Absence of Changes in Antidiuretic Hormone, Angiotensin II, and Atrial Natriuretic Peptide With Clozapine Treatment of Polydipsia-Hyponatremia: 2 Case Reports
J Clin Psychiatry 1998;59:415-419
© Copyright 2014 Physicians Postgraduate Press, Inc.
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Background: Polydipsia-hyponatremia is a poorly understood disorder that
causes considerable mortality and morbidity. Hyponatremia in polydipsia-hyponatremia has
been attributed to disturbances in antidiuretic hormone (ADH) function. Improvements in
polydipsia-hyponatremia during clozapine treatment offered the chance to see if levels of
ADH and other hormones associated with osmoregulation changed with improvement in
biochemical and clinical measures of polydipsia-hyponatremia.
Method: In this preliminary, longitudinal study, we studied 2 male
schizophrenic patients (DSM-III-R) who had polydipsia-hyponatremia. Measures were (1)
biochemical and clinical: serum sodium and osmolality, urine osmolality and specific
gravity, normalized diurnal weight gain, and estimated urine volume and (2) endocrine:
ADH, angiotensin II, atrial natriuretic peptide, and prolactin. Measures were collected
during 2 months of baseline (typical neuroleptic) and 6 months of clozapine treatment.
Results: Single-case statistical procedures showed significant changes in
sodium levels (a.m. and p.m.), estimated urine volume, and a.m. urine specific gravity in
both patients and significantly decreased diurnal weight gain in 1 patient. Both serum and
urine osmolality showed improvement, but values did not reach statistical significance.
Low baseline ADH levels persisted through 6 months of clozapine treatment and showed no
changes in the context of improvements in serum sodium and osmolality. No significant
changes were seen in levels of angiotensin II and atrial natriuretic peptide.
Conclusion: Given the limitations of this study, there is some evidence
to suggest that the improvements in serum sodium and osmolality during clozapine treatment
of polydipsia-hyponatremia may not be related to serum levels of ADH, although altered ADH
receptor function cannot be ruled out. These data need to be extended in larger samples.