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==Overview==
==Overview==
[[SIADH]] may be [[classified]] into several sub-types based on the pattern of [[AVP]]( [[arginine vasopressin]]) secretions across a range of plasma osmolalities: Type A, type B, type C, type D.
[[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 [[reset osmostat]] – such that secretion of AVP occurs at lower plasma [[osmolalities]] than normal.  
*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 [[tumours]] 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]].
*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]]


|-
|-
| 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


|-
|-
| 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;" |
* Type D:
* 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 . <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>  


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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
TypeA
  • 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 plasmaosmolality and plasmaAVP is lost
  • Commonly seen in lung cancer
  • Some studies have shown that some lung tumours synthesize AVP, and that tumour tissue stains positive for AVPmRNA
  • 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 lowerosmotic threshold for thirst appreciation in this type of SIADH
  • This type of SIADH is also characteristic of nasopharyngeal tumours, which also stain positive for AVPmRNA
Type B
  • Accounts for (20–40%) of the cases
  • Theosmoticthreshold 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 severehyponatraemia
  • Although most tumors manifest type ASIADH, some also present with type B SIADH, so thepattern of abnormalAVP (arginine vasopressin) secretion cannot be utilized to predict the causation of SIADH
TypeC
  • 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
  • This variant may be due to dysfunction of inhibitory neurons in thehypothalamus, leading to persistent low-grade basal AVP secretion
Type D
  • Is a rare clinical picture of SIADH with low or undetectableAVP levels and no detectable abnormality in circulating AVP response
  • It is thought that a nephrogenic SIADH (NSIAD) may be responsible for this picture
  • Gain-of-functionmutations 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
  • 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[1]

References

  1. 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.

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