Endocrine Abstracts

Objective: TRH induces GH secretion presumably by expression of TRH receptor dedifferentiated in pitutiary tumors, but it is not clear how the TRH elegantly stimulates GH secretion in tumoral states.

Design: The aim of this study was to investigate how GH-producing pituitary adenomas respond to TRH with respect to GH secretion and how it differs according to octreotide responses and their sizes of tumor.

Method: GH levels of 45 patients with newly diagnosed acromegaly were measured using a TRH stimulation test (TST), insulin tolerance test (ITT), and an octreotide suppression test (OST) sequentially. These values were compared according to the size of tumors and the response pattern to the OST.

Results: Thirty-six of 45 tumors were macroadenomas, and 23/36 macroadenomas appeared to be non-responders during the OST. Stimulated GH levels during the TST were not significantly different according to the size of tumor (P=0.212), even though baseline and recovered GH after stimulation had significant difference during the TST (P<0.024). Also, microadenomas and macroadenomas with non-responders had significantly different GH during the TST, but not the ITT (P=0.073).

Conclusion: According to the TST, dedifferentiation of tumor was firstly influenced by tumor size and then, OST responsiveness. Regardless of the tumor size, the effect of hypoglycemia to stimulate GH secretion was equivalent, though the result of the OST played a significant role to determine the responsiveness to hypoglycemia in macroadenomas.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.