Psoriasis risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
Common risk factors in the development of psoriasis are [[Gene|genes]] which increase the susceptibility of developing psoriasis and environmental triggers. The presence of these risk factors may lead to [[Autoimmunity|auto-immunity]] and development of psoriasis. | |||
==Risk Factors== | ==Risk Factors== | ||
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=== Common Risk Factors === | === Common Risk Factors === | ||
==== Genetics ==== | ==== Genetics ==== | ||
* The human [[genome]] has at least nine different [[Locus (genetics)|loci]] | * The human [[genome]] has at least nine different [[Locus (genetics)|loci]] implicated in 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 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> | * 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> | ||
* Psoriatic arthritis (PsA) has been | * Psoriatic arthritis (PsA) has been shown to be associated with [[human leukocyte antigen]] ([[Human leukocyte antigen|HLA]]) [[Human leukocyte antigen|class 1]].<ref name="pmid15708927">{{cite journal |vauthors=Gladman DD, Antoni C, Mease P, Clegg DO, Nash P |title=Psoriatic arthritis: epidemiology, clinical features, course, and outcome |journal=Ann. Rheum. Dis. |volume=64 Suppl 2 |issue= |pages=ii14–7 |year=2005 |pmid=15708927 |pmc=1766874 |doi=10.1136/ard.2004.032482 |url=}}</ref> | ||
==== Immune system ==== | ==== Immune system ==== | ||
* Both [[Innate immunity|innate]] and [[adaptive immunity]] | * Both [[Innate immunity|innate]] and [[adaptive immunity]] are involved in the development of psoriasis. | ||
* The key [[Cytokine|cytokines]] of [[immune system]] | * The key [[Cytokine|cytokines]] of [[immune system]] involved in the development of psoriasis are [[tumor necrosis factor-alpha]] and [[interferon alpha]]. | ||
* The [[LFA-1|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. | * The [[LFA-1|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: | * Within the [[immune system]], the development of psoriasis is based upon four key pathways/interactions: | ||
** [[Antigen]] presentation | ** [[Antigen]] presentation | ||
** [[NF-κB]] signaling | ** [[NF-κB]] signaling | ||
** IL-23/IL-17 axis | ** IL-23/IL-17 axis | ||
** Type I IFN pathway | ** [[Interferon type I|Type I interferon]] (IFN) pathway | ||
==== Environmental and behavioral ==== | ==== Environmental and behavioral ==== | ||
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 | 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 |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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*[[Infection]] ([[Streptococcal Infection|Streptococcal]], [[HIV]]) | *[[Infection]] ([[Streptococcal Infection|Streptococcal]], [[HIV]]) | ||
*Seasonal variation | *Seasonal variation | ||
*Medications ([[ | *Medications ([[lithium]], [[beta blockers]], [[Pegylated interferon-alpha-2b|pegylated interferon alpha-2b]], [[siltuximab]]) | ||
*[[Obesity]] | *[[Obesity]] | ||
*Skin injury | *Skin injury | ||
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==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category:Dermatology]] | [[Category:Dermatology]] | ||
Latest revision as of 23:52, 29 July 2020
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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
Common risk factors in the development of psoriasis are genes which increase the susceptibility of developing psoriasis and environmental triggers. The presence of these risk factors may lead to auto-immunity and development of psoriasis.
Risk Factors
Common Risk Factors
Genetics
- The human genome has at least nine different loci implicated in 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]
- Psoriatic arthritis (PsA) has been shown to be associated with human leukocyte antigen (HLA) class 1.[4]
Immune system
- Both innate and adaptive immunity are involved in the development of psoriasis.
- The key cytokines of immune system involved in the development of 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, the development of psoriasis is based upon four key pathways/interactions:
- Antigen presentation
- NF-κB signaling
- IL-23/IL-17 axis
- Type I interferon (IFN) pathway
Environmental and behavioral
The environmental factors implicated in the development or aggravation of psoriasis are:[5][6][7][8][9][10][11]
- 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.
- ↑ Gladman DD, Antoni C, Mease P, Clegg DO, Nash P (2005). "Psoriatic arthritis: epidemiology, clinical features, course, and outcome". Ann. Rheum. Dis. 64 Suppl 2: ii14–7. doi:10.1136/ard.2004.032482. PMC 1766874. PMID 15708927.
- ↑ [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. "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.
- ↑ [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.