple measurement of IGF1 concentration off rhGH treatment. Clearly, low IGF1 levels are evidence of persistent severe GHD in subjects with genetic GHD or panhypopituitarism. However, normal IGF1 levels never rule out severe GHD and CO-GHD with normal IGF1 levels must undergo a provocative test. The appropriate GH cut-off limit is specific for each provocative test. As shown by the ROC curve analysis, in late adolescents and young adults, the lowest normal GH peak response to ITT is 6.1 mg/l while that to GHRHCARG test is 19.0 mg/l. These cut-off limits, however, are just indicative as being variable as a function of the assay used. No other test is validated for retesting. As GHRHCARG test mostly explores the GH-releasable pool, normal GH response would be verified by a second ITT in order to rule out subtle hypothalamic defect. European Journal of Endocrinology 159 S45-S52

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“…41 For GHD, we utilized the glucagon stimulation test, which is a well-validated test for this purpose. 32,33,36,[42][43][44] Given that a majority of this cohort was obese and that peak GH levels are negatively correlated with BMI for all types of GH stimulation testing, including glucagon, GHRH/arginine, and the insulin tolerance tests, it was necessary to use a BMI-adjusted definition for GHD with a control cohort of overweight subjects.…”

Section: Defining Hormonal Deficiencymentioning

confidence: 99%

“…31,32 Because of this known inverse relationship with BMI and peak GH after stimulation testing with glucagon, GHRH/arginine, and insulin tolerance testing, GHD was defined at 3 cut points, adjusted for BMI using a normal non-head-injured control cohort referred to the Dynamic Endocrine Testing Unit at the Oregon Health & Science University (Portland, OR) for assessment of possible GHD with low normal to low serum IGF-1 levels. 27,[33][34][35][36] From 119 men tested, individuals were excluded if they had a previous history of pituitary or hypothalamic tumor, other hypothalamic or pituitary disorder, pituitary surgery or irradiation, or TBI. Thirty individuals from these 119 men met the criteria and made up the control group.…”

Section: Pituitary Hormonal Testingmentioning

confidence: 99%

Prevalence of Pituitary Hormone Dysfunction, Metabolic Syndrome, and Impaired Quality of Life in Retired Professional Football Players: A Prospective Study

Kelly

Chaloner

Evans

et al. 2014

Journal of Neurotrauma

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Hypopituitarism is common after moderate and severe traumatic brain injury (TBI). Herein, we address the association between mild TBI (mTBI) and pituitary and metabolic function in retired football players. Retirees 30-65 years of age, with one or more years of National Football League (NFL) play and poor quality of life (QoL) based on Short Form 36 (SF-36) Mental Component Score (MCS) were prospectively enrolled. Pituitary hormonal and metabolic syndrome (MetS) testing was performed. Using a glucagon stimulation test, growth hormone deficiency (GHD) was defined with a standard cut point of 3 ng/mL and with a more stringent body mass index (BMI)-adjusted cut point. Subjects with and without hormonal deficiency (HD) were compared in terms of QoL, International Index of Erectile Function (IIEF) scores, metabolic parameters, and football career data. Of 74 subjects, 6 were excluded because of significant non-football-related TBIs. Of the remaining 68 subjects (mean age, 47.3 -10.2 years; median NFL years, 5; median NFL concussions, 3; mean BMI, 33.8 -6.0), 28 (41.2%) were GHD using a peak GH cutoff of < 3 ng/mL. However, with a BMI-adjusted definition of GHD, 13 of 68 (19.1%) were GHD. Using this BMI-adjusted definition, overall HD was found in 16 (23.5%) subjects: 10 (14.7%) with isolated GHD; 3 (4.4%) with isolated hypogonadism; and 3 (4.4%) with both GHD and hypogonadism. Subjects with HD had lower mean scores on the IIEF survey ( p = 0.016) and trended toward lower scores on the SF-36 MCS ( p = 0.113). MetS was present in 50% of subjects, including 5 of 6 (83%) with hypogonadism, and 29 of 62 (46.8%) without hypogonadism ( p = 0.087). Age, BMI, median years in NFL, games played, number of concussions, and acknowledged use of performance-enhancing steroids were similar between HD and non-HD groups. In summary, in this cohort of retired NFL players with poor QoL, 23.5% had HD, including 19% with GHD (using a BMI-adjusted definition), 9% with hypogonadism, and 50% had MetS. Although the cause of HD is unclear, these results suggest that GHD and hypogonadism may contribute to poor QoL, erectile dysfunction, and MetS in this population. Further study of pituitary function is warranted in athletes sustaining repetitive mTBI.

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Growth hormone release after glucagon as a reliable test of growth hormone assessment in adults

Abstract: The glucagon GH test is reliable and provides a clear separation between GH-deficient and normal adults. A single glucagon test with a cut-off of 3 microg/l for the GH peak is diagnostic of GH deficiency in adults and could be considered and studied as an alternative to the ITT.

Cited by 123 publications

References 28 publications

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

Retesting the childhood-onset GH-deficient patient

Prevalence of Pituitary Hormone Dysfunction, Metabolic Syndrome, and Impaired Quality of Life in Retired Professional Football Players: A Prospective Study

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