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__NOTOC__
{{Eczema}}
{{Eczema}}
{{CMG}}, {{AE}} [[User:Edzelco|Edzel Lorraine Co, D.M.D., M.D.]]
{{CMG}}, {{AE}} {{EdzelCo}}


==Overview==
==Overview==
The [[etiology]] of [[eczema]] is multifactorial and complex. This involves aberrations in [[genetic]] components, [[adverse effect]]s of certain [[medication]]s, and some environmental factors.


==Causes==
==Etiology of Eczema==
Damage from the [[Enzyme|enzymatic]] activity of allergens is usually prevented by the body's own [[protease inhibitor]]s, such as, LEKTI,  produced from the gene [[SPINK5]]. Mutations in this gene are known to cause Netherton’s syndrome, which is a [[congenital]] [[erythroderma]]. These patients nearly always develop atopic disease, including hay fever, food allergy, urticaria and asthma. Such evidence supports the hypothesis that skin damage from allergens may be the cause of eczema, and may provide a venue for further treatment. <ref name="pmid11544479">{{cite journal |author=Walley AJ, Chavanas S, Moffatt MF, ''et al'' |title=Gene polymorphism in Netherton and common atopic disease |journal=Nat. Genet. |volume=29 |issue=2 |pages=175–8 |year=2001 |pmid=11544479 |doi=10.1038/ng728}}</ref>


Another study identified a gene that the researchers believe to be the cause of inherited eczema and some related disorders.  The gene produces the protein [[filaggrin]], the lack of which causes dry skin and impaired skin barrier function.<ref name=filaggrin>Palmer, C.N. ''et al.'' (2006) Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. ''Nature Genetics''  '''38'''(4), 441-6. PMID 16550169</ref>
===Genetic problem===
*Damage from the [[Enzyme|enzymatic]] activity of [[allergens]] is usually prevented by the body's own [[protease inhibitor]]s, such as ''[[LEKTI]]'', produced from the gene ''[[SPINK5]]''.
*Lack of [[filaggrin]] [[gene]] causes [[dry skin]]. <ref name="pmid16550169">{{cite journal| author=Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP | display-authors=etal| title=Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis. | journal=Nat Genet | year= 2006 | volume= 38 | issue= 4 | pages= 441-6 | pmid=16550169 | doi=10.1038/ng1767 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16550169 }} </ref>


A recent study indicated that two specific chemicals found in the blood are connected to the itching sensations associated with eczema. The chemicals are [[Brain-derived neurotrophic factor]] (BDNF) and [[Substance P]].<ref name="BBC-blood chemicals">{{cite news |author= |title= 'Blood chemicals link' to eczema -- Scientists have identified two blood chemicals linked to itchy eczema, offering new treatment possibilities. |url= http://news.bbc.co.uk/2/hi/health/6962450.stm |date= 26 August 2007 |publisher=BBC News |accessdate=2007-10-16}}</ref>
===Eczema as an Adverse Drug Reaction===
*[[Eczema]] can also be brought about by some adverse effects of [[medications]].
*Below is a list of commonly prescribed medications with [[eczema]] as the common [[adverse drug effect]] '''(Table 1)'''.


===Life Threatening Causes===


===Common Causes===


===Causes by Organ System===
{| style="border: 0px; font-size: 90%; margin: 1px; width: " align="center" 500px;"
{|style="width:80%; height:100px" border="1"
| valign="top" |
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" |'''Cardiovascular'''
|+<big>''' Table 1. List of [[medications]] with [[eczema]] as its [[adverse effect]].'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
! align="center" style="background: #00CED1; width: 500px;" |{{fontcolor|#FFF|[[Medication]]}}
|-
|-
|bgcolor="LightSteelBlue"| '''Chemical/Poisoning'''
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Cidofovir]]'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Flurbiprofen]]'''
| '''Dental'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Olaparib]]'''
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Siltuximab]]'''
| '''Drug Side Effect'''
|bgcolor="Beige"|  [[Cidofovir]], [[Flurbiprofen]], [[Olaparib]], [[Siltuximab]], [[Sorafenib]], [[Tiagabine]]
|-
|-
|-bgcolor="LightSteelBlue"
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Sorafenib]]'''
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
| align="center" style="padding: 2px 2px; background: #F5F5F5;" |'''[[Tiagabine]]'''
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal/Orthopedic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional/Metabolic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Ophthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose/Toxicity'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Renal/Electrolyte'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Rheumatology/Immunology/Allergy'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| No underlying causes
|-
|-
|}
|}
===Causes in Alphabetical Order===
: List the causes of the disease in alphabetical order. You may need to list across the page, as seen [[Jaundice causes#Causes in Alphabetical Order|here]]
{{col-begin|width=80%}}
{{col-break|width=33%}}
*[[Cidofovir]]
*[[Flurbiprofen]]
*[[Siltuximab]]
*[[Sorafenib]]
*[[Tiagabine]]
{{col-break|width=33%}}
{{col-break|width=33%}}
{{col-end}}


==References==
==References==
{{reflist|2}}
{{reflist|2}}
 
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Latest revision as of 07:43, 13 November 2023

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, DMD, MD[2]

Overview

The etiology of eczema is multifactorial and complex. This involves aberrations in genetic components, adverse effects of certain medications, and some environmental factors.

Etiology of Eczema

Genetic problem

Eczema as an Adverse Drug Reaction


 Table 1. List of medications with eczema as its adverse effect.
Medication
Cidofovir
Flurbiprofen
Olaparib
Siltuximab
Sorafenib
Tiagabine

References

  1. ↑ Palmer CN, Irvine AD, Terron-Kwiatkowski A, Zhao Y, Liao H, Lee SP; et al. (2006). "Common loss-of-function variants of the epidermal barrier protein filaggrin are a major predisposing factor for atopic dermatitis". Nat Genet. 38 (4): 441–6. doi:10.1038/ng1767. PMID 16550169.
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