Methods: The retrospective observational study of all consecutive cases of pituitary adenoma treated with ETS in Hospital Kuala Lumpur (HKL) between 2006 and 2015. Age, sex, pre- and post-operative hormone level, tumour size, and complications were noted.
Results: A total of 67 patients were diagnosed with non-functioning pituitary adenoma throughout this period. Of these, 11 patients had both visual and hormonal improvement post-operation. Of the 27 patients with tumour invaded into the cavernous sinus, 13 showed an improved vision. In the adenoma patients who had impaired hormonal function before the surgery, the hormone level normalised post-surgery in 42 patients. Moreover, 39 patients were diagnosed with functioning pituitary adenoma. Ten patients recovered from acromegaly and four patients recovered from Cushing disease within seven days post-operative. Also, five patients with functioning adenoma suffered complications.
Conclusion: Outcome for the preservation and hormone recovery in non-functioning pituitary adenoma group was satisfactory, with only one patient's hormonal level worsening. No visual deterioration and mortality were detected throughout this study. A dedicated team specialised in endoscopic transsphenoidal pituitary surgery further improved the outcome of this surgical method.
METHODS: Medline (1946-) and Embase (1947-) were searched until 23rd January 2019 for original studies. A meta-analysis was performed of remission and recurrence rates. Studies were excluded if patients had prior radiosurgery/radiotherapy, mixed pathologies or interventions without separated data, follow-up not reported or population size
RESULTS: We show that Rasd1 is expressed in vasopressin neurons of the PVN and SON, within which mRNA levels are induced by hyperosmotic cues. Dexamethasone treatment of AtT20 cells decreased forskolin stimulation of c-Fos, Nr4a1 and phosphorylated CREB expression, effects that were mimicked by overexpression of Rasd1, and inhibited by knockdown of Rasd1. These effects were dependent upon isoprenylation, as both farnesyltransferase inhibitor FTI-277 and CAAX box deletion prevented Rasd1 inhibition of cAMP-induced gene expression. Injection of lentiviral vector into rat SON expressing Rasd1 diminished, whereas CAAX mutant increased, cAMP inducible genes in response to osmotic stress.
CONCLUSIONS: We have identified two mechanisms of Rasd1 induction in the hypothalamus, one by elevated glucocorticoids in response to stress, and one in response to increased plasma osmolality resulting from osmotic stress. We propose that the abundance of RASD1 in vasopressin expressing neurons, based on its inhibitory actions on CREB phosphorylation, is an important mechanism for controlling the transcriptional responses to stressors in both the PVN and SON. These effects likely occur through modulation of cAMP-PKA-CREB signaling pathway in the brain.