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Neurohypophyseal peptide function during early postoperative diabetes insipidus
Brain : a Journal of Neurology
|June 1, 1987
Summary
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.