Syndrome of inappropriate antidiuretic hormone classification: Difference between revisions
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==Overview== | ==Overview== | ||
[[SIADH]] may be | [[SIADH]] may be classified into several sub-types based on the pattern of [[AVP]] ([[arginine vasopressin]]) secretion across a range of plasma osmolalities into type A, type B, type C and type D. | ||
==Classification== | ==Classification== | ||
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| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeA]] | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeA]] | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
* This type accounts for the most common form which constitutes about 60-70% of SIADH | * This type accounts for the most common form which constitutes about 60-70% of SIADH | ||
* There is excessive, random secretion of AVP, and linear relationship between plasma[[ osmolality]] and plasma[[ AVP]] is lost | * There is excessive, random secretion of AVP, and linear relationship between plasma[[ osmolality]] and plasma[[ AVP]] is lost | ||
*Commonly seen in [[lung cancer]] | *Commonly seen in [[lung cancer]] | ||
* Some studies have shown that some lung tumours synthesize AVP, and that [[tumour]] tissue stains positive for AVP[[ mRNA]] | * Some studies have shown that some lung tumours synthesize AVP, and that [[tumour]] tissue stains positive for AVP[[ mRNA]] | ||
*Plasma [[AVP]] concentrations in type A SIADH are not suppressed [[physiologically]] by drinking , which makes patients vulnerable to the development of severe [[hyponatremia]] | *Plasma [[AVP]] concentrations in type A SIADH are not suppressed [[physiologically]] by drinking , which makes patients vulnerable to the development of severe [[hyponatremia]] | ||
* Studies have also demonstrated a lower[[ osmotic]] threshold for [[thirst]] appreciation in this type of [[SIADH]] | * Studies have also demonstrated a lower[[ osmotic]] threshold for [[thirst]] appreciation in this type of [[SIADH]] | ||
* This type of SIADH is also characteristic of [[nasopharyngeal tumours]], which also stain positive for AVP[[ mRNA]] | * This type of SIADH is also characteristic of [[nasopharyngeal tumours]], which also stain positive for AVP[[ mRNA]] | ||
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*Accounts for (20–40%) of the cases | *Accounts for (20–40%) of the cases | ||
*The[[ osmotic]][[ threshold ]]for AVP release is lowered – a | *The[[ osmotic]][[ threshold ]]for AVP release is lowered – a reset osmostat – such that secretion of AVP occurs at lower plasma [[osmolalities]] than normal | ||
*AVP is suppressed at plasma osmolalities below the lower, reset threshold, further over-[[hydration]] leads to suppression of AVP release, which protects against the progression to severe[[ hyponatraemia]] | *AVP is suppressed at plasma osmolalities below the lower, reset threshold, further over-[[hydration]] leads to suppression of AVP release, which protects against the progression to severe[[ hyponatraemia]] | ||
*Although most | *Although most tumors manifest type A[[ SIADH]], some also present with type B SIADH, so the[[ pattern]] of [[abnormal]][[ AVP]] (arginine vasopressin) secretion cannot be utilized to predict the [[causation]] of [[SIADH]] | ||
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| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeC]] | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[TypeC]] | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
* A rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the [[osmotic]] threshold | * A rare condition characterized by failure to suppress AVP secretion at plasma osmolalities below the [[osmotic]] threshold | ||
* Plasma [[AVP]] concentrations are thus inappropriately high at low plasma osmolalities, but there is a normal relationship between plasma osmolality and plasma AVP at physiological plasma osmolalities | * Plasma [[AVP]] concentrations are thus inappropriately high at low plasma osmolalities, but there is a normal relationship between plasma osmolality and plasma AVP at physiological plasma osmolalities | ||
*This variant may be due to dysfunction of inhibitory neurons in the[[ hypothalamus]], leading to persistent low-grade basal AVP secretion | *This variant may be due to dysfunction of inhibitory neurons in the[[ hypothalamus]], leading to persistent low-grade basal AVP secretion | ||
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| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Type D]] | | style="padding: 5px 5px; background: #DCDCDC; font-weight: bold; text-align:center;" |[[Type D]] | ||
| style="padding: 5px 5px; background: #F5F5F5;" | | | style="padding: 5px 5px; background: #F5F5F5;" | | ||
* Is a rare clinical picture of [[SIADH]] with low or undetectable[[ AVP]] levels and no detectable abnormality in circulating AVP response | |||
*Is a rare clinical picture of [[SIADH]] with low or undetectable[[ AVP]] levels and no detectable abnormality in circulating AVP response | *It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture | ||
*It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture | *Gain-of-function[[ mutations]] in the V2 receptor leading to a clinical picture of SIADH, with undetectable AVP levels, have been described | ||
*Gain-of-function[[ mutations]] in the V2 receptor leading to a clinical picture of SIADH, with undetectable AVP levels, have been described | *The identified mutations had different [[nucleotide]] substitutions causing different levels of V2 receptor activation | ||
*The identified mutations had different [[nucleotide]] substitutions causing different levels of V2 receptor activation | *This syndrome appears to be inherited in an X-linked manner,although heterozygous females may have varying degrees of inappropriate antidiuresis. Owing to variable expressivity of the [[gene]] involved,[[ NSIAD]] may be clinically undetectable for years, until other contributing factors in later life lead to clinically significant hyponatraemia<ref name="pmid20164214">{{cite journal |vauthors=Hannon MJ, Thompson CJ |title=The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences |journal=Eur. J. Endocrinol. |volume=162 Suppl 1 |issue= |pages=S5–12 |year=2010 |pmid=20164214 |doi=10.1530/EJE-09-1063 |url=}}</ref> | ||
*This syndrome appears to be inherited in an X-linked manner,although heterozygous females may have varying degrees of inappropriate antidiuresis. Owing to variable expressivity of the [[gene]] involved,[[ NSIAD]] may be clinically undetectable for years, until other contributing factors in later life lead to clinically significant hyponatraemia | |||
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Revision as of 20:35, 24 August 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
SIADH may be classified into several sub-types based on the pattern of AVP (arginine vasopressin) secretion across a range of plasma osmolalities into type A, type B, type C and type D.
Classification
SIADH may be classified in to several sub-types based on the pattern ofAVPsecretion across a range of plasma osmolalities:
Classification | Features |
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TypeA |
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Type B |
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TypeC |
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Type D |
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References
- ↑ Hannon MJ, Thompson CJ (2010). "The syndrome of inappropriate antidiuretic hormone: prevalence, causes and consequences". Eur. J. Endocrinol. 162 Suppl 1: S5–12. doi:10.1530/EJE-09-1063. PMID 20164214.