ECE2019 ePoster Presentations Pituitary and Neuroendocrinology (37 abstracts)
Kyung Hee University School of Medicine, Seoul, Republic of Korea.
Acromegaly is an insidious disease that results from excessive growth hormone (GH) secretion from the pituitary tumor. Major advances have occurred in the understanding of some aspects of acromegaly, such as the biology of pituitary tumors, physiology, molecular mechanisms of GH secretion. In a point of GH producing pituitary adenoma, it was located in a pituitary gland, even though macroadenoma. Macroadenoma was bigger than normal pituitary, remnant normal pituitary gland existed with shrunken state. So, GH was secreted from the both pools of GH of the normal remnant pituitary gland and GH producing adenoma respectively. These GH secretory phenomena by blood glucose were interpreted as physiologic response with pituitary GH pools. Neuroendocrinologist must investigate characteristics and dynamic patterns of these two different pools of GH at the time of diagnosis for the GH behavior of acromegalics. The physiologic GH pools were mainly regulated by blood glucose levels. Hyperglycemia could suppress GH secretion from the normal pituitary via somatostatinergic pathway, and somewhat influence to block GH secretion from the GH producing pituitary tumor. For checking it, we used oral glucose tolerance test (oGTT) with 75 grams of glucose solution. Also, hypoglycemia below 40 mg/dL induced by regular insulin (insulin tolerance test, ITT) could stimulate GH secretion from the normal pituitary gland at 60 to 90 minutes after insulin injection. The GH secretory dynamic pattern would be normal, if the peak GH level was over 5 μg/L during test. These GH secretory phenomena by blood glucose were interpreted as physiologic response with pituitary GH pools.
During medical treatment, we also tested previously mentioned 4 different active tests reflected to GH secretory status from the normal pituitary and tumor tissues. Average treatment period was 10.5 (6.324.5) years for cured patients and 9.4 (4.914.0) years for uncured patients. After medical treatment, cured patients showed that complete responder rate was 100% (8/8) for TRH stimulation test (TST), 87.5% (7/8) for insulin tolerance test (ITT), and 100% (8/8) for octreotide suppression test (OST). Uncured patients showed that complete responder rate was 75% (6/8) for TST, 75% (6/8) for ITT and 25% (2/8) for OST. Fully completed responders of these 3 dynamic tests revealed that 50% (4/8) from cured group, and 25% (2/8) at the time of pre-treatment. After treatment, full responded patients of these 3 different tests were 87.5 (7/8) from cured group, and only 12.5% (1/8) from uncured group.