Evaluation of GH reserve in patients with adrenal incidentalomas and biochemical evidence of subclinical autonomous glucocorticoid hypersecretion.
OBJECTIVE
Although it is well established that overt hypercortisolism in patients with active Cushing's syndrome leads to a profound suppression of stimulated GH secretion, the role of subclinical autonomous glucocorticoid hypersecretion (SAGH), currently detected with increasing frequency in patients with adrenal incidentalomas, on GH secretory reserve has received little attention. The aim of the present study was to evaluate whether SAGH in patients presented with adrenal incidentalomas has a negative effect on GH secretory reserve.


METHODS
Sixteen patients with overt Cushing's syndrome (CS) and 36 patients with adrenal incidentalomas were investigated. The latter group was further divided in 23 patients who demonstrated an adequate suppression of cortisol levels (of < 70 nmol/l) following the low-dose dexamethasone suppression test (LDDST) and in 13 patients, who failed to suppress (cortisol levels post-LDDST > 70 nmol/l). The former group was defined as normocortisolaemic (NC) and the latter group as representing patients with SAGH. The combined pyridostigmine + GHRH test (PD + GHRH) was used to assess the GH secretory reserve of these patients.


RESULTS
Peak GH levels following PD + GHRH administration were significantly lower in CS patients compared to both the NC and SAGH group of patients with adrenal incidentalomas (2.2 +/- 0.7 vs. 18.9 +/- 2.6 and 21.5 +/- 3.6 microg/l, respectively, P < 0.05); no difference was observed in peak GH responses between the NC and SAGH group of patients. A subnormal GH response (defined as GH(max) < 12.8 microg/l) was observed in all 16 patients with CS. However, only seven NC and three SAGH patients failed to respond adequately. Correlation analysis revealed a negative correlation between peak GH response to PD + GHRH and plasma cortisol concentrations in CS patients (R =-0.6, P = 0.012), while in patients with adrenal incidentalomas such a correlation was absent. Contrary to patients with CS in whom body mass index (BMI) was not correlated to peak GH, a significant negative correlation between peak GH response to PD + GHRH and BMI was disclosed in patients with adrenal incidentalomas (R =-0.49, P = 0.003). In these patients, again contrary to CS patients, a significant negative correlation was also found between peak GH post PD + GHRH and age (R = -0.46, P = 0.002).


CONCLUSIONS
In conclusion, our results provide evidence that, contrary to patients with overt CS, SAGH does not affect the GH secretory response to provocative stimulation.
Tzanela
M
M
Department of Endocrinology, Diabetes and Metabolism, Evangelismos Hospital, Athens, Greece.
Zianni
D
D
Stylianidou
Ch
Ch
Karavitaki
N
N
Tsagarakis
S
S
Thalassinos
N C
NC
D000236:Adenoma / Q000097:blood* / Q000378:metabolism*; D000306:Adrenal Cortex Neoplasms / Q000097:blood* / Q000378:metabolism*; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D002800:Cholinesterase Inhibitors; D003907:Dexamethasone; D005260:Female; D005938:Glucocorticoids; D013006:Growth Hormone / Q000097:blood*; D013007:Growth Hormone-Releasing Hormone; D006801:Humans; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism*; D033162:Incidental Findings; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011729:Pyridostigmine Bromide; D018709:Statistics, Nonparametric
D002800:Cholinesterase Inhibitors; D005938:Glucocorticoids; D003907:Dexamethasone; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D011729:Pyridostigmine Bromide; D006854:Hydrocortisone