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Diminished glucocorticoid negative feedback in polydipsic hyponatremic schizophrenic patients
Morris B Goldman1, Gordon Wood, Megan B Goldman
1Department of Psychiatry, University of Chicago and Psychiatric Institute, Chicago, Illinois 60637, USA. m-goldman@uchicago.edu
The Journal of Clinical Endocrinology and Metabolism
|November 23, 2006
Summary
Schizophrenia patients with primary polydipsia, especially those with hyponatremia, show impaired glucocorticoid negative feedback. This dysfunction suggests hippocampal mineralocorticoid abnormalities in these patients.
Area of Science:
- Neuroendocrinology
- Psychiatry
Background:
- Diminished glucocorticoid negative feedback is observed in schizophrenia, particularly in patients with primary polydipsia.
- Hyponatremic polydipsic patients exhibit neuroendocrine abnormalities linked to hippocampal pathology.
Purpose of the Study:
- To investigate the effect of cortisol on plasma ACTH.
- To assess glucocorticoid feedback under conditions sensitive to hippocampal influence.
Main Methods:
- Repeated measures design at an inpatient clinical research center.
- Administration of metyrapone and hydrocortisone infusion.
- Measurement of plasma ACTH and cortisol levels in patient groups and healthy volunteers.
Main Results:
- Polydipsic hyponatremic patients showed no significant ACTH decline during cortisol infusion.
- Elevated ACTH levels were observed in hyponatremic patients for any given cortisol level.
- Other groups exhibited cortisol-induced ACTH decline, most pronounced in non-water-imbalanced patients.
Conclusions:
- Marked impairment of glucocorticoid negative feedback in polydipsic hyponatremic schizophrenic patients.
- Findings are consistent with hippocampal mineralocorticoid dysfunction in this patient group.
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