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| {{Psoriasis}} | | {{Psoriasis}} |
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| {{CMG}} | | {{CMG}}; {{AE}} {{HK}} |
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| ==Overview== | | ==Overview== |
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| | There are no established causes of psoriasis. The development of psoriasis is secondary to a combination of [[Gene|genes]] and exposure to specific external factors or triggers, which increase an individual's risk of developing psoriasis. These [[Risk factor|risk factors]] lead to complex interactions between the [[genetics]], [[immune system]], and the environment. To view the factors which may increase one's susceptibility to the development psoriasis, [[psoriasis risk factors|click here]]. |
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| ==Causes== | | ==Causes== |
| ===Common Causes===
| | *The development of psoriasis is secondary to a combination of [[Gene|genes]] and exposure to specific external factors or triggers, which increase an individual's risk of developing psoriasis. |
| | | *The presence of these [[Risk factor|risk factors]] may cause an activation of the [[immune system]], which can lead to disease. |
| The cause of psoriasis is not fully understood. There are two main hypotheses about the process that occurs in the development of the disease. The first considers psoriasis as primarily a disorder of excessive growth and reproduction of skin cells. The problem is simply seen as a fault of the [[epidermis (skin)|epidermis]] and its [[keratinocytes]]. The second hypothesis sees the disease as being an [[immune-mediated disease|immune-mediated disorder]] in which the excessive reproduction of skin cells is secondary to factors produced by the [[immune system]]. [[T cell]]s (which normally help protect the body against infection) become active, migrate to the [[dermis]] and trigger the release of [[cytokines]] ([[tumor necrosis factor-alpha]] TNFα, in particular) which cause inflammation and the rapid production of skin cells. It is not known what initiates the activation of the T cells. | | '''To view the factors which may increase one's susceptibility to the development of psoriasis, [[psoriasis risk factors|click here]].''' |
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| The immune-mediated model of psoriasis has been supported by the observation that [[immunosuppressant]] medications can clear psoriasis plaques. However, the role of the immune system is not fully understood, and it has recently been reported that an [[animal model]] of psoriasis can be triggered in mice lacking T cells.<!--
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| --><ref name=Zenz>{{cite journal |author=Zenz R, Eferl R, Kenner L, ''et al'' |title=Psoriasis-like skin disease and arthritis caused by inducible epidermal deletion of Jun proteins |journal=Nature |volume=437 |issue=7057 |pages=369–75 |year=2005 |pmid=16163348 |doi=10.1038/nature03963}}</ref> [[Animal model]]s, however, reveal only a few aspects resembling human psoriasis.
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| Psoriasis is a fairly [[idiosyncratic]] disease. The majority of people's experience of psoriasis is one in which it may worsen or improve for no apparent reason. Studies of the factors associated with psoriasis tend to be based on small (usually hospital based) samples of individuals. These studies tend to suffer from representative issues, and an inability to tease out [[causal]] associations in the face of other (possibly unknown) intervening factors. Conflicting findings are often reported. Nevertheless, the first outbreak is sometimes reported following [[stress (medicine)|stress]] (physical and mental), skin injury, and [[streptococcal infection]]. Conditions that have been reported as accompanying a worsening of the disease include infections, stress, and changes in season and [[climate]]. Certain medicines, including [[lithium salt]] and [[beta blocker]]s, have been reported to trigger or aggravate the disease. Excessive alcohol consumption, smoking and obesity may exacerbate psoriasis or make the management of the condition difficult.<ref>[http://www.skincarephysicians.com/psoriasisnet/triggers.html] 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>
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| Individuals suffering from the advanced effects of the [[HIV|Human immunodeficiency virus]], or HIV, often exhibit psoriasis.<ref>[http://www.medscape.com/viewarticle/556533][http://dermatology.cdlib.org/132/reviews/HIV/fife.html] 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> This presents a paradox to researchers as traditional therapies that reduce [[T-cell]] counts generally cause psoriasis to improve. Yet, as CD4-T-cell counts decrease with the progression of HIV, psoriasis worsens.<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> In addition, HIV is typically characterized by a strong [[T helper cell|Th2]] [[cytokine]] profile, whereas psoriasis vulgaris is characterized by a strong [[T helper cell|Th1]] secretion pattern.<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> It's hypothesized that the diminished CD4-T-Cell presence causes an over-activation of CD8-T-Cells, which are responsible for the exacerbation of psoriasis in HIV positive patients. It is important to remember that most individuals with psoriasis are otherwise healthy and the presence of HIV accounts for less than 1% of cases. The prevalence of psoriasis in the HIV positive population ranges from 1 to 6 percent, which is about 3 times higher than the normal population.<ref>[http://www.nsc.gov.sg/cgi-bin/WB_ContentGen.pl?id=401&gid=83] 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>
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| Psoriasis occurs more likely in dry skin than oily or well-moisturized skin, and specifically after an external skin injury such as a scratch or cut. This is believed to be caused by an infection, in which the infecting organism thrives under dry skin conditions with minimal skin oil, which otherwise protects skin from infections. The case for psoriasis is opposite to the case of [[athlete's foot]], which occurs because of a fungus infection under wet conditions as opposed to dry in psoriasis. This infection induces inflammation, which causes the symptoms commonly associated with psoriasis, such as itching and rapid skin turnover, and leads to drier skin as the infecting organism absorbs the moisture that would otherwise go to the skin. To prevent dry skin and reduce psoriasis symptoms, it is advised to not use shower scrubs, as they not only damage skin by leaving tiny scratches, they also scrape off the naturally occurring skin oil. Additionally, moisturizers can be applied to moisturize the skin, and lotions used to promote skin oil gland functions.
| | ==References== |
| | {{Reflist|2}} |
| | {{WH}} |
| | {{WS}} |
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| ===Causes in Alphabetical Order===
| | [[Category:Dermatology]] |
| | [[Category:Disease]] |