Syndrome of inappropriate antidiuretic hormone secretion

 

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Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by excessive unsuppressible release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes an unrelenting increase in solute-free water being returned by the tubules of the kidney to the venouscirculation.

The causes of SIADH are grouped into six categories: 1) central nervous system diseases that directly stimulate the hypothalamus, the site of control of ADH secretion; 2) various cancers that synthesize and secrete ectopic ADH; 3) various lung diseases; 4) numerous drugs that chemically stimulate the hypothalamus; 5) inherited mutations; and 6) miscellaneous largely transient conditions.[1]

ADH is derived from a preprohormone precursor that is synthesized in cells in the hypothalamus and stored in vesicles in the posterior pituitary. Appropriate ADH secretion is regulated by osmoreceptors on the hypothalamic cells that synthesize and store ADH: plasma hypertonicity activates these receptors, ADH is released into the blood stream, the kidney increases solute-free water return to the circulation, and the hypertonicity is alleviated. Inappropriate (increased) ADH secretion causes an unrelenting increase in solute-free water (“free water”) absorption by the kidneys, with two consequences. First, in the extracellular fluid (ECF) space, there is a dilution of blood solutes, causing hypoosmolality, including a low sodium concentration – hyponatremia. Then virtually simultaneously, in the intracellular space, cells swell, i.e. intracellular volume increases. Swelling of brain cells causes various neurological abnormalities which in severe or acute cases can result in convulsions, coma, and death.

Potential treatments of SIADH include restriction of fluid intake, correction of an identifiable reversible underlying cause, and/or medication which promotes solute-free water excretion by the kidney. The presence of cerebral edema may necessitate intravenous isotonic or hypertonic saline administration.[1] SIADH was originally described in 1957 in two people with small-cell carcinoma of the lung.[2]

  1. Ellison, David H.; Berl, Tomas (2007). “The Syndrome of Inappropriate Antidiuresis”. New England Journal of Medicine. 356 (20): 2064–72. doi:10.1056/NEJMcp066837. PMID 17507705. [needs update]
  2. ^ Jump up to: a b Schwartz, William B.; Bennett, Warren; Curelop, Sidney; Bartter, Frederic C. (1957). “A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone”. The American Journal of Medicine. 23 (4): 529–42. doi:10.1016/0002-9343(57)90224-3. PMID 13469824. reproduced as a Milestone in Nephrology with author commentary in Schwartz, William B.; Bennett, Warren; Curelop, Sidney; Bartter, Frederic C. (2001). “A syndrome of renal sodium loss and hyponatremia probably resulting from inappropriate secretion of antidiuretic hormone. 1957” (PDF). Journal of the American Society of Nephrology. 12 (12): 2860–70. PMID 11729259.

AN antidiuretic is a substance that helps to control fluid balance in an animal’s body by reducing urination,[1] opposing diuresis.[2] Its effects are opposite that of a diuretic. The major endogenous antidiuretics are antidiuretic hormone (ADH; also called vasopressin) and oxytocin. Both of those are also used exogenously as medications in people whose bodies need extra help with fluid balance via suppression of diuresis. In addition, there are various other antidiuretic drugs, some molecularly close to ADH or oxytocin and others not. Antidiuretics reduce urine volume, particularly in diabetes insipidus (DI), which is one of their main indications.

The antidiuretic hormone class includes vasopressin (ADH), argipressin, desmopressin, lypressin, ornipressin, oxytocin, and terlipressin. Miscellaneous others include chlorpropamide and carbamazepine.

 

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