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Journal of Clinical Endocrinology & Metabolism Vol. 67, No. 3 571-575
doi:10.1210/jcem-67-3-571
Copyright © 1988 by the Endocrine Society.
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Plasma Atrial Natriuretic Hormone Levels in Patients With the Syndrome of Inappropriate Antidiuretic Hormone Secretion*

C. MANOOGIAN, M. PANDIAN, L. EHRLICH, D. FISHER and R. HORTON

University of Southern California School of Medicine Los Angeles, California 90033
Nichols Institute San Juan Capistrano, California 00000
Harbor-University of California-Los Angeles Torrance, California 00000

This study explored whether atrial natriuretic hormone (ANH) might be involved in the escape from salt and water retention that occurs in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Sixteen patients with low serum Na+ concentrations [123 ± 1 (±SE) mmol/L] were studied. Each patient excreted urine that was hyperosmolar (mean, 391 ± 46 mosmol/kg) in relation to serum osmolality (mean, 258 ± 4 mosmol/kg). Sodium excretion (81 ± 20 mmol/L) also was inappropriate to the low serum Na+ level. The probable causes of SIADH were head trauma (4), pneumonia (5), lung cancer (3), and chlorpropamide therapy (4). In the nontumor patients, plasma and/or urinary vasopressin (AVP) concentrations were in the normal range, but inappropriate for serum osmolality. Urinary AVP values of 50 pg/mL or more (>46 pmol/L) were found in the three tumor patients. The mean plasma ANH concentration was 6-fold higher than that in normal subjects [296 ± 51 vs. 51 ± 13 pg/mL (100 ± 20 vs. 17 ± 4 pmol/L); P < 0.01]. Six SIADH patients were studied again after brief (1-3 days) water restriction. Although serum osmolality increased in each, their plasma AVP concentrations decreased very little, and urinary AVP excretion and plasma ANH did not change. These results indicate that plasma ANH levels are markedly increased in patients with SIADH. Their increased ANH secretion may antagonize water retention resulting from the inappropriate AVP secretion.

* This work was supported by grants from the NIH (HL-21112 and HD-06335).

Received November 9, 1987.




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Copyright © 1988 by The Endocrine Society