 | This article needs more reliable medical references for verification or relies too heavily on primary sources. (January 2019) |  |
| Syndrome of inappropriate antidiuretic hormone secretion | |
|---|---|
| Other names | Schwartz-Bartter syndrome, syndrome of inappropriate antidiuresis (SIAD) |
| Specialty | Endocrinology |
| Symptoms | Lack of appetite, nausea, vomiting, abdominal pain, seizures and coma[1] |
The syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD),[2] is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source.[1] Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia (a low plasma osmolality and low sodium levels).[2]
The causes of SIADH are commonly grouped into categories including: central nervous system diseases that directly stimulate the hypothalamus to release ADH, various cancers that synthesize and secrete ectopic ADH, various lung diseases, numerous drugs that may stimulate the release of ADH, enhance ADH effects, act as ADH analogues in the body, or stimulate the vasopressin receptor 2 at the kidney (the site of ADH action); or inherited mutations leading to a gain of function of the vasopressin-2 receptor (a very rare occurrence).[2] Inappropriate antidiuresis may also be due to acute stressors such as exercise, pain, severe nausea or during the post-operative state. In 17–60% of people, the cause of inappropriate antidiuresis is never found.[2]
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 reabsorption and return to the circulation, and the hypertonicity is alleviated.[2] A decrease in the effective circulating volume of blood (the volume of arterial blood effectively perfusing tissues) also stimulates an appropriate, physiologic release of ADH.[2] Inappropriate (increased) ADH secretion causes a physiologically inappropriate water reabsorption by the kidneys. This causes the extracellular fluid (ECF) space to become hypo-osmolar, including a low sodium concentration (hyponatremia).[2] In the intracellular space, cells swell as intracellular volume increases as water moves from an area of low solute concentration (extracellular space) to an area of high solute concentration (the cells' interior). In severe or acute hypoosmolar hyponatremia, swelling of brain cells causes various neurological abnormalities, which in severe or acute cases can result in convulsions, coma, and death. The symptoms of chronic syndrome of inappropriate antidiuresis are more vague, and may include cognitive impairment, gait abnormalities, or osteoporosis.[2]
The main treatment of inappropriate antidiuresis is to identify and treat the underlying cause, if possible. This usually causes plasma osmolality and sodium levels to return to normal in several days.[2] In those in which an underlying cause cannot be found, or is untreatable, treatments are targeted to alleviating correcting the hypoosmolality and hyponatremia.[2] These include restriction of fluid intake, using salt tablets (sometimes with diuretics), urea supplements, or increasing the protein intake.[2] The vasopressin receptor 2 blocker tolvaptan may also be used.[2] The presence of cerebral edema, or other moderate to severe symptoms, may necessitate intravenous hypertonic saline administration with close monitoring of the serum sodium levels to avoid overcorrection.[2]
SIADH was originally described in 1957 in two people with small-cell carcinoma of the lung.[3]
- ^ a b Babar SM (October 2013). "SIADH associated with ciprofloxacin". The Annals of Pharmacotherapy. 47 (10): 1359–63. doi:10.1177/1060028013502457. PMID 24259701. S2CID 36759747.
- ^ a b c d e f g h i j k l m Adrogué, Horacio J.; Madias, Nicolaos E. (19 October 2023). "The Syndrome of Inappropriate Antidiuresis". New England Journal of Medicine. 389 (16): 1499–1509. doi:10.1056/NEJMcp2210411. PMID 37851876. S2CID 264305156.
- ^ 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. doi:10.1681/ASN.V12122860. PMID 11729259.