Eczema risk factors: Difference between revisions
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==Risk Factors== | ==Risk Factors== | ||
*[[Genetics]] is the strongest identifiable factor associated with development of [[eczema]]. <ref name="pmid27212086">{{cite journal| author=Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G | display-authors=etal| title=The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves. | journal=J Allergy Clin Immunol | year= 2016 | volume= 138 | issue= 2 | pages= 500-508.e24 | pmid=27212086 | doi=10.1016/j.jaci.2016.02.020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27212086 }} </ref> | *<u>Hereditary factors</u> | ||
*[[ | **[[Genetics]] is the strongest identifiable factor associated with development of [[eczema]]. <ref name="pmid27212086">{{cite journal| author=Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G | display-authors=etal| title=The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves. | journal=J Allergy Clin Immunol | year= 2016 | volume= 138 | issue= 2 | pages= 500-508.e24 | pmid=27212086 | doi=10.1016/j.jaci.2016.02.020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27212086 }} </ref> | ||
*34 [[genetic loci]] have been identified based on [[genome-wide association studies]] that accounts for almost 20% of [[eczema]] [[inheritance]]. <ref name="pmid26482879">{{cite journal| author=Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP | display-authors=etal| title=Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis. | journal=Nat Genet | year= 2015 | volume= 47 | issue= 12 | pages= 1449-1456 | pmid=26482879 | doi=10.1038/ng.3424 | pmc=4753676 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26482879 }} </ref> | **[[Family history]] and ''[[FLG]]'' [[gene mutation]]. <ref name="pmid19203656">{{cite journal| author=Sicherer SH, Leung DY| title=Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2008. | journal=J Allergy Clin Immunol | year= 2009 | volume= 123 | issue= 2 | pages= 319-27 | pmid=19203656 | doi=10.1016/j.jaci.2008.12.025 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19203656 }} </ref> | ||
* The [[profilaggrin]] [[protein]] of the ''[[FLG]]'' [[gene]] maintains the intactness of the [[skin]]. <ref name="pmid19386895">{{cite journal| author=Sandilands A, Sutherland C, Irvine AD, McLean WH| title=Filaggrin in the frontline: role in skin barrier function and disease. | journal=J Cell Sci | year= 2009 | volume= 122 | issue= Pt 9 | pages= 1285-94 | pmid=19386895 | doi=10.1242/jcs.033969 | pmc=2721001 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19386895 }} </ref> | **34 [[genetic loci]] have been identified based on [[genome-wide association studies]] that accounts for almost 20% of [[eczema]] [[inheritance]]. <ref name="pmid26482879">{{cite journal| author=Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP | display-authors=etal| title=Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis. | journal=Nat Genet | year= 2015 | volume= 47 | issue= 12 | pages= 1449-1456 | pmid=26482879 | doi=10.1038/ng.3424 | pmc=4753676 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26482879 }} </ref> | ||
*Peanut [[allergy]], [[herpes virus]], and [[contact dermatitis]] were found to be associated with ''[[FLG]]'' [[gene mutation]].<ref name="pmid25282559">{{cite journal| author=Leung DY, Guttman-Yassky E| title=Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches. | journal=J Allergy Clin Immunol | year= 2014 | volume= 134 | issue= 4 | pages= 769-79 | pmid=25282559 | doi=10.1016/j.jaci.2014.08.008 | pmc=4186710 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25282559 }} </ref> <ref name="pmid21991953">{{cite journal| author=Irvine AD, McLean WH, Leung DY| title=Filaggrin mutations associated with skin and allergic diseases. | journal=N Engl J Med | year= 2011 | volume= 365 | issue= 14 | pages= 1315-27 | pmid=21991953 | doi=10.1056/NEJMra1011040 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21991953 }} </ref> | **The [[profilaggrin]] [[protein]] of the ''[[FLG]]'' [[gene]] maintains the intactness of the [[skin]]. <ref name="pmid19386895">{{cite journal| author=Sandilands A, Sutherland C, Irvine AD, McLean WH| title=Filaggrin in the frontline: role in skin barrier function and disease. | journal=J Cell Sci | year= 2009 | volume= 122 | issue= Pt 9 | pages= 1285-94 | pmid=19386895 | doi=10.1242/jcs.033969 | pmc=2721001 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19386895 }} </ref> | ||
*[[ | **Peanut [[allergy]], [[herpes virus]], and [[contact dermatitis]] were found to be associated with ''[[FLG]]'' [[gene mutation]].<ref name="pmid25282559">{{cite journal| author=Leung DY, Guttman-Yassky E| title=Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches. | journal=J Allergy Clin Immunol | year= 2014 | volume= 134 | issue= 4 | pages= 769-79 | pmid=25282559 | doi=10.1016/j.jaci.2014.08.008 | pmc=4186710 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25282559 }} </ref> <ref name="pmid21991953">{{cite journal| author=Irvine AD, McLean WH, Leung DY| title=Filaggrin mutations associated with skin and allergic diseases. | journal=N Engl J Med | year= 2011 | volume= 365 | issue= 14 | pages= 1315-27 | pmid=21991953 | doi=10.1056/NEJMra1011040 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21991953 }} </ref> | ||
*<u>Environmental factors</u> | |||
** People living in places with low humidity, cold temperature, and low ultraviolet light exposure tend to have a higher [[risk]] of [[eczema]] development according to US ecological records. <ref name="pmid23334343">{{cite journal| author=Silverberg JI, Hanifin J, Simpson EL| title=Climatic factors are associated with childhood eczema prevalence in the United States. | journal=J Invest Dermatol | year= 2013 | volume= 133 | issue= 7 | pages= 1752-9 | pmid=23334343 | doi=10.1038/jid.2013.19 | pmc=3646081 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23334343 }} </ref> | |||
==References== | ==References== | ||
{{reflist|2}} | {{reflist|2}} | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Associate Editor(s)-in-Chief: Edzel Lorraine Co, D.M.D., M.D.
Overview
Risk factors of eczema include family history and FLG gene mutation.
Risk Factors
- Hereditary factors
- Genetics is the strongest identifiable factor associated with development of eczema. [1]
- Family history and FLG gene mutation. [2]
- 34 genetic loci have been identified based on genome-wide association studies that accounts for almost 20% of eczema inheritance. [3]
- The profilaggrin protein of the FLG gene maintains the intactness of the skin. [4]
- Peanut allergy, herpes virus, and contact dermatitis were found to be associated with FLG gene mutation.[5] [6]
- Environmental factors
References
- ↑ Feld M, Garcia R, Buddenkotte J, Katayama S, Lewis K, Muirhead G; et al. (2016). "The pruritus- and TH2-associated cytokine IL-31 promotes growth of sensory nerves". J Allergy Clin Immunol. 138 (2): 500–508.e24. doi:10.1016/j.jaci.2016.02.020. PMID 27212086.
- ↑ Sicherer SH, Leung DY (2009). "Advances in allergic skin disease, anaphylaxis, and hypersensitivity reactions to foods, drugs, and insects in 2008". J Allergy Clin Immunol. 123 (2): 319–27. doi:10.1016/j.jaci.2008.12.025. PMID 19203656.
- ↑ Paternoster L, Standl M, Waage J, Baurecht H, Hotze M, Strachan DP; et al. (2015). "Multi-ancestry genome-wide association study of 21,000 cases and 95,000 controls identifies new risk loci for atopic dermatitis". Nat Genet. 47 (12): 1449–1456. doi:10.1038/ng.3424. PMC 4753676. PMID 26482879.
- ↑ Sandilands A, Sutherland C, Irvine AD, McLean WH (2009). "Filaggrin in the frontline: role in skin barrier function and disease". J Cell Sci. 122 (Pt 9): 1285–94. doi:10.1242/jcs.033969. PMC 2721001. PMID 19386895.
- ↑ Leung DY, Guttman-Yassky E (2014). "Deciphering the complexities of atopic dermatitis: shifting paradigms in treatment approaches". J Allergy Clin Immunol. 134 (4): 769–79. doi:10.1016/j.jaci.2014.08.008. PMC 4186710. PMID 25282559.
- ↑ Irvine AD, McLean WH, Leung DY (2011). "Filaggrin mutations associated with skin and allergic diseases". N Engl J Med. 365 (14): 1315–27. doi:10.1056/NEJMra1011040. PMID 21991953.
- ↑ Silverberg JI, Hanifin J, Simpson EL (2013). "Climatic factors are associated with childhood eczema prevalence in the United States". J Invest Dermatol. 133 (7): 1752–9. doi:10.1038/jid.2013.19. PMC 3646081. PMID 23334343.