Acromegaly due to a growth hormone-releasing hormone-secreting bronchial carcinoid tumor: further information on the abnormal responsiveness of the somatotroph cells and their recovery after successful treatment
Boizel, R.; Halimi, S.; Labat, F.; Cohen, R.; Bachelot, I.
Journal of Clinical Endocrinology and Metabolism 64(2): 304-308
1987
ISSN/ISBN: 0021-972X
PMID: 3098773
DOI: 10.1210/jcem-64-2-304
Accession: 039161508
We studied GH secretion in a patient with acromegaly and a bronchial carcinoid tumor before and again after surgical removal of this tumor. Before removal of the carcinoid tumor, plasma GH increased slightly after glucose loading (OGTT) and markedly TRH (650%) and insulin (440%) treatment. Plasma GH did not change after GH-releasing hormone (GHRH), LHRH, or L-dopa administration. Somatostatin (SRIH) infusion lowered plasma GH. No change in plasma immunoreactive GHRH (IR-GHRH) occurred after TRH, glucose, insulin, or SRIH administration. Two weeks after removal of the carcinoid tumor, TRH induced GH secretion (250%) when the IR-GHRH level was undetectable and somatomedin-C was within normal limits. Fifteen weeks after surgery, the patient had normal GH secretion. In conclusion, 1) no pattern of GH secretion is diagnostic of acromegaly due to ectopic GHRH secretion, but the lack of GH response to exogenous GHRH and a large rsponse during hypoglycemia may be features of this conditions. 2) When acromegaly and abnormal GH responsiveness are induced by a GHRH-secreting tumor, the increases in plasma GH after TRH, glucose, and insulin administration are not mediated by GHRH. 3) After removal of the GHRH-secreting tumor, persistent paradoxical GH response to TRH does not require abnormally high IR-GHRH levels and does not preclude complete recovery.