Psoriasis risk factors: Difference between revisions
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==Overview== | ==Overview== | ||
The most potent risk factor in the development of psoriasis is autoimmunity. Other risk factors include genetic predisposition and environmental factors. | The most potent risk factor in the development of psoriasis is [[autoimmunity]]. Other risk factors include genetic predisposition and environmental factors. | ||
==Risk Factors== | ==Risk Factors== | ||
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* 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 known 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> | * Psoriatic arthritis (PsA) has been known 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> | ||
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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]
- Psoriatic arthritis (PsA) has been known to be associated with human leukocyte antigen (HLA) class 1.[4]
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:[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 (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.