Diagnostic reliability of a single IGF‐I measurement in 237 adults with total anterior hypopituitarism and severe GH deficiency

Aimaretti, Gianluca; Corneli, G.; Baldelli, Roberto; Somma, Carolina Di; Gasco, Valentina; Durante, Cosimo; Ausiello, Livia; Rovere, Silvia; Grottoli, Silvia; Tamburrano, G.; Ghigo, Ezio

doi:10.1046/j.1365-2265.2003.01794.x

Cited by 60 publications

(59 citation statements)

References 44 publications

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“…These findings have been confirmed by others who also proposed an IGF1 cut-off limit of around K2 S.D. All agree that the diagnostic reliability of low IGF1 levels is satisfactory when patients with CO severe GHD or multiple pituitary deficits are considered, particularly below 40 years of age (2,4,(11)(12)(13)(14)(15). These patients therefore do not require a GH stimulation test to make the diagnosis of adult GHD; however, it remains that patients suspected for GHD showing normal IGF1 levels must undergo provocative tests (2,4).…”

Section: How To Testsupporting

confidence: 74%

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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Section: How To Testsupporting

confidence: 74%

Retesting the childhood-onset GH-deficient patient

Gasco¹,

Corneli

Beccuti³

et al. 2008

European Journal of Endocrinology

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“…These findings suggest that IGF-1 concentrations might be even less informative in the suspected diagnosis of GHD in these patients as compared with other GHD patients (18,19). Therefore, we can conclude that it is recommendable to periodically investigate all cured acromegalic patients with dynamic GH secretion evaluation, such as GHRH plus arginine test, independently from previous treatment for acromegaly and from IGF-1 levels.…”

Section: Discussionmentioning

confidence: 62%

Prevalence of GH deficiency in cured acromegalic patients: impact of different previous treatments

Ronchi¹,

Giavoli²,

Ferrante³

et al. 2009

European Journal of Endocrinology

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Objective: Radiotherapy (RT) for pituitary adenomas, including GH-secreting ones, frequently leads to GH deficiency (GHD). Data on the effects of surgery alone (S) on dynamic GH secretion are limited. The aim of the study was to investigate the occurrence of GHD in acromegalic patients treated with different therapeutic options. Design and methods: Fifty-six patients in remission from acromegaly, (33 F & 23 M, age: 54G13 years, body mass index (BMI): 28.4G4.1 kg/m 2 , 21 with adequately substituted pituitary deficiencies) treated by S alone (nZ33, group 1) or followed by RT (nZ23, group 2), were investigated for GHD by GHRH plus arginine testing, using BMI-adjusted cut-offs. Several metabolic and cardiovascular parameters (waist circumference, body fat percentage, blood pressure, fasting and post-oral glucose tolerance test glucose, HbA1c, insulin resistance and lipid profile) were evaluated in all the patients and 28 control subjects with known diagnosis of GHD. Results: Serum GH peak after challenge was 8.0G9.7 mg/l, without any correlation with post-glucose GH nadir and IGF-1 levels. The GH response indicated severe GHD in 34 patients (61%) and partial GHD in 15 patients (27%). IGF-1 were below the normal range in 14 patients (25%). The frequency of GHD was similar in the two treatment groups (54% in group 1 and 70% in group 2). No significant differences in metabolic parameters were observed between acromegalic patients and controls with GHD. Conclusions: Severe GHD may occur in about 60% of patients treated for acromegaly, even when cured after S alone. Thus, a stimulation test (i.e. GHRH plus arginine) is recommended in all cured acromegalic patients, independently from previous treatment.

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“…However, the reliability of serum IGF-1 as an indicator of GH deficiency is being debated (Aimaretti et al, 1998(Aimaretti et al, , 2003Granada et al, 2000). Specifically, the consensus guidelines for the diagnosis and treatment of adults with GH deficiency conclude that, ''a normal IGF-1 does not rule out GH deficiency'' (Ho, 2007).…”

Section: Kasturi and Steinmentioning

confidence: 99%

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

Kasturi

Stein

2009

Journal of Neurotrauma

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In humans, traumatic brain injury (TBI) causes pathological changes in the hypothalamus (HT) and the pituitary. One consequence of TBI is hypopituitarism, with deficiency of single or multiple hormones of the anterior pituitary (AP), including growth hormone (GH). At present no animal model of TBI with ensuing hypopituitarism has been demonstrated. The main objective of this study was to investigate whether cortical contusion injury (CCI) could induce long-term reduction of serum GH in rats. We also tested the hypothesis that TBI to the medial frontal cortex (MFC) would induce inflammatory changes in the HT and AP. Methods: Nine young adult male rats were given sham surgery (n ¼ 4) or controlled impact contusions (n ¼ 5) of the MFC. Two months postinjury they were killed, trunk blood collected and their brains and AP harvested. GH was measured in serum and AP using ELISA and Western blot respectively. Interleukin-1b (IL-1b) and glial fibrillary acidic protein (GFAP) were measured in the cortex (Cx), HT, and AP by Western blot. Results: Lesion rats had significantly (p < 0.05) lower levels of GH in the AP and serum, unaltered serum IGF-1, and significantly (p < 0.05) higher levels of IL-1b in the Cx and HT and GFAP in the Cx, HT, and AP compared to that of shams. Conclusion: CCI leads to a long-term depletion of serum GH in male rats. This chronic change in GH post-TBI is probably the result of systemic and persistent inflammatory changes observed at the level of HT and AP, the mechanism of which is not yet known.

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Diagnostic reliability of a single IGF‐I measurement in 237 adults with total anterior hypopituitarism and severe GH deficiency

Cited by 60 publications

References 44 publications

Retesting the childhood-onset GH-deficient patient

Retesting the childhood-onset GH-deficient patient

Prevalence of GH deficiency in cured acromegalic patients: impact of different previous treatments

Traumatic Brain Injury Causes Long-Term Reduction in Serum Growth Hormone and Persistent Astrocytosis in the Cortico-Hypothalamo-Pituitary Axis of Adult Male Rats

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