ECE2019 Poster Presentations Pituitary and Neuroendocrinology 3 (73 abstracts)
Endocrinology Research Centre, Moscow, Russian Federation.
Introduction: Hyponatremia after transnasal neurosurgery for pituitary adenomas is a serious and not so rare complication. It often occurs in a delayed manner after patients discharge and is a major cause of readmission. The pathogenesis of postneurosurgical hyponatremia is not clear yet.
Aims: To study the role of posterior pituitary hormones (antidiuretic hormone (ADH) and apelin) and reaction of renin-aldosterone system (RAS) at hyponatremia manifestation.
Materials and methods: The study included 13 patients with debut of hyponatremia after transnasal adenomectomy, three men and 10 women, with median age 58 years [46; 62], without decompensated pituitary deficiencies or desmopressin treatment. Median decrease in blood sodium level was 122 mmol/l [117; 126]. The control group consisted of healthy female volunteers of median age 24 years [23; 25]. Apelin-12 and copeptin (as surrogate for ADH) were measured by EIA (Phoenix Pharmaceuticals, Inc). Renin and aldosterone evaluated by Cobas 6000 (Roche Diagnostics).
Results: In patients with hyponatremia there were no significant differences compared to controls in levels of copeptin (0.382 ng/ml [0.274; 0.451] vs. 0.273 [0.200; 0.431], P>0.05), increased levels of apelin-12 (0.111 ng/ml [0.098; 0.242] 0.072 [0.052; 0.109], P=0.02), decreased concentrations of aldosterone (220 mmol/l [112; 345] vs. 594 [272; 979], P=0.03) and no significant changers in renin activity (1.1 [0.6; 2.0] vs. 1.2 [0.6; 2.1], P>0.05). Strong positive correlations were seen for apelin and blood sodium (r=0.64, P<0.01), plasma osmolality (0.67, P=0.009), and urine osmolality (0.83, P=0.003).
Conclusions: In case of hyponatremia after transnasal adenomectomy, there is not only an unsuppressed by hyponatremia blood levels of a surrogate marker of secretion of ADH, copeptin, but also an increase in its counterregulatory hormone apelin, which may correspond to increased secretion from damaged terminals of axons of magnocellular neurons along with ADH or increased secretion in response to hyponatremia and hypervolemia. RAS appears to be depressed.