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Syndrome of inappropriate antidiuretic hormone hypersecretion

Syndrome of inappropriate antidiuretic hormone secretion
Synonym Schwartz-Bartter syndrome, syndrome of inappropriate antidiuresis(SIAD)
Explanation of SIADH
Classification and external resources
Specialty Endocrinology
ICD-10 E22.2
ICD-9-CM 253.6
DiseasesDB 12050
MedlinePlus 003702
eMedicine emerg/784 med/3541 ped/2190
MeSH D007177
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Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive release of antidiuretic hormone from the posterior pituitary gland or another source. The increase in blood volume (hypervolemia) often results in true hyponatremia in which the plasma sodium levels are lowered and total body fluid is increased. Although the sodium level is low, SIADH is brought about by an excess of water rather than a deficit of sodium.

It was originally described in people with small-cell carcinoma of the lung, but it can be caused by a number of underlying medical conditions. The treatment may consist of fluid intake restriction, various medicines, and management of the underlying cause. Salt administration may help prevent brain swelling by increasing attractive force to keep water in the bloodstream, preventing fluid buildup in tissue. SIADH was first described in 1957.

Patients with SIADH will be euvolemic with:

Urinalysis will reveal a highly concentrated urine with a high fractional excretion of sodium (high sodium urine content compared to the serum sodium).Certain prominent physical findings may be seen only in severe or rapid-onset hyponatremia, such as seizure and other neurological signs.

Causes of SIADH include conditions that dysregulate ADH secretion in the central nervous system, tumors that secrete ADH, drugs that increase ADH secretion, and many others. A list of common causes is below:

The normal function of ADH on the kidneys is to control the amount of water reabsorbed by kidney nephrons. ADH acts in the distal portion of the renal tubule (Distal Convoluted Tubule) as well as on the collecting duct and causes the retention of water, but not solute. Hence, ADH activity effectively dilutes the blood (decreasing the concentrations of solutes such as sodium), causing hyponatremia; this is compounded by the fact that the body responds to water retention by decreasing aldosterone, thus allowing even more sodium wasting. For this reason, a high urinary sodium excretion will be seen.


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