Diagnostic utility of the glucagon stimulation test in comparison to the insulin tolerance test in patients following pituitary surgery

Berg, C; Meinel, T.; Lahner, Harald; Yuece, Ali; Mann, Klaus; Petersenn, Stephan

doi:10.1530/eje-09-0824

Cited by 92 publications

(86 citation statements)

References 36 publications

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“…On the other hand, the study by Berg et al was a retrospective study that revealed an optimal peak GH cut-off value of 2.5 ng/ml with 95 % sensitivity and 79 % specificity using ROC analysis. 21 This study also reported lower peak GH levels with GST compared with ITT (5.1 versus 6.7 ng/ml; p<0.01), but a significant positive correlation between peak GH levels during ITT and GST (r=0.88; p<0.0001).…”

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tesupporting

confidence: 57%

“…Nevertheless, these 21,22,28 and previous studies 20,23,24,31 did not specifically evaluate patients with glucose intolerance and frank diabetes and, for this reason, the characteristic of the GST and its reliability in testing for GHD in this population remains unclear. To address this question, we evaluated GSTs performed in 515 patients, and found that BMI, fasting, peak, and nadir glucose levels correlated negatively with peak GH levels.…”

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 97%

“…14 The utilization of the GST for the assessment of GH reserve was first described in 1969 by Mitchell et al 19 Since then, the GST has been shown by various investigators to have a GH secretory potency that is similar to or only slightly less than the ITT, suggesting that it is more reliable than other classic agents such as ARG or clonidine for separating GHD patients from normal subjects. [20][21][22][23][24] The true mechanism by which glucagon induces GH release is still a mystery. Some of the hypothesized mechanisms include the glycemic fluctuations during the test where blood glucose levels increase initially before decreasing later in the test, 25 the generation of a peptidyl fragment associated with the GH-and adrenocorticotropic hormone (ACTH)-releasing activity, 26 and the induction of norepinephrine secretion in stimulating GH release via a-receptors.…”

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 99%

“…Berg et al 21 evaluated GHD in patients with pituitary disorders. The first two studies 22,28 were prospective studies that compared the diagnostic characteristics of GST to ITT and included a control group which was matched for age and sex in both studies and for body mass index (BMI) in one study.…”

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 99%

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Glucagon Stimulation Testing in Adult Growth Hormone Deficiency A 2014 Update

Yuen

2014

US Endocrinology

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Growth hormone deficiency (GHD) in adults is characterized by alterations in body composition, carbohydrate and lipid metabolism, bone mineral density, cardiovascular risk profile, and quality of life.1 Treatment with GH replacement has been shown to improve many, but not all, of these abnormalities. 2 By contrast, untreated GHD is associated with increased mortality and morbidity that was previously observed in adults with hypopituitarism. 3,4 These findings were substantiated in two large surveys based on national Danish registries, 5,6 where the morbidity of adults with GHD was found to be approximately threefold higher than that of a healthy population. This result was independent of gender and applied to patients with childhood-onset and adult-onset GHD, with mortality of childhoodonset GHD far exceeding that of adult-onset GH deficient patients. 6Current published consensus guidelines recommend the evaluation of adult GHD to be based on clinical findings, medical history and using the appropriate GH stimulation test for biochemical confirmation, 7-9 with the exception of patients with three or more pituitary hormone deficiencies and low serum insulin-like growth factor 1 (IGF-1) levels. 10 Serum IGF-1 levels should not be used alone to diagnose adult GHD and the maximum or peak GH secretion following GH stimulation testing is used as a surrogate of the capacity of the pituitary to release GH. The insulin tolerance test (ITT) is widely considered as the gold standard test for evaluation of GH deficiency and has been endorsed by several consensus guidelines. [7][8][9]11 However, this test is labor intensive, may be unpleasant for some patients, has potential risks, and is contraindicated in elderly patients and in patients with seizure disorders and ischemic heart disease. AbstractGrowth hormone deficiency (GHD) is a well-recognized clinical syndrome in adults, and its diagnosis is established through one or more GH stimulation tests. The decision to perform GH stimulation testing should be based on medical history and clinical findings, and using appropriate GH stimulation test/s for biochemical confirmation. The insulin tolerance test (ITT) remains the diagnostic test of choice; however, this test is labor intensive, contraindicated in the elderly and in adults with seizure disorders and ischemic heart disease, can be unpleasant for the patient, and is potentially hazardous. With the discontinuation of the growth hormone releasing hormone (GHRH) analog (Geref ® ) in the US in 2008, the glucagon stimulation test (GST) has gained increasing popularity as the alternative test to the ITT because of its availability, reproducibility, safety, lack of influence by gender and hypothalamic cause of GH deficiency (GHD), and relatively few contraindications. In this article, recommendations for performing this test, the potential drawbacks in conducting and caveats in interpreting this test, and its future perspectives are discussed.

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Section: Historical Perspective Of the Use Of Glucagon Stimulation Tesupporting

confidence: 57%

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 97%

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 99%

Section: Historical Perspective Of the Use Of Glucagon Stimulation Tementioning

confidence: 99%

See 2 more Smart Citations

Glucagon Stimulation Testing in Adult Growth Hormone Deficiency A 2014 Update

Yuen

2014

US Endocrinology

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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%

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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