GROWTH-HORMONE RESPONSE TO THE HYPOTHALAMIC SOMATOSTATINERGIC ACTIVITY IN ACROMEGALIC PATIENTS

Oral glucose administration suppresses the TRH-induced TSH response by enhancing the hypothalamic somatostatinergic activity (HSA). We asses sed the HSA in 13 acromegalic patients by measuring glucose-induced su ppression of TRH-stimulated TSH secretion. The HSA showed wide variati on with up to 64% suppression. The mean HSA of the patients (25 +/- 6% ) did not differ from that in normal young men (19 +/- 4%) in our prev ious study. Six patients had normal or low HSA, and the other 7 patien ts had high HSA. The mean TRH-stimulated HSS, levels of the patients w ith normal or low HSA was significantly lower than that of the patient s with high HSA (5.13 +/- 0.10 cs. 11.30 +/- 2.80 mU/L). The HSA did n ot relate to sex, age, tumor size, basal GH levels, the paradoxical re sponses to TRH and GnRH, octreotide response, or the gsp oncogene. In the combined glucose-TRH test, glucose pretreatment completely suppres sed the paradoxical increase in GH level at 30 min in 4 patients. Howe ver, it could suppress the paradoxical GH response by only 6-51% in th e other 5 patients who also showed the paradoxical response in TRH tes t. The tumor diameter of patients with good response to the HSA was si gnificantly larger than that of the patients with poor response (31 +/ - 5 vs. 14 +/- 2 mm) as was the the tumor grade (3.3 +/- 0.3 vs. 1.7 /- 0.2). This study supports the idea that a reduction of HSA is not a primary cause of acromegaly, and the HSA seems to increase to suppres s the autonomous secretion of GH from the pituitary adenomas. HSA as w ell as the response of tumors to HSA do not determine tumor growth.