Changes of GH Axis after Transsphenoidal Adenomectomy in 1766 Patients with Pituitary Adenoma
Presentation Number: SUN 423
Date of Presentation: April 2nd, 2017
Cheol Ryong Ku*1, Jae Won Hong2, Daham Kim1, Seunghee Han3, Se Hee Park1, Young Ki Lee1, Sun Ho Kim1 and Eun Jig Lee1
1Yonsei University College of Medicine, Seoul, Korea, Republic of (South), 2Inje University Ilsan Paik Hospital, Korea, Republic of (South), 3Yonsei University College of Medicine, Seoul
Objective: Impaired GH secretion usually accompanied in patients with pituitary adenoma after transsphenoidal adenomectomy (TSA). Although surgery itself could induce the GH deficiencies, changes of pituitary hormones and removal of mass effect after TSA might influence on the secretory function of GH axis. In this study, we evaluated the changes of GH axis in patients with pituitary adenoma after TSA.
Research Design and Methods: From the cohorts of Severance Hospital Pituitary Tumor Clinic, GH axis had been evaluated in patients with pituitary adenoma after TSA. GH deficiency (GHD) was defined when the peak serum GH level was less than 3.0 ng/mL in insulin tolerance tests (ITT) which were conducted before TSA and at least 2 times at 1.5 years intervals after TSA.
Results: The GH axis of 1766 patients with pituitary adenoma had been evaluated 2.77±1.54 times with ITT for 4.77±3.75 years. The enrolled patients were consisted of 536 (30.4%) in GH secreting pituitary adenoma, 90 (5.1%) in Cushing disease, 255 (14.4%) in prolactinoma, 32 (1.8%) in TSH secreting pituitary adenoma, and 853 (48.3%) in nonfunctioning pituitary adenoma (NFPA). There were no differences in number of ITT and follow up duration between patients with each pituitary adenoma. The frequency of preoperative GHD was significantly higher in patients with Cushing disease (68/90; 75.6%) than subjects with prolactinoma, TSH secreting pituitary adenoma, and NFPA (66/255; 25.9%, 6/32; 18.8%, and 511/853; 60.0%, respectively) (P < 0.001). After TSA, newly developed GH deficiencies were diagnosed in 49/534 (9.2%) in GH secreting pituitary adenoma, 9/22 (40.9%) in Cushing disease, 17/189 (9.0%) in prolactinoma, 1/26 (3.8%) in TSH secreting pituitary adenoma, and 46/342 (13.5%) in NFPA. Among the patients with GHD before TSA, the recovery rates of GH axis were 25/68 (36.8%) in Cushing disease, 37/66 (56.1%) in prolactinoma, 4/6 (66.7%) in TSH secreting pituitary adenoma, and 158/511 (30.9%) in NFPA. Younger age (42.22±12.49 vs. 48.05±12.95, P=0.014), female gender (135/338; 39.9% vs. 91/315; 28.9% P<0.001), and low grade Hardy classification (31/60; 51.7% vs. 42/67; 62.7%, 122/409; 29.8% vs. 31/117; 26.5%, Hardy I, II, III, and IV, respectively, P<0.001) were significantly associated with recovery of GH axis from GHD after TSA.
Conclusions: Several clinical factors including classification of pituitary adenoma were significantly associated with changes of GH axis before and after TSA. These data provide the first clinical evidence that differentiating evaluations for GHD should be applied according to the classification of pituitary hormones.
Nothing to Disclose: CRK, JWH, DK, SH, SHP, YKL, SHK, EJL