Psoriasis risk factors: Difference between revisions
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==== Genetics ==== | ==== Genetics ==== | ||
* The human [[genome]] has at least nine different [[Locus (genetics)|loci]], which lead to the development of psoriasis (PSORS1-9).<ref name="pmid16916825">{{cite journal |vauthors=Smith CH, Barker JN |title=Psoriasis and its management |journal=BMJ |volume=333 |issue=7564 |pages=380–4 |year=2006 |pmid=16916825 |pmc=1550454 |doi=10.1136/bmj.333.7564.380 |url=}}</ref> | * The human [[genome]] has at least nine different [[Locus (genetics)|loci]], which lead to the development of psoriasis (PSORS1-9).<ref name="pmid16916825">{{cite journal |vauthors=Smith CH, Barker JN |title=Psoriasis and its management |journal=BMJ |volume=333 |issue=7564 |pages=380–4 |year=2006 |pmid=16916825 |pmc=1550454 |doi=10.1136/bmj.333.7564.380 |url=}}</ref> | ||
* PSORS-1, a part of the [[major histocompatibility complex]] (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to | * PSORS-1, a part of the [[major histocompatibility complex]] (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to 50% of genetic susceptibility to the disease.<ref name="pmid16138103">{{cite journal |vauthors=Bowcock AM, Krueger JG |title=Getting under the skin: the immunogenetics of psoriasis |journal=Nat. Rev. Immunol. |volume=5 |issue=9 |pages=699–711 |year=2005 |pmid=16138103 |doi=10.1038/nri1689 |url=}}</ref> | ||
* The second most well-characterized disease-susceptibility [[locus]] (''PSORS2'') is found within 17q24–q25. | * The second most well-characterized disease-susceptibility [[locus]] (''PSORS2'') is found within 17q24–q25. | ||
* [[Missense mutation|Missense mutations]] in CARD14 gene lead to activation of the [[NF-κB]] pathway. | * [[Missense mutation|Missense mutations]] in CARD14 gene lead to activation of the [[NF-κB]] pathway. | ||
* Another major gene involved in the development of psoriasis is a [[Human leukocyte antigen|HLA class]] I [[allele]], specifically HLA-Cw6.<ref name="pmid7387872">{{cite journal |vauthors=Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M |title=Psoriasis and HLA-Cw6 |journal=Br. J. Dermatol. |volume=102 |issue=2 |pages=179–84 |year=1980 |pmid=7387872 |doi= |url=}}</ref> | * Another major [[gene]] involved in the development of psoriasis is a [[Human leukocyte antigen|HLA class]] I [[allele]], specifically HLA-Cw6.<ref name="pmid7387872">{{cite journal |vauthors=Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M |title=Psoriasis and HLA-Cw6 |journal=Br. J. Dermatol. |volume=102 |issue=2 |pages=179–84 |year=1980 |pmid=7387872 |doi= |url=}}</ref> | ||
==== Immune system ==== | ==== Immune system ==== | ||
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** [[NF-κB]] signaling | ** [[NF-κB]] signaling | ||
** IL-23/IL-17 axis | ** IL-23/IL-17 axis | ||
** Type I IFN pathway | ** Type I IFN pathway | ||
==== Environmental and behavioral ==== | ==== Environmental and behavioral ==== | ||
The | The environmental factors implicated in the development or aggravation of psoriasis are:<ref>[http://www.skincarephysicians.com/psoriasisnet/triggers.html <nowiki>[1]</nowiki>] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.</ref><ref>{{cite journal |author=Behnam SM, Behnam SE, Koo JY |title=Smoking and psoriasis |journal=Skinmed |volume=4 |issue=3 |pages=174–6 |year=2005 |pmid=15891254 |doi= |url=http://www.lejacq.com/articleDetail.cfm?pid=SKINmed_4;3:174}}</ref><ref>[http://www.medscape.com/viewarticle/556533 <nowiki>[2]</nowiki>][http://dermatology.cdlib.org/132/reviews/HIV/fife.html <nowiki>[3]</nowiki>] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.</ref><ref>{{cite journal |author=Ortonne JP, Lebwohl M, Em Griffiths C |title=Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis |journal=Eur J Dermatol |volume=13 |issue=2 |pages=117–23 |year=2003 |pmid=12695125 |doi= |url=http://www.john-libbey-eurotext.fr/medline.md?issn=1167-1122&vol=13&iss=2&page=117}}</ref><ref>{{cite journal |author=Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG |title=The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients |journal=J. Invest. Dermatol. |volume=113 |issue=5 |pages=752–9 |year=1999 |month=November |pmid=10571730 |doi=10.1046/j.1523-1747.1999.00749.x |url=}}</ref><ref>[http://www.nsc.gov.sg/cgi-bin/WB_ContentGen.pl?id=401&gid=83 <nowiki>[4]</nowiki>] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.</ref><ref name="pmid15199399">{{cite journal |vauthors=Nickoloff BJ, Nestle FO |title=Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities |journal=J. Clin. Invest. |volume=113 |issue=12 |pages=1664–75 |year=2004 |pmid=15199399 |pmc=420513 |doi=10.1172/JCI22147 |url=}}</ref> | ||
*[[Stress]] (physical and mental) | *[[Stress]] (physical and mental) | ||
*[[Smoking]] | *[[Smoking]] | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]
Overview
The most potent risk factor in the development of psoriasis is autoimmunity. Other risk factors include genetic predisposition and environmental factors.
Risk Factors
Common Risk Factors
Genetics
- The human genome has at least nine different loci, which lead to the development of psoriasis (PSORS1-9).[1]
- PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to 50% of genetic susceptibility to the disease.[2]
- The second most well-characterized disease-susceptibility locus (PSORS2) is found within 17q24–q25.
- Missense mutations in CARD14 gene lead to activation of the NF-κB pathway.
- Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.[3]
Immune system
- Both innate and adaptive immunity is involved in the development of psoriasis.
- The key cytokines of immune system, which lead to psoriasis are tumor necrosis factor-alpha and interferon alpha.
- The LFA-1 integrin is also important in the immune pathogenesis of psoriasis and has been known to be a target for medications used for the management of psoriasis.
- Within the immune system, development of psoriasis is based upon four key pathways/interactions:
Environmental and behavioral
The environmental factors implicated in the development or aggravation of psoriasis are:[4][5][6][7][8][9][10]
- Stress (physical and mental)
- Smoking
- Excessive alcohol consumption
- Infection (Streptococcal, HIV)
- Seasonal variation
- Medications (Lithium, Beta blockers, pegylated interferon alpha-2b, Siltuximab)
- Obesity
- Skin injury
- Skin dryness
References
- ↑ Smith CH, Barker JN (2006). "Psoriasis and its management". BMJ. 333 (7564): 380–4. doi:10.1136/bmj.333.7564.380. PMC 1550454. PMID 16916825.
- ↑ Bowcock AM, Krueger JG (2005). "Getting under the skin: the immunogenetics of psoriasis". Nat. Rev. Immunol. 5 (9): 699–711. doi:10.1038/nri1689. PMID 16138103.
- ↑ Tiilikainen A, Lassus A, Karvonen J, Vartiainen P, Julin M (1980). "Psoriasis and HLA-Cw6". Br. J. Dermatol. 102 (2): 179–84. PMID 7387872.
- ↑ [1] Psoriasis Triggers at Psoriasis Net. SkinCarePhysicians.com 9-28-05. American Academy of Dermatology, 2008.
- ↑ Behnam SM, Behnam SE, Koo JY (2005). "Smoking and psoriasis". Skinmed. 4 (3): 174–6. PMID 15891254.
- ↑ [2][3] Fife, Jeffes, Koo, Waller. Unraveling the Paradoxes of HIV-associated Psoriasis: A Review of T-cell Subsets and Cytokine Profiles. 5-18-07. Retrieved 5-13-08.
- ↑ Ortonne JP, Lebwohl M, Em Griffiths C (2003). "Alefacept-induced decreases in circulating blood lymphocyte counts correlate with clinical response in patients with chronic plaque psoriasis". Eur J Dermatol. 13 (2): 117–23. PMID 12695125.
- ↑ Austin LM, Ozawa M, Kikuchi T, Walters IB, Krueger JG (1999). "The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients". J. Invest. Dermatol. 113 (5): 752–9. doi:10.1046/j.1523-1747.1999.00749.x. PMID 10571730. Unknown parameter
|month=ignored (help) - ↑ [4] A Case Report of Severe Psoriasis in a Patient with AIDS: The Role of the HIV Virus and the Therapeutic Challenges Involved. Vol: 13 No 2, 2002. National Skin Center. Retrieved 05-13-08.
- ↑ Nickoloff BJ, Nestle FO (2004). "Recent insights into the immunopathogenesis of psoriasis provide new therapeutic opportunities". J. Clin. Invest. 113 (12): 1664–75. doi:10.1172/JCI22147. PMC 420513. PMID 15199399.