Atopic dermatitis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Although it is such a common disease, relatively little is understood about the underlying causes of | Although it is such a common disease, relatively little is understood about the underlying causes of atopic eczema.<ref name=kluken>Klüken, H., Wienker, T., & Bieber, T. Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution. Allergy 58 (2003): pp 5-12. </ref> While AE is associated with allergic asthma and allergic rhinitis, the connection between the diseases has not been established.<ref name=kluken/> Twin studies have consistently shown that the disease has a higher rate of concordance in identical as compared to fraternal twins, which also indicates that genetics plays a role in its development.<ref name=kluken/> However, the rate of concordance between identical twins is far from 100%, and the changing frequency of the disease over time points to the environmental factors—nutrition or hygiene, for instance—that also play a role in disease susceptibility.<ref name=schreiber>Schreiber, S. et al. Genetics of Crohn Disease, an archetypal inflammatory barrier disease. Nature Reviews Genetics 6 (2005), pp. 376-388.</ref> | ||
Genomic research into the cause of multigenic diseases is still in its infancy: few genes have ever been identified that contribute to multigenic human disorders.<ref name=schreiber/> Researchers have attempted to do this in past whole-genome screens for AE and related diseases, but their results have been inconsistent. A few of the pertinent loci have been validated by replication in further studies (chromosome 2q, chromosome 6p, and chromosome 12q, for example),<ref>Lyle J. Palmer and William O.C.M. Cookson. [http://www.genome.org/cgi/content/full/10/9/1280 Genomic Approaches to Understanding Asthma.] Genome Research Vol. 10, Issue 9, 1280-1287, September 2000.</ref> but most have not been. | Genomic research into the cause of multigenic diseases is still in its infancy: few genes have ever been identified that contribute to multigenic human disorders.<ref name=schreiber/> Researchers have attempted to do this in past whole-genome screens for AE and related diseases, but their results have been inconsistent. A few of the pertinent loci have been validated by replication in further studies (chromosome 2q, chromosome 6p, and chromosome 12q, for example),<ref>Lyle J. Palmer and William O.C.M. Cookson. [http://www.genome.org/cgi/content/full/10/9/1280 Genomic Approaches to Understanding Asthma.] Genome Research Vol. 10, Issue 9, 1280-1287, September 2000.</ref> but most have not been. | ||
Associations with ATOD1, ATOD2, ATOD3, ATOD4, ATOD5 and ATOD6 have been identified.<ref name="urlOMIM - DERMATITIS, ATOPIC">{{cite web |url=http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=603165 |title=OMIM - DERMATITIS, ATOPIC |format= |work= |accessdate=2008-09-19}}</ref> | Associations with ATOD1, ATOD2, ATOD3, ATOD4, ATOD5 and ATOD6 have been identified.<ref name="urlOMIM - DERMATITIS, ATOPIC">{{cite web |url=http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=603165 |title=OMIM - DERMATITIS, ATOPIC |format= |work= |accessdate=2008-09-19}}</ref> | ||
==References== | ==References== | ||
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Pathophysiology
Although it is such a common disease, relatively little is understood about the underlying causes of atopic eczema.[1] While AE is associated with allergic asthma and allergic rhinitis, the connection between the diseases has not been established.[1] Twin studies have consistently shown that the disease has a higher rate of concordance in identical as compared to fraternal twins, which also indicates that genetics plays a role in its development.[1] However, the rate of concordance between identical twins is far from 100%, and the changing frequency of the disease over time points to the environmental factors—nutrition or hygiene, for instance—that also play a role in disease susceptibility.[2]
Genomic research into the cause of multigenic diseases is still in its infancy: few genes have ever been identified that contribute to multigenic human disorders.[2] Researchers have attempted to do this in past whole-genome screens for AE and related diseases, but their results have been inconsistent. A few of the pertinent loci have been validated by replication in further studies (chromosome 2q, chromosome 6p, and chromosome 12q, for example),[3] but most have not been.
Associations with ATOD1, ATOD2, ATOD3, ATOD4, ATOD5 and ATOD6 have been identified.[4]
References
- ↑ 1.0 1.1 1.2 Klüken, H., Wienker, T., & Bieber, T. Atopic eczema/dermatitis syndrome – a genetically complex disease. New advances in discovering the genetic contribution. Allergy 58 (2003): pp 5-12.
- ↑ 2.0 2.1 Schreiber, S. et al. Genetics of Crohn Disease, an archetypal inflammatory barrier disease. Nature Reviews Genetics 6 (2005), pp. 376-388.
- ↑ Lyle J. Palmer and William O.C.M. Cookson. Genomic Approaches to Understanding Asthma. Genome Research Vol. 10, Issue 9, 1280-1287, September 2000.
- ↑ "OMIM - DERMATITIS, ATOPIC". Retrieved 2008-09-19.