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Ectopic ADH secretion

Ectopic ADH secretion is the release of antidiuretic hormone (ADH, also called vasopressin, or AVP) from a place in the body where it is not normally produced. ADH is a substance produced naturally by the hypothalamus and released by the pituitary gland. This hormone controls the amount of water your body loses through the urine.

Ectopic means "out of place."

Alternative Names

SIADH; Syndrome of inappropriate antidiuretic hormone secretion


Ectopic ADH secretion is rare. The most common cause of ectopic ADH secretion is cancer. Certain lung cancers and some head and neck tumors are the most common cancers that cause this problem. In very rare cases, other tumors can cause ectopic ADH secretion.


The ectopic, unregulated release of ADH makes it harder for the body to excrete water in the urine. Too much water is kept in the blood and dilutes many substances in the blood. Low blood sodium level (hyponatremia) can result.

Often, there are no symptoms from a low sodium level. But changes in mental status, including confusion, decreased memory, and strange behavior can occur. In rare cases, a low blood sodium level can cause seizures .


Treatment is aimed at removing the cause of the problem. For example, surgery is done to remove a tumor producing ADH.

Limiting fluid intake is another common treatment. This helps prevent excess fluid from building up in the body. Patients in the hospital with ectopic ADH secretion that does not respond to other treatments may be given medicines to block the effects of ADH on the kidneys so that excess water is be excreted by the kidneys.


Robinson AG, Verbalis JG. Posterior pituitary. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, eds. Williams Textbook of Endocrinology. 12th ed. Philadelphia, PA: Elsevier Saunders; 2011:chap 10.

Updated: 11/7/2013

Brent Wisse, MD, Associate Professor of Medicine, Division of Metabolism, Endocrinology & Nutrition, University of Washington School of Medicine. Also reviewed by David Zieve, MD, MHA, Bethanne Black, and the A.D.A.M. Editorial team. 11/07/13

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