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===Medical and Neurologic causes===
{| style="width:70%; height:100px" border="1"
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" | '''Neurologic disorders
| style="width:75%" bgcolor="Beige" ; border="1" | Cerebral neoplasms, cerebral trauma and post concussive syndromes ,Cerebrovascular disease, [[subarachnoid hemorrhage]], [[Migraine]], [[encephalitis]],[[ cerebral syphilis]], [[Multiple sclerosis]],[[Wilsons disease]],[[Huntington disease]],[[Epilepsy]]
|-
|- bgcolor="LightSteelBlue"
| ''' Endocrine disorder'''
| bgcolor="Beige" | [[ Pituitary dysfunction]], [[Thyroid]] dysfunction, [[ parathyroid dysfunction]], [[Adrenal dysfunction]],[[ pheochromocytoma]]
|-
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" | '''Systemic conditions'''
| style="width:75%" bgcolor="Beige" ; border="1" | Hypoxia, Cardiovascular disease, pulmonary insufficiency, [[anemia]]
|-
|- bgcolor="LightSteelBlue"
| '''Inflammatory disorders'''
| bgcolor="Beige" | [[ Lupus erythematosus]], [[rheumatoid arthritis]], [[ polyarteritis nodosa]], [[temporal arteritis]]
|-
|- bgcolor="LightSteelBlue"
| '''Deficiency states'''
| bgcolor="Beige" | Vitamin B12 deficiency, [[ pellagra]]
|- bgcolor="LightSteelBlue"
| '''Miscellaneous '''
| bgcolor="Beige" | [[ hypoglycemia]], [[carcinoid syndrome]], [[ uremia]], [[premenstrual syndrome]], [[porphyria]]
|-
|- bgcolor="LightSteelBlue"
| '''Substances'''
| bgcolor="Beige" | [[Caffeine]],[[cannabis]],[[Hallucinogens]], [[theophylline]], [[amphetamines]],[[yohimbine]],[[sympathomimetics]], [[mercury]], [[Arsenic]],[[organophosphates]],[[benzene]]
|-
|- bgcolor="LightSteelBlue"
| '''Withdrawal'''
| bgcolor="Beige" | [[alcohol]],[[caffeine]], [[opiods]],[[antihypertensives]]


|}
_NOTOC _
{{CMG}};{{AE}}{{Vbe}}


siadh classification
==Causes==
==Classification==
[[Hypogammaglobulinemia]] is caused by:


[[SIADH]] may be classified in to several sub-types based on the pattern of AVP secretion across a range of plasma osmolalities:
Immunodeficiency secondary to:
*[[Uremia]]
*Protein losing enteropathy
*[[Nephrotic syndrome]]
*Malnutrition
*Cirrhosis
*Hemodialysis
* Intestinal lymphangiectasia


*Type A : is the commonest form of [[SIADH]] responsible for a much higher proportion of SIADH, at around 60–70%. Characteristically, type A patients exhibit excessive, random secretion of AVP, with loss of the close linear relationship between plasma osmolality and plasma[[ AVP]]. Type A is common in [[lung cancer]]; in[[ vitro studie]]s have demonstrated 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]]. 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.
* Protein-losing gastroenteropathy
*[[Nephrotic syndrome]]
*[[Thymoma]] <ref name="pmid29881497">{{cite journal |vauthors=Aouadi S, Ghrairi N, Braham E, Kaabi M, Maâlej S, Elgharbi LD |title=[Acquired hypogammaglobulinemia associated with thymoma: Good syndrome] |language=French |journal=Pan Afr Med J |volume=28 |issue= |pages=253 |date=2017 |pmid=29881497 |pmc=5989270 |doi=10.11604/pamj.2017.28.253.11352 |url=}}</ref>
* Medications :
** Gold
**D-Penicillamine
**Sulfasalazin
**Anticonvulsants
**Glucocorticoids
**Methotrexate
**Calcineurin inhibitors
** Rituximab<ref name="pmid29755528">{{cite journal |vauthors=Shoukat BA, Ali O, Kumar D, Bilal Gilani M, Zahid A, Aslam Joiya S, Anwar Malik M |title=Hypogammaglobulinemia Observed One Year after Rituximab Treatment for Idiopathic Thrombocytopenic Purpura |journal=Case Rep Med |volume=2018 |issue= |pages=2096186 |date=2018 |pmid=29755528 |pmc=5884289 |doi=10.1155/2018/2096186 |url=}}</ref><ref name="pmid29752554">{{cite journal |vauthors=Farhat L, Dara J, Duberstein S, De A |title=Secondary Hypogammaglobulinemia After Rituximab for Neuromyelitis Optica: A Case Report |journal=Drug Saf Case Rep |volume=5 |issue=1 |pages=22 |date=May 2018 |pmid=29752554 |pmc=5948191 |doi=10.1007/s40800-018-0087-y |url=}}</ref><ref name="pmid29627491">{{cite journal |vauthors=Thorlacius H, Jerkeman A, Marginean FE, Toth E |title=Colorectal malakoplakia in a patient with hypogammaglobulinemia |journal=Gastrointest. Endosc. |volume= |issue= |pages= |date=April 2018 |pmid=29627491 |doi=10.1016/j.gie.2018.04.001 |url=}}</ref>


* Environmental hazards:
** Ionizing radiation
**Toxins


*Type B: is also common (20–40%). The osmotic[[ threshold ]]for AVP release is lowered – a [[reset osmostat]] – such that secretion of AVP occurs at lower plasma [[osmolalities]] than normal. Because [[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 secretion cannot be utilized to predict the [[causation]] of SIADH.
*Infections
 
** Viral(Herpes, Measles)
 
**Bacterial(Mycobacterial)
*Type C :is 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 the hypothalamus, leading to persistent low-grade basal AVP secretion.
**Parasitic(Malaria, helminthic infections)
 
 
*Type D: 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 . 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. 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>

Latest revision as of 14:23, 3 August 2018


_NOTOC _ Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Causes

Hypogammaglobulinemia is caused by:

Immunodeficiency secondary to:

  • Protein-losing gastroenteropathy
  • Nephrotic syndrome
  • Thymoma [1]
  • Medications :
    • Gold
    • D-Penicillamine
    • Sulfasalazin
    • Anticonvulsants
    • Glucocorticoids
    • Methotrexate
    • Calcineurin inhibitors
    • Rituximab[2][3][4]
  • Environmental hazards:
    • Ionizing radiation
    • Toxins
  • Infections
    • Viral(Herpes, Measles)
    • Bacterial(Mycobacterial)
    • Parasitic(Malaria, helminthic infections)
  1. ↑ Aouadi S, Ghrairi N, Braham E, Kaabi M, Maâlej S, Elgharbi LD (2017). "[Acquired hypogammaglobulinemia associated with thymoma: Good syndrome]". Pan Afr Med J (in French). 28: 253. doi:10.11604/pamj.2017.28.253.11352. PMC 5989270. PMID 29881497.
  2. ↑ Shoukat BA, Ali O, Kumar D, Bilal Gilani M, Zahid A, Aslam Joiya S, Anwar Malik M (2018). "Hypogammaglobulinemia Observed One Year after Rituximab Treatment for Idiopathic Thrombocytopenic Purpura". Case Rep Med. 2018: 2096186. doi:10.1155/2018/2096186. PMC 5884289. PMID 29755528.
  3. ↑ Farhat L, Dara J, Duberstein S, De A (May 2018). "Secondary Hypogammaglobulinemia After Rituximab for Neuromyelitis Optica: A Case Report". Drug Saf Case Rep. 5 (1): 22. doi:10.1007/s40800-018-0087-y. PMC 5948191. PMID 29752554.
  4. ↑ Thorlacius H, Jerkeman A, Marginean FE, Toth E (April 2018). "Colorectal malakoplakia in a patient with hypogammaglobulinemia". Gastrointest. Endosc. doi:10.1016/j.gie.2018.04.001. PMID 29627491.
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