Which Patients Do Not Require a GH Stimulation Test for the Diagnosis of Adult GH Deficiency?

Hartman, Mark L.; Crowe, Brenda; Biller, Beverly M. K.; Ho, Ken K. Y.; Clemmons, David R.; Chipman, John J.

doi:10.1210/jcem.87.2.8216

Cited by 254 publications

(137 citation statements)

References 24 publications

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…By analyzing the clinical characteristics and biochemical testing results of over 800 patients with either adult-onset hypothalamic or pituitary disease or CO-GHD, it has been demonstrated that adult GHD can be predicted with 95% accuracy by the presence of either three or four pituitary hormone deficits or a low IGF1 level (10). These findings have been confirmed by others who also proposed an IGF1 cut-off limit of around K2 S.D.…”

Section: How To Testmentioning

confidence: 75%

Retesting the childhood-onset GH-deficient patient

Gasco¹,

Corneli

Beccuti³

et al. 2008

European Journal of Endocrinology

View full text Add to dashboard Cite

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

show abstract

Section: How To Testmentioning

confidence: 75%

Retesting the childhood-onset GH-deficient patient

Gasco¹,

Corneli

Beccuti³

et al. 2008

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…For the purpose of ROC analysis, we assumed the patients with TPHD to be GHD, according to other studies and to the statement derived from the Growth Hormone Research Society consensus (1,34,36,37). The PHD group (patients without or with no more than two PHD) included subjects with either normal or impaired GH secretion.…”

Section: Discussionmentioning

confidence: 99%

The cut-off limits of the GH response to GH-releasing hormone-arginine test related to body mass index

et al. 2005

View full text Add to dashboard Cite

Objective: The diagnosis of growth hormone (GH) deficiency (GHD) in adults is based on a reduced peak GH response to provocative tests, such as the insulin tolerance test (ITT) and the GH-releasing hormone-arginine (GHRH-ARG) test. However, the cut-off limits of peak GH response in lean subjects are not reliable in obese patients; this is noteworthy since adult GHD is often associated with obesity. Aim of this study was to evaluate the diagnostic cut-off limits of peak GH response to the GHRH-ARG test in overweight and obese as well as in lean population. Design and methods: The GH responses to the GHRH-ARG test were studied in 322 patients with organic hypothalamic-pituitary disease and in 318 control subjects. Patients were subdivided into two groups on the basis of the number of pituitary hormone deficits, except for GH deficiency: (a) patients with total pituitary hormone deficit (TPHD) and (b) patients without or with no more than two pituitary hormone deficits (PHD). Both patients and control subjects were divided into three subgroups according to body mass index (BMI): lean (BMI , 25 kg/m 2 ), overweight (BMI $ 25 and , 30 kg/m 2 ) and obese (BMI $30 kg/m 2 ). TPHD patients were assumed to be GH deficient, whereas PHD patients may include subjects with either normal or impaired GH secretion. The statistical analysis was carried out by the Receiver-Operating Characteristic curve analysis (Medcalc 7.2). The diagnostic cut-off points were calculated for lean, overweight and obese subjects to provide optimal separation of GH-deficient patients and control subjects according to two criteria: (1) a balance between high sensitivity and high specificity; (2) to provide the highest pair of sensitivity/specificity values for GH deficiency. Results: In the lean population the best pair of values, with highest sensitivity as 98.7% and highest specificity as 83.7%, was found using a peak GH cut-off point of 11.5 mg/l. In the overweight population the best pair of values, 96.7 and 75.5%, respectively, was found using a peak GH cut-off point of 8.0 mg/l. In the obese population the best pair of values, 93.5 and 78.3%, respectively, was found using a peak GH cut-off point of 4.2 mg/l. Applying the above mentioned cut-off points, among PHD patients we found that 80 subjects (72%) were GHD whereas 31 (28%) had normal GH secretion. Conclusions: In conclusion the GHRH-ARG test is a reliable tool for the diagnosis of adult GH deficiency in lean, overweight and obese patients, provided that specific BMI-related cut-off limits are assumed.European Journal of Endocrinology 153 257-264

show abstract

“…The current consensus is that patients with appropriate clinical history should have the diagnosis of GHD confirmed by a provocative test of GH secretion (89,90). In TBI patients GHD has been diagnosed by means of classical provocative tests (glucagon, ITT or GHRH plus ARG), but the suspected GHD in these patients was not supported by an appropriate clinical context, except for TBI history.…”

Section: Kelly Et Al (30)mentioning

confidence: 99%

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

185

152

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

show abstract

Which Patients Do Not Require a GH Stimulation Test for the Diagnosis of Adult GH Deficiency?

Cited by 254 publications

References 24 publications

Retesting the childhood-onset GH-deficient patient

Retesting the childhood-onset GH-deficient patient

The cut-off limits of the GH response to GH-releasing hormone-arginine test related to body mass index

Hypopituitarism after traumatic brain injury

Contact Info

Product

Resources

About