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Neurohypophyseal peptide function during early postoperative diabetes insipidus
Insights
Post-surgery diabetes insipidus (DI) in children is not caused by low vasopressin (AVP) levels. Instead, it may stem from inactive AVP precursors released from the damaged neurohypophysis, causing kidney resistance to AVP.
Area of Science:
- Pediatric Endocrinology
- Neurosurgery
- Nephrology
Background:
- Neurohypophyseal function is critical for fluid balance.
- Pituitary and suprasellar surgeries can impact neurohypophyseal function.
- Diabetes insipidus (DI) is a potential complication following such surgeries.
Purpose of the Study:
- To investigate neurohypophyseal function in children post-pituitary or suprasellar surgery.
- To determine the cause of early postoperative diabetes insipidus (DI).
- To assess vasopressin (AVP) levels and AVP precursor activity in relation to DI onset and resolution.
Main Methods:
- Studied 11 children undergoing pituitary or suprasellar surgery with hormone replacement.
- Monitored plasma vasopressin (AVP), neurophysin I, and oxytocin levels.
- Utilized high-performance liquid chromatography (HPLC) for AVP characterization.
- Administered desamino-8-D-arginine vasopressin (DDAVP) and conducted water deprivation tests.
Main Results:
- Nine out of 11 children developed DI within 12 hours of surgery.
- Plasma AVP levels were initially high at DI onset (3.9 +/- 1.2 pmol/l) and decreased significantly by day 2.
- HPLC revealed AVP immunoreactivity peaks coeluting with synthetic AVP.
- Urinary AVP excretion rate was higher on postoperative day 6 compared to day 14.
Conclusions:
- Early postoperative DI is likely due to biologically inactive AVP precursors from the damaged neurohypophysis, leading to renal resistance.
- Circulating AVP levels are not decreased at the onset of DI.
- Urinary AVP excretion patterns suggest dynamic changes in AVP processing or release post-surgery.
Abstract:
Neurohypophyseal function has been investigated in 11 children undergoing pituitary or suprasellar surgery. All had corticosteroid and thyroxine replacement; 9 developed diabetes insipidus (DI) within 1-12 h of operation. At the onset of DI, the plasma vasopressin (AVP) concentration was 3.9 +/- 1.2 pmol/l, considerably higher values usually associated with cranial DI (less than 0.9 pmol/l). AVP fell significantly to 1.1 +/- 0.2 pmol/l by the second day of DI. There was a similar change of levels of the AVP prohormone/carrier peptide, neurophysin I, but plasma oxytocin did not change significantly. High performance liquid chromatography of plasma at the onset of DI revealed a major peak that coeluted with synthetic AVP and two smaller peaks of AVP immunoreactivity. Seven patients required very large doses of desamino-8-D-arginine vasopressin (DDAVP) during the first day; 4 needed smaller doses on day 2. Water deprivation tests were performed on days 6 and 14 after operation in 5 patients with prolonged DI (2 with a triple response). There were no differences in plasma AVP on the two occasions but urinary AVP excretion rate was significantly higher on day 6 (2.4 +/- 0.8 pmol/h) than day 14 (0.7 +/- 0.3 pmol/h). It is concluded that early postoperative DI is not due to decreased levels of circulating AVP but may be related to the release of biologically inactive precursors from the damaged neurohypophysis. These may lead to renal refractoriness to AVP. There is a higher urinary AVP excretion rate on day 6 than day 14 after operation in both patients with a triple response and those with uninterrupted DI. Other factors may determine whether or not a transient resolution phase of DI occurs.