View source for Psoriasis

{{Short description|Autoimmune diseases of the skin}}
{{good article}}
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{{Use dmy dates|date=July 2023}}
{{Infobox medical condition
| name            = Psoriasis
| image           = Psoriasis on back1.jpg
| caption         = Back and arms of a person with severe psoriasis
| pronounce       = {{IPAc-en|s|ə|ˈ|r|aɪ|ə|s|ᵻ|s|,_|p|s|-|,_|s|ɒ|-|,_|s|ɔː|-|,_|s|oʊ|-}}{{refn|{{cite book | vauthors = Jones D |author-link=Daniel Jones (phonetician) |title=English Pronouncing Dictionary | veditors = Roach P, Hartmann J, Setter J |place=Cambridge |publisher=Cambridge University Press |orig-date=1917 |year=2003 |isbn=978-3-12-539683-8 }}}}{{refn|{{MerriamWebsterDictionary|Psoriasis}}}}
| specialty       = [[Dermatology]] (primarily); <br />[[immunology]], [[rheumatology]] and other specialties (e.g., [[cardiology]] and [[vascular medicine]], [[nephrology]], [[hepatology]]/[[gastroenterology]], [[endocrinology]], [[hematology]]) (indirectly/by association)
| symptoms        = [[erythema|Red]] (purple on darker skin), itchy, scaly patches of skin<ref name=Menter2008/>
| complications   = [[Psoriatic arthritis]]<ref name=Lancet2015/>
| onset           = Adulthood<ref name=NIH2015/>
| duration        = Long-term<ref name=Lancet2015/>
| causes          = [[Genetic disease]] triggered by environmental factors<ref name=Menter2008 />
| risks           =
| diagnosis       = Based on symptoms<ref name=Lancet2015/>
| differential    = 
| prevention      = 
| treatment       = [[corticosteroid|Steroid creams]], [[vitamin D3|vitamin D<sub>3</sub>]] cream, [[ultraviolet light]], [[immunosuppressive drug]]s such as [[methotrexate]] and [[Biologics for immunosuppression|biologics]]<ref name=NIH2015/>
| medication      = 
| prognosis       = 
| frequency       = 79.7 million<ref name=GBD2015Pre>{{cite journal | vauthors = ((GBD 2015 Disease and Injury Incidence and Prevalence Collaborators)) | title = Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015 | journal = Lancet | volume = 388 | issue = 10053 | pages = 1545–1602 | date = October 2016 | pmid = 27733282 | pmc = 5055577 | doi = 10.1016/S0140-6736(16)31678-6 }}</ref> / 2–4%<ref name=Parisi2013/>
| deaths          = 
}}

'''Psoriasis''' is a [[Chronic condition|long-lasting]], noncontagious [[autoimmune disease]] characterized by [[skin plaque|patches of abnormal skin]].<ref name=Lancet2015/><ref name=NIH2015/> These areas are [[erythema|red]], pink, or purple, [[Xeroderma|dry]], [[itch]]y, and scaly.<ref name=Menter2008/><ref>{{cite book |vauthors=LeMone P, Burke K, Dwyer T, Levett-Jones T, Moxham L, Reid-Searl K |title=Medical-Surgical Nursing |date=2015 |publisher=Pearson Higher Education AU |isbn=978-1-4860-1440-8 |page=454 |url=https://books.google.com/books?id=MDXiBAAAQBAJ&pg=PA454 |access-date=8 May 2020 |archive-date=14 January 2023 |archive-url=https://web.archive.org/web/20230114031931/https://books.google.com/books?id=MDXiBAAAQBAJ&pg=PA454 |url-status=live }}</ref> Psoriasis varies in severity from small localized patches to complete body coverage.<ref name="Menter2008">{{Cite journal |last1=Menter |first1=Alan |last2=Gottlieb |first2=Alice |last3=Feldman |first3=Steven R. |last4=Van Voorhees |first4=Abby S. |last5=Leonardi |first5=Craig L. |last6=Gordon |first6=Kenneth B. |last7=Lebwohl |first7=Mark |last8=Koo |first8=John Y.M. |last9=Elmets |first9=Craig A. |last10=Korman |first10=Neil J. |last11=Beutner |first11=Karl R. |last12=Bhushan |first12=Reva |date=2008 |title=Guidelines of care for the management of psoriasis and psoriatic arthritis |url=https://linkinghub.elsevier.com/retrieve/pii/S0190962208002739 |journal=Journal of the American Academy of Dermatology |language=en |volume=58 |issue=5 |pages=826–850 |doi=10.1016/j.jaad.2008.02.039|url-access=subscription }}</ref> [[Injury]] to the skin can trigger psoriatic skin changes at that spot, which is known as the [[Koebner phenomenon]].<ref name=Ely2010>{{cite journal | vauthors = Ely JW, Seabury Stone M | title = The generalized rash: part II. Diagnostic approach | journal = American Family Physician | volume = 81 | issue = 6 | pages = 735–9 | date = March 2010 | pmid = 20229972 | url = http://www.aafp.org/afp/2010/0315/p735.html | url-status = live | archive-url = https://web.archive.org/web/20140202152931/http://www.aafp.org/afp/2010/0315/p735.html | archive-date = 2 February 2014 }}</ref>

The five main types of psoriasis are plaque, [[Guttate psoriasis|guttate]], [[Inverse psoriasis|inverse]], [[Pustular psoriasis|pustular]], and [[Psoriatic erythroderma|erythrodermic]].<ref name=NIH2015/> Plaque psoriasis, also known as psoriasis vulgaris, makes up about 90% of cases.<ref name=Lancet2015/> It typically presents as red patches with white scales on top.<ref name=Lancet2015/> Areas of the body most commonly affected are the back of the forearms, shins, [[navel]] area, and scalp.<ref name=Lancet2015/> Guttate psoriasis has drop-shaped lesions.<ref name=NIH2015/> Pustular psoriasis presents as small, noninfectious, [[pus]]-filled [[blister]]s.<ref name=Jain2012/> Inverse psoriasis forms red patches in skin folds.<ref name=NIH2015/> Erythrodermic psoriasis occurs when the rash becomes very widespread and can develop from any of the other types.<ref name=Lancet2015/> [[Nail (anatomy)|Fingernails]] and toenails are affected in most people with psoriasis at some point in time.<ref name=Lancet2015/> This may include pits in the nails or changes in nail color.<ref name=Lancet2015>{{cite journal | vauthors = Boehncke WH, Schön MP | title = Psoriasis | journal = Lancet | volume = 386 | issue = 9997 | pages = 983–94 | date = September 2015 | pmid = 26025581 | doi = 10.1016/S0140-6736(14)61909-7 | s2cid = 208793879 }}</ref>

Psoriasis is generally thought to be a [[genetic disease]] that is triggered by environmental factors.<ref name=Menter2008 /> If one [[twin]] has psoriasis, the other twin is three times more likely to be affected if the twins are [[identical twins|identical]] than if they are [[fraternal twins|nonidentical]].<ref name=Lancet2015/> This suggests that genetic factors predispose to psoriasis.<ref name=Lancet2015/> Symptoms often worsen during winter and with certain medications, such as [[beta blockers]] or [[NSAIDs]].<ref name=Lancet2015/> Infections and [[psychological stress]] can also play a role.<ref name=Menter2008/><ref name=NIH2015/> The underlying mechanism involves the [[immune system]] reacting to [[Keratinocyte|skin cell]]s.<ref name=Lancet2015/> Diagnosis is typically based on the signs and symptoms.<ref name=Lancet2015/>

There is no known cure for psoriasis, but various treatments can help control the symptoms.<ref name=Lancet2015/> These treatments include [[corticosteroid|steroid creams]], [[vitamin D3|vitamin D<sub>3</sub>]] cream, [[ultraviolet light]], [[immunosuppressive drug]]s, such as [[methotrexate]], and [[Biopharmaceutical|biologic]] therapies targeting specific immunologic pathways.<ref name=NIH2015/> About 75% of skin involvement improves with creams alone.<ref name=Lancet2015/> The disease affects 2–4% of the population.<ref name=Parisi2013>{{cite journal | vauthors = Parisi R, Symmons DP, Griffiths CE, Ashcroft DM | title = Global epidemiology of psoriasis: a systematic review of incidence and prevalence | journal = The Journal of Investigative Dermatology | volume = 133 | issue = 2 | pages = 377–85 | date = February 2013 | pmid = 23014338 | doi = 10.1038/jid.2012.339 | others = Identification and Management of Psoriasis and Associated ComorbidiTy (IMPACT) project team | doi-access = free | title-link = doi }}</ref> Men and women are affected with equal frequency.<ref name=NIH2015/> The disease may begin at any age, but typically starts in adulthood.<ref name=NIH2015>{{cite web|title=Questions and Answers About Psoriasis|url=https://www.niams.nih.gov/health-topics/psoriasis|website=National Institute of Arthritis and Musculoskeletal and Skin Diseases|access-date=22 April 2017|url-status=live|archive-url=https://web.archive.org/web/20170422134800/https://www.niams.nih.gov/health_info/psoriasis/|archive-date=22 April 2017|date=12 April 2017}}</ref> Psoriasis is associated with an increased risk of [[psoriatic arthritis]], [[lymphoma]]s, [[cardiovascular disease]], [[Crohn's disease]], and [[Depression (mood)|depression]].<ref name=Lancet2015/> Psoriatic arthritis affects up to 30% of individuals with psoriasis.<ref name=Jain2012>{{cite book| vauthors = Jain S |title=Dermatology: illustrated study guide and comprehensive board review|year=2012|publisher=Springer|isbn=978-1-4419-0524-6|pages=83–87|url=https://books.google.com/books?id=r4Xzi0LKROcC&q=dermatology&pg=PA86|url-status=live|archive-url=https://web.archive.org/web/20170908183432/https://books.google.com/books?id=r4Xzi0LKROcC&lpg=PP1&dq=dermatology&pg=PA86|archive-date=8 September 2017}}</ref>

The word "psoriasis" is from [[Greek language|Greek]] {{lang|grc|ψωρίασις}} meaning {{gloss|itching condition}} or {{gloss|being itchy}},<ref name="Ritchlin2007">{{cite book| vauthors = Ritchlin C, Fitzgerald I |title=Psoriatic and Reactive Arthritis: A Companion to Rheumatology|year=2007|publisher=Mosby|location=Maryland Heights, MI|isbn=978-0-323-03622-1|page=4|url=https://books.google.com/books?id=RN-B2g2YjmAC&pg=PA4|edition=1st |url-status=live|archive-url=https://web.archive.org/web/20170108132906/https://books.google.com/books?id=RN-B2g2YjmAC&pg=PA4&lpg=PA4|archive-date=8 January 2017}}</ref> from [[wikt:psora|{{Transliteration|grc|psora}}]] {{gloss|itch}}, and [[wikt:-iasis#Suffix|{{Transliteration|grc|-iasis}}]] {{gloss|action, condition}}.

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==Signs and symptoms==

===Plaque psoriasis===
[[File:Psoriasis2010.JPG|thumbnail|Psoriatic plaque, showing a silvery center surrounded by a reddened border]]
Psoriasis vulgaris (also known as chronic stationary psoriasis or plaque-like psoriasis) is the most common form and affects 85–90% of people with psoriasis.<ref name="Palfreeman2013"/> Plaque psoriasis typically appears as raised areas of [[Inflammation|inflamed]] skin covered with silvery-white, scaly skin. These areas are called plaques and are most commonly found on the elbows, knees, [[scalp]], and back.<ref name="Palfreeman2013"/><ref name=DAVIDSONS2010>{{cite book| veditors = Colledge NR, Walker BR, Ralston SH |title=Davidson's principles and practice of medicine.|year=2010|publisher=Churchill Livingstone/Elsevier|location=Edinburgh|isbn=978-0-7020-3084-0|edition=21st | pages=1260–1 }}</ref>

<gallery>
Image:Psoriasis2010a.JPG|Plaques of psoriasis
Image:Psoriasis.jpg|A person's arm covered with plaque psoriasis
File:Psoriasis of the palms.jpg|Psoriasis of the palms
Riehl Zumbusch Tafel LII (1).jpg|Psoriasis of the scalp
</gallery>

=== Other forms ===
Additional types of psoriasis comprise about 10% of cases. They include pustular, inverse, napkin, guttate, oral, and seborrheic-like forms.<ref name="Andrews">{{cite book | vauthors = James W, Berger T, Elston D |title=Andrews' Diseases of the Skin: Clinical Dermatology |publisher=Saunders |year=2005 |isbn=978-0-7216-2921-6 |edition=10th|pages=191–7 }}</ref>

====Pustular psoriasis====
[[File:Psoriasis manum.jpg|thumbnail|Severe generalized pustular psoriasis]]
[[Pustular psoriasis]] appears as raised bumps filled with noninfectious pus ([[pustules]]).<ref>{{cite journal | vauthors = Robinson A, Van Voorhees AS, Hsu S, Korman NJ, Lebwohl MG, Bebo BF, Kalb RE | title = Treatment of pustular psoriasis: from the Medical Board of the National Psoriasis Foundation | journal = Journal of the American Academy of Dermatology | volume = 67 | issue = 2 | pages = 279–88 | date = August 2012 | pmid = 22609220 | doi = 10.1016/j.jaad.2011.01.032 }}</ref> The skin under and surrounding the pustules is red and tender.<ref name="Raychaudhuri2014" /> Pustular psoriasis can either be localized or more widespread throughout the body. Two types of localized pustular psoriasis include psoriasis pustulosa palmoplantaris and [[Dermatitis repens|acrodermatitis continua of Hallopeau]]; both forms are localized to the hands and feet.<ref name="Rendon2019" />

==== Inverse psoriasis ====
[[Inverse psoriasis]] (also known as flexural psoriasis) appears as smooth, inflamed patches of skin. The patches frequently affect [[skin fold]]s, particularly around the [[genitals]] (between the thigh and groin), the [[armpit]]s, in the skin folds of an overweight abdomen (known as [[panniculus]]), between the buttocks in the intergluteal cleft, and under the [[breasts]] in the [[inframammary fold]]. Heat, trauma, and infection are thought to play a role in the development of this atypical form of psoriasis.<ref name="Weigle2013" />

==== Napkin psoriasis ====
[[Napkin psoriasis]] is a subtype of psoriasis common in infants under the age of two and is characterized by red papules with silver scales in the diaper area that may extend to the torso or limbs.<ref name="Gudjonsson2012" /><ref>{{Cite journal |last1=Afsar |first1=Fatma Sule |last2=Uysal |first2=Sila Seremet |last3=Salis |first3=Fatma Muderrisoglu |last4=Calli |first4=Aylin Orgen |date=May 2016 |title=Napkin psoriasis |url=https://onlinelibrary.wiley.com/doi/10.1111/ped.12916 |journal=Pediatrics International |language=en |volume=58 |issue=5 |pages=420–422 |doi=10.1111/ped.12916 |pmid=27103532 |issn=1328-8067|url-access=subscription }}</ref> Napkin psoriasis is often misdiagnosed as [[irritant diaper dermatitis|napkin dermatitis]] (diaper rash).<ref name="Gelmetti2009">{{cite journal | vauthors = Gelmetti C | title = Therapeutic moisturizers as adjuvant therapy for psoriasis patients | journal = American Journal of Clinical Dermatology | volume = 10 | issue = Suppl 1 | pages = 7–12 | date = January 2009 | pmid = 19209948 | doi = 10.2165/0128071-200910001-00002 | s2cid = 9513914 }}</ref> It typically improves as children age and may later present in more common forms as [[plaque psoriasis]] or [[inverse psoriasis]].<ref>{{Cite journal |last=Mahé |first=Emmanuel |date=November 2016 |title=Childhood psoriasis |url=http://www.john-libbey-eurotext.fr/medline.md?doi=10.1684/ejd.2016.2932 |journal=European Journal of Dermatology |volume=26 |issue=6 |pages=537–548 |doi=10.1684/ejd.2016.2932 |pmid=27900946 |issn=1167-1122|url-access=subscription }}</ref>

==== Guttate psoriasis ====
[[File:Psoriasis en gouttes enfant 2.jpg|thumbnail|Example of [[guttate psoriasis]]]]
[[Guttate psoriasis]] is an inflammatory condition characterized by numerous small, scaly, red or pink, droplet-like lesions (papules). These numerous papules appear over large areas of the body, primarily the [[Torso|trunk]], limbs, and scalp, but typically spare the palms and soles. Guttate psoriasis is often triggered by a [[Group A beta-hemolytic streptococcus|streptococcal]] infection ([[Pharynx|oropharyngeal]] or perianal) and typically occurs 1–3 weeks post-infection. [[Guttate psoriasis]] is most commonly seen in children and young adults, and diagnosis is typically made based on history and clinical exam findings.<ref name=Saleh22>{{cite book |vauthors=Saleh D, Tanner LS |chapter=Guttate Psoriasis |date=August 2022 |title=((StatPearls [Internet])) |location=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=29494104}}</ref> Skin [[biopsy]] can also be performed which typically shows a psoriasiform reaction pattern characterized by epidermal [[hyperplasia]] with elongation of the [[Rete pegs|rete ridges]].<ref name=Saleh22/>

There is no firm evidence regarding the best management for guttate psoriasis; however, first-line [[therapy]] for mild guttate psoriasis typically includes topical corticosteroids.<ref name=Saleh22/><ref>{{cite journal |vauthors=Chalmers RJ, O'Sullivan T, Owen CM, Griffiths CE |title=A systematic review of treatments for guttate psoriasis |journal=Br J Dermatol |date=2001 |volume=145 |issue=6 |pages=891–4 |doi= 10.1046/j.1365-2133.2001.04505.x |pmid=11899141|s2cid=27381477 |doi-access=free }}</ref> [[Light therapy|Phototherapy]] can be used for moderate or severe guttate psoriasis. Biologic treatments have not been well studied in the treatment of guttate psoriasis.<ref name=Saleh22/>

Guttate psoriasis has a better [[prognosis]] than plaque psoriasis and typically resolves within 1–3 weeks; however, up to 40% of patients with guttate psoriasis eventually convert to plaque psoriasis.<ref name=Saleh22/><ref name="Weigle2013">{{cite journal | vauthors = Weigle N, McBane S | title = Psoriasis | journal = American Family Physician | volume = 87 | issue = 9 | pages = 626–33 | date = May 2013 | pmid = 23668525 | url = http://www.aafp.org/afp/2013/0501/p626.html | archive-url = https://web.archive.org/web/20150215233455/http://www.aafp.org/afp/2013/0501/p626.html | url-status = live | archive-date = 15 February 2015 }}</ref>

==== Erythrodermic psoriasis ====
[[Psoriatic erythroderma]] (erythrodermic psoriasis) involves widespread inflammation and exfoliation of the skin over most of the body surface, often involving greater than 90% of the body surface area.<ref name="Rendon2019">{{cite journal | vauthors = Rendon A, Schäkel K | title = Psoriasis Pathogenesis and Treatment | journal = International Journal of Molecular Sciences | volume = 20 | issue = 6 | page = 1475 | date = March 2019 | pmid = 30909615 | doi = 10.3390/ijms20061475 | pmc = 6471628 | doi-access = free | title-link = doi }}</ref> It may be accompanied by severe dryness, itching, swelling, and pain. It can develop from any type of psoriasis.<ref name="Rendon2019" /> It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic [[glucocorticoid]]s.<ref name="Zattra2012">{{cite journal | vauthors = Zattra E, Belloni Fortina A, Peserico A, Alaibac M | title = Erythroderma in the era of biological therapies | journal = European Journal of Dermatology | volume = 22 | issue = 2 | pages = 167–71 | date = May 2012 | pmid = 22321651 | doi = 10.1684/ejd.2011.1569 }}</ref> This form of psoriasis can be fatal as the extreme inflammation and exfoliation disrupt the body's ability to [[Thermoregulation|regulate temperature]] and perform barrier functions.<ref name="DermNZ">{{cite web | vauthors = Stanway A | title=Erythrodermic psoriasis | url=http://dermnetnz.org/scaly/erythrodermic-psoriasis.html | publisher=DermNet NZ | access-date=16 March 2014 | url-status=live | archive-url=https://web.archive.org/web/20140202222207/http://dermnetnz.org/scaly/erythrodermic-psoriasis.html | archive-date=2 February 2014 }}</ref>

==== Mouth ====
Psoriasis in the mouth is very rare, in contrast to [[lichen planus]], another common papulosquamous disorder that commonly involves both the skin and mouth.<ref name="Yesudian2012">{{cite journal | vauthors = Yesudian PD, Chalmers RJ, Warren RB, Griffiths CE | title = In search of oral psoriasis | journal = Archives of Dermatological Research | volume = 304 | issue = 1 | pages = 1–5 | date = January 2012 | pmid = 21927905 | doi = 10.1007/s00403-011-1175-3 | s2cid = 33434341 }}</ref> When psoriasis involves the oral [[Mucous membrane|mucosa]] (the lining of the mouth), it may be asymptomatic,<ref name="Yesudian2012"/> but it may appear as white or grey-yellow plaques.<ref name="Yesudian2012"/> [[Fissured tongue]] is the most common finding in those with oral psoriasis and has been reported to occur in 6.5–20% of people with psoriasis affecting the skin. The microscopic appearance of oral mucosa affected by [[geographic tongue]] (migratory stomatitis) is very similar to the appearance of psoriasis.<ref>{{cite book | vauthors = Greenberg MS, Glick M, Ship JA | title = Burket's oral medicine | year = 2008 | publisher = BC Decker | location = Hamilton, Ont | isbn = 978-1-55009-345-2 | pages = 103–4 | edition = 11th }}</ref> A recent study found an association between the two conditions, and it suggests that geographic tongue might be a predictor for psoriasis.<ref>{{Cite journal |last1=González-Álvarez |first1=Laura |last2=García-Martín |first2=José M. |last3=García-Pola |first3=María José |date=May 2019 |title=Association between geographic tongue and psoriasis: A systematic review and meta-analyses |journal=Journal of Oral Pathology & Medicine|volume=48 |issue=5 |pages=365–372 |doi=10.1111/jop.12840 |issn=1600-0714 |pmid=30739339|hdl=10651/52321 |hdl-access=free }}</ref>

==== Seborrheic-like psoriasis ====
[[Seborrheic-like psoriasis]] is a common form of psoriasis with clinical aspects of psoriasis and [[seborrheic dermatitis]], and it may be difficult to distinguish from the latter. This form of psoriasis typically manifests as red plaques with greasy scales in areas of higher [[sebum]] production such as the [[scalp]], [[forehead]], [[nasolabial fold|skin folds next to the nose]], the skin surrounding the mouth, skin on the chest above the [[sternum]], and in [[intertriginous|skin folds]].<ref name="Gudjonsson2012"/>

===Psoriatic arthritis===
[[Psoriatic arthritis]] is a form of chronic inflammatory [[arthritis]] that has a highly variable clinical presentation and frequently occurs in association with skin and nail psoriasis.<ref name="Chimenti2013">{{cite journal | vauthors = Chimenti MS, Saraceno R, Chiricozzi A, Giunta A, Chimenti S, Perricone R | title = Profile of certolizumab and its potential in the treatment of psoriatic arthritis | journal = Drug Design, Development and Therapy | volume = 7 | pages = 339–48 | date = April 2013 | pmid = 23620660 | pmc = 3633576 | doi = 10.2147/DDDT.S31658 | doi-access = free }}</ref><ref name="Goldenstein2012"/> It typically involves painful inflammation of the joints and [[Synovitis|surrounding connective tissue]] and can occur in any joint, but most commonly affects the joints of the fingers and toes. This can result in a sausage-shaped swelling of the fingers and toes known as [[dactylitis]].<ref name="Chimenti2013"/> Psoriatic arthritis can also affect the hips, knees, spine ([[spondylitis]]), and [[sacroiliac joint]] ([[sacroiliitis]]).<ref name="Krawczyk2013">{{cite journal | vauthors = Krawczyk-Wasielewska A, Skorupska E, Samborski W | title = Sacroiliac joint pain as an important element of psoriatic arthritis diagnosis | journal = Postepy Dermatologii I Alergologii | volume = 30 | issue = 2 | pages = 108–12 | date = April 2013 | pmid = 24278057 | pmc = 3834688 | doi = 10.5114/pdia.2013.34161 }}</ref> About 30% of individuals with psoriasis will develop psoriatic arthritis.<ref name="Palfreeman2013">{{cite journal | vauthors = Palfreeman AC, McNamee KE, McCann FE | title = New developments in the management of psoriasis and psoriatic arthritis: a focus on apremilast | journal = Drug Design, Development and Therapy | volume = 7 | pages = 201–10 | date = March 2013 | pmid = 23569359 | pmc = 3615921 | doi = 10.2147/DDDT.S32713 | doi-access = free }}</ref> Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.<ref name="Goldenstein2012">{{cite journal | vauthors = Goldenstein-Schainberg C, Favarato MH, Ranza R | title = Current and relevant concepts in psoriatic arthritis | journal = Revista Brasileira de Reumatologia | volume = 52 | issue = 1 | pages = 98–106 | date = January–February 2012 | pmid = 22286649 | doi = 10.1590/s0482-50042012000100010 | doi-access = free | title-link = doi }}</ref>

===Nail changes===
[[File:Luszczyca paznokcia.jpg|thumbnail|Psoriasis of a fingernail, with visible pitting]]
[[File:NailPsoriasis.JPG|thumb|Effect of psoriasis on the toenails]]
[[Psoriatic nails|Psoriasis can affect the nails]] and produces a variety of changes in the appearance of fingers and toenails. Nail psoriasis occurs in 40–45% of people with psoriasis affecting the skin, and has a lifetime incidence of 80–90% in those with psoriatic arthritis.<ref name="Tan2012">{{cite journal | vauthors = Tan ES, Chong WS, Tey HL | title = Nail psoriasis: a review | journal = American Journal of Clinical Dermatology | volume = 13 | issue = 6 | pages = 375–88 | date = December 2012 | pmid = 22784035 | doi = 10.2165/11597000-000000000-00000 | s2cid = 8561015 }}</ref> These changes include pitting of the nails (pinhead-sized depressions in the nail is seen in 70% with nail psoriasis), [[leukonychia|whitening of the nail]], [[splinter hemorrhage|small areas of bleeding from capillaries under the nail]], yellow-reddish discoloration of the nails known as the oil drop or salmon spots, dryness, thickening of the skin under the nail (subungual hyperkeratosis), loosening and separation of the nail ([[onycholysis]]), and crumbling of the nail.<ref name="Tan2012"/>

===Medical signs===
In addition to the appearance and distribution of the rash, specific [[medical sign]]s may be used by medical practitioners to assist with diagnosis. These may include [[Auspitz's sign]] (pinpoint bleeding when the scale is removed), [[Koebner phenomenon]] (psoriatic skin lesions induced by trauma to the skin),<ref name="Gudjonsson2012">{{cite book|vauthors=Gudjonsson JE, Elder JT, Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K |title=Fitzpatrick's Dermatology in General Medicine|year=2012|publisher=McGraw-Hill|isbn=978-0-07-166904-7|edition=8th|chapter=18: Psoriasis }}</ref> and [[Pruritus|itching]] and pain localized to papules and plaques.<ref name="Weigle2013"/><ref name="Gudjonsson2012"/>

==Causes==
The cause of psoriasis is not fully understood. Genetics, seasonal changes, skin damage, climate, [[Immunodeficiency|immunocompromised]] state, specific infections, and the use of some medications have been connected with different types of psoriasis.<ref name="Prieto2013" /><ref name=":0" />

===Genetics===
{{See also|List of human leukocyte antigen alleles associated with cutaneous conditions}}
Around one-third of people with psoriasis report a [[family history (medicine)|family history]] of the disease, and researchers have identified genetic [[locus (genetics)|loci]] associated with the condition. [[twin|Identical twin]] studies suggest a 70% chance of a twin developing psoriasis if the other twin has the disorder. The risk is around 20% for fraternal twins. These findings suggest both a genetic susceptibility and an environmental response in developing psoriasis.<ref name=Krueger>{{cite journal | vauthors = Krueger G, Ellis CN | title = Psoriasis--recent advances in understanding its pathogenesis and treatment | journal = Journal of the American Academy of Dermatology | volume = 53 | issue = 1 Suppl 1 | pages = S94–100 | date = July 2005 | pmid = 15968269 | doi = 10.1016/j.jaad.2005.04.035 }}</ref>

Psoriasis has a strong hereditary component, and many genes are associated with it, but how those genes work together is unclear. Most of the identified genes relate to the [[immune system]], particularly the [[major histocompatibility complex]] (MHC) and [[T cells]]. Genetic studies are valuable due to their ability to identify molecular mechanisms and pathways for further study and potential medication targets.<ref name=Nestle>{{cite journal | vauthors = Nestle FO, Kaplan DH, Barker J | title = Psoriasis | journal = The New England Journal of Medicine | volume = 361 | issue = 5 | pages = 496–509 | date = July 2009 | pmid = 19641206 | doi = 10.1056/NEJMra0804595 | s2cid = 203791161 | doi-access = free }}</ref>

Classic genome-wide [[linkage analysis]] has identified nine loci on different [[chromosome]]s associated with psoriasis. They are called psoriasis susceptibility 1 through 9 (''[[PSORS1]]'' through ''PSORS9''). Within those loci are genes on pathways that lead to inflammation. Certain variations ([[mutation]]s) of those genes are commonly found in psoriasis.<ref name=Nestle/> [[Genome-wide association study|Genome-wide association scans]] have identified other genes that are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal [[proteins]], which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.<ref name=Nestle/>

The major determinant is ''PSORS1'', which probably accounts for 35–50% of psoriasis heritability.<ref>{{cite journal | vauthors = Smith CH, Barker JN | title = Psoriasis and its management | journal = BMJ | volume = 333 | issue = 7564 | pages = 380–4 | date = August 2006 | pmid = 16916825 | pmc = 1550454 | doi = 10.1136/bmj.333.7564.380 }}</ref> It controls genes that affect the immune system or encode skin proteins that are overabundant in psoriasis. ''PSORS1'' is located on [[chromosome 6]] in the MHC, which controls important immune functions. Three genes in the ''PSORS1'' locus have a strong association with psoriasis vulgaris: ''HLA-C'' variant ''HLA-Cw6'',<ref name="Prieto2013"/> which encodes an MHC class I protein; ''[[CCHCR1]]'', variant WWC, which encodes a [[coiled coil]] protein overexpressed in psoriatic [[epidermis]]; and ''[[CDSN]]'', variant allele 5, which encodes [[corneodesmosin]], a protein expressed in the granular and [[cornified layer]]s of the epidermis and upregulated in psoriasis.<ref name=Nestle/>

Two major immune system genes under investigation are interleukin-12 subunit beta (''IL12B'') on [[Chromosome 5 (human)|chromosome 5q]], which expresses interleukin-12B; and ''[[IL23R]]'' on chromosome 1p, which expresses the interleukin-23 receptor and is involved in T cell differentiation. Interleukin-23 receptor and ''IL12B'' have both been strongly linked with psoriasis.<ref name="Prieto2013"/> T cells are involved in the inflammatory process that leads to psoriasis.<ref name=Nestle/> These genes are on the pathway that upregulates tumor necrosis factor-α and [[NF-κB|nuclear factor κB]], two genes involved in inflammation.<ref name=Nestle/> The first gene directly linked to psoriasis was identified as the ''[[CARD14]] ''gene located in the ''PSORS2'' locus. A rare mutation in the gene encoding for the ''[[CARD14]]''-regulated protein, plus an environmental trigger, was enough to cause plaque psoriasis (the most common form of psoriasis).<ref name = Jordan1>{{cite journal | vauthors = Jordan CT, Cao L, Roberson ED, Duan S, Helms CA, Nair RP, Duffin KC, Stuart PE, Goldgar D, Hayashi G, Olfson EH, Feng BJ, Pullinger CR, Kane JP, Wise CA, Goldbach-Mansky R, Lowes MA, Peddle L, Chandran V, Liao W, Rahman P, Krueger GG, Gladman D, Elder JT, Menter A, Bowcock AM | title = Rare and common variants in CARD14, encoding an epidermal regulator of NF-kappaB, in psoriasis | journal = American Journal of Human Genetics | volume = 90 | issue = 5 | pages = 796–808 | date = May 2012 | pmid = 22521419 | pmc = 3376540 | doi = 10.1016/j.ajhg.2012.03.013 }}</ref><ref name = Jordan2>{{cite journal | vauthors = Jordan CT, Cao L, Roberson ED, Pierson KC, Yang CF, Joyce CE, Ryan C, Duan S, Helms CA, Liu Y, Chen Y, McBride AA, Hwu WL, Wu JY, Chen YT, Menter A, Goldbach-Mansky R, Lowes MA, Bowcock AM | title = PSORS2 is due to mutations in CARD14 | journal = American Journal of Human Genetics | volume = 90 | issue = 5 | pages = 784–95 | date = May 2012 | pmid = 22521418 | pmc = 3376640 | doi = 10.1016/j.ajhg.2012.03.012 }}</ref>

===Lifestyle===
Conditions reported as worsening the disease include chronic infections, stress, and changes in season and [[climate]].<ref name="Prieto2013"/> Other factors that might worsen the condition include hot water, scratching psoriasis skin lesions, [[Xeroderma|skin dryness]], [[Alcoholism|excessive alcohol consumption]], [[cigarette smoking]], and [[obesity]].<ref name=Prieto2013/><ref name=Clarke2011>{{cite journal | vauthors = Clarke P | title = Psoriasis | journal = Australian Family Physician | volume = 40 | issue = 7 | pages = 468–73 | date = July 2011 | pmid = 21743850 | url = http://www.racgp.org.au/download/documents/AFP/2011/July/201107clark.pdf | access-date = 4 March 2014 | archive-date = 27 June 2019 | archive-url = https://web.archive.org/web/20190627155636/https://www.racgp.org.au/download/documents/AFP/2011/July/201107clark.pdf | url-status = live }}</ref><ref name=Richard2013/><ref name=Shu2019>{{cite journal | vauthors = Ko SH, Chi CC, Yeh ML, Wang SH, Tsai YS, Hsu MY | title = Lifestyle changes for treating psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | article-number = CD011972 | date = July 2019 | issue = 7 | pmid = 31309536 | pmc = 6629583 | doi = 10.1002/14651858.CD011972.pub2 | id = CD011972 }}</ref> The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019.<ref name=Shu2019 />

===HIV===
The rate of psoriasis in [[human immunodeficiency virus]]-positive (HIV) individuals is comparable to that of HIV-negative individuals, but psoriasis tends to be more severe in people infected with HIV.<ref name="Cedeno2011"/> A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with psoriasis than in those without the infection.<ref name="Cedeno2011"/> The immune response in those infected with HIV is typically characterized by [[cytokine|cellular signals]] from [[T helper cell|T<sub>h</sub>2 subset of CD4+ helper T cells]],<ref name="Fife2007">{{cite journal | vauthors = Fife DJ, Waller JM, Jeffes EW, Koo JY | title = Unraveling the paradoxes of HIV-associated psoriasis: a review of T-cell subsets and cytokine profiles | journal = Dermatology Online Journal | volume = 13 | issue = 2 | page = 4 | date = May 2007 | doi = 10.5070/D34SF63339 | pmid = 17498423 | url = http://dermatology.cdlib.org/132/reviews/HIV/fife.html | url-status = live | archive-url = https://web.archive.org/web/20080421173119/http://dermatology.cdlib.org/132/reviews/HIV/fife.html | archive-date = 21 April 2008 }}</ref> whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of [[Th1 cell|T<sub>h</sub>1 subset of CD4+ helper T cells]] and [[T helper 17 cell|T<sub>h</sub>17 helper T cells]].<ref name="Wong2013">{{cite journal | vauthors = Wong T, Hsu L, Liao W | title = Phototherapy in psoriasis: a review of mechanisms of action | journal = [[Journal of Cutaneous Medicine and Surgery]] | volume = 17 | issue = 1 | pages = 6–12 | date = January–February 2013 | pmid = 23364144 | pmc = 3736829 | doi = 10.2310/7750.2012.11124 }}</ref><ref name="Martin2013">{{cite journal | vauthors = Martin DA, Towne JE, Kricorian G, Klekotka P, Gudjonsson JE, Krueger JG, Russell CB | title = The emerging role of IL-17 in the pathogenesis of psoriasis: preclinical and clinical findings | journal = The Journal of Investigative Dermatology | volume = 133 | issue = 1 | pages = 17–26 | date = January 2013 | pmid = 22673731 | pmc = 3568997 | doi = 10.1038/jid.2012.194 }}</ref> The diminished CD4+ T cell presence is thought to cause overactivation of CD8+ T cells, which are responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy.<ref name=Rice>{{cite web |title=Images of Memorable Cases: Case 34 |quote=This AIDS patient presented with a pruritic eruption over most of his body |work=Connexions |publisher=Rice University |url=http://cnx.org/content/m14956/latest/ |access-date=21 December 2009 |archive-date=10 July 2012 |archive-url=https://archive.today/20120710172141/http://cnx.org/content/m14956/latest/ |url-status=live }}</ref> In those with long-term, well-controlled psoriasis, new HIV infection can trigger a severe flare-up of psoriasis and/or psoriatic arthritis.{{Medical citation needed|date=October 2019}}

=== Microbes ===
Psoriasis has been described as occurring after [[strep throat]], and may be worsened by skin or gut colonization with ''[[Staphylococcus aureus]]'', ''[[Malassezia]]'' spp., and ''[[Candida albicans]]''.<ref name=":0">{{cite journal | vauthors = Fry L, Baker BS | title = Triggering psoriasis: the role of infections and medications | journal = Clinics in Dermatology | volume = 25 | issue = 6 | pages = 606–15 | date = 2007 | pmid = 18021899 | doi = 10.1016/j.clindermatol.2007.08.015 }}</ref> Guttate psoriasis often affects children and adolescents and can be triggered by a recent [[group A streptococcal infection]] ([[tonsillitis]] or [[pharyngitis]]).<ref name="Rendon2019" />

===Medications===
Drug-induced psoriasis may occur with [[beta blocker]]s,<ref name=Jain2012 /> [[lithium]],<ref name=Jain2012 /> [[antimalarial medication]]s,<ref name=Jain2012 /> [[nonsteroidal anti-inflammatory drug]]s,<ref name=Jain2012 /> [[terbinafine]], [[calcium channel blockers]], [[captopril]], [[glyburide]], [[granulocyte colony-stimulating factor]],<ref name=Jain2012 /> [[interleukin]]s, [[interferon]]s,<ref name=Jain2012 /> [[Hypolipidemic agent|lipid-lowering medications]],<ref name="Andrews"/>{{rp|197}} and paradoxically [[TNF inhibitor]]s such as [[infliximab]] or [[adalimumab]].<ref name="Guerra2013">{{cite journal | vauthors = Guerra I, Gisbert JP | title = Onset of psoriasis in patients with inflammatory bowel disease treated with anti-TNF agents | journal = Expert Review of Gastroenterology & Hepatology | volume = 7 | issue = 1 | pages = 41–8 | date = January 2013 | pmid = 23265148 | doi = 10.1586/egh.12.64 | s2cid = 207210831 }}</ref> Withdrawal of [[corticosteroid]]s (topical steroid cream) can aggravate psoriasis due to the [[rebound effect]].<ref name=Weller2008>{{cite book|vauthors=Weller R, Hunter JA, Savin J, Dahl M|title=Clinical dermatology|year=2008|publisher=Blackwell|location=Malden, MA|isbn=978-1-4443-0009-3|pages=54–70|url=https://books.google.com/books?id=5RHM0Nerk9gC&q=dermatology|edition=4th|access-date=19 November 2020|archive-date=24 February 2024|archive-url=https://web.archive.org/web/20240224040825/https://books.google.com/books?id=5RHM0Nerk9gC&q=dermatology|url-status=live}}</ref>

==Pathophysiology==
Psoriasis is characterized by an abnormally excessive and rapid growth of the [[epidermis (skin)|epidermal layer of the skin]].<ref name="Ouyang2010">{{cite journal | vauthors = Ouyang W | title = Distinct roles of IL-22 in human psoriasis and inflammatory bowel disease | journal = Cytokine & Growth Factor Reviews | volume = 21 | issue = 6 | pages = 435–41 | date = December 2010 | pmid = 21106435 | doi = 10.1016/j.cytogfr.2010.10.007 }}</ref> Abnormal production of skin cells (especially during [[wound repair]]) and an overabundance of skin cells result from the sequence of pathological events in psoriasis.<ref name="Raychaudhuri2014"/> The sequence of pathological events in psoriasis is thought to start with an initiation phase in which an event (skin trauma, infection, or drugs) leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease.<ref name="Nestle" /><ref name="Rendon2019" /> Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days.<ref name="Parrish2012"/> These changes are believed to stem from the premature maturation of [[keratinocyte]]s induced by an inflammatory cascade in the [[dermis]] involving [[dendritic cell]]s, [[macrophage]]s, and T cells (three subtypes of immune cells).<ref name="Palfreeman2013"/><ref name="Cedeno2011">{{cite journal | vauthors = Cedeno-Laurent F, Gómez-Flores M, Mendez N, Ancer-Rodríguez J, Bryant JL, Gaspari AA, Trujillo JR | title = New insights into HIV-1-primary skin disorders | journal = Journal of the International AIDS Society | volume = 14 | issue = 5 | page = 5 | date = January 2011 | pmid = 21261982 | pmc = 3037296 | doi = 10.1186/1758-2652-14-5 | doi-access = free }}</ref> These immune cells move from the [[dermis]] to the epidermis and secrete inflammatory chemical signals (cytokines) such as [[IL36G|interleukin-36γ]], [[tumor necrosis factor-α]], [[Interleukin 1 family|interleukin-1β]], [[interleukin-6]], and [[interleukin-22]].<ref name=Nestle/><ref>{{cite journal | vauthors = Baliwag J, Barnes DH, Johnston A | title = Cytokines in psoriasis | journal = Cytokine | volume = 73 | issue = 2 | pages = 342–50 | date = June 2015 | pmid = 25585875 | pmc = 4437803 | doi = 10.1016/j.cyto.2014.12.014 | series = Skin Disease, Immune Response and Cytokines }}</ref> These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate.<ref name=Nestle/> One hypothesis is that psoriasis involves a defect in [[regulatory T cell]]s, and in the regulatory cytokine [[interleukin-10]].<ref name=Nestle/> The inflammatory cytokines found in psoriatic nails and joints (in the case of psoriatic arthritis) are similar to those of psoriatic skin lesions, suggesting a common inflammatory mechanism.<ref name="Rendon2019" />

Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of psoriasis.<ref name="Roberson2010">{{cite journal | vauthors = Roberson ED, Bowcock AM | title = Psoriasis genetics: breaking the barrier | journal = Trends in Genetics | volume = 26 | issue = 9 | pages = 415–23 | date = September 2010 | pmid = 20692714 | pmc = 2957827 | doi = 10.1016/j.tig.2010.06.006 }}</ref><ref name="Ramos2012">{{cite journal | vauthors = Ramos-e-Silva M, Jacques C | title = Epidermal barrier function and systemic diseases | journal = Clinics in Dermatology | volume = 30 | issue = 3 | pages = 277–9 | date = May–June 2012 | pmid = 22507041 | doi = 10.1016/j.clindermatol.2011.08.025 }}</ref>

[[Deoxyribonucleic acid]] (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis<ref name="Dombrowski2012">{{cite journal | vauthors = Dombrowski Y, Schauber J | title = Cathelicidin LL-37: a defense molecule with a potential role in psoriasis pathogenesis | journal = Experimental Dermatology | volume = 21 | issue = 5 | pages = 327–30 | date = May 2012 | pmid = 22509827 | doi = 10.1111/j.1600-0625.2012.01459.x | s2cid = 24119451 }}</ref> and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α.<ref name="Dombrowski2012"/> In response to these chemical messages from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signal downstream inflammatory cells to arrive and stimulate additional inflammation.<ref name=Nestle/>

[[Dendritic cell]]s bridge the [[innate immune system]] and [[adaptive immune system]]. They are increased in psoriatic lesions<ref name="Ouyang2010"/> and induce the proliferation of T cells and type 1 helper T cells (T<sub>h</sub>1). Targeted [[immunotherapy]], as well as [[psoralen]] and [[ultraviolet A]] ([[PUVA]]) therapy, can reduce the number of dendritic cells and favors a [[Th2 cell|T<sub>H</sub>2 cell]] cytokine secretion pattern over a T<sub>h</sub>1/T<sub>h</sub>17 cell cytokine profile.<ref name=Nestle/><ref name="Wong2013"/> Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and [[interleukin-17]].<ref name="Mudigonda2012">{{cite journal | vauthors = Mudigonda P, Mudigonda T, Feneran AN, Alamdari HS, Sandoval L, Feldman SR | title = Interleukin-23 and interleukin-17: importance in pathogenesis and therapy of psoriasis | journal = Dermatology Online Journal | volume = 18 | issue = 10 | page = 1 | date = October 2012 | doi = 10.5070/D33N39N8XM | pmid = 23122008 }}</ref> Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22.<ref name="Ouyang2010"/><ref name="Mudigonda2012"/> Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete [[neutrophil]]-attracting cytokines.<ref name="Mudigonda2012"/>

==Diagnosis==
[[File:Micrograph of psoriasis vulgaris.jpg|thumb|Micrograph of psoriasis vulgaris. Confluent [[parakeratosis]], psoriasiform epidermal hyperplasia [(A), EH], hypogranulosis, and an influx of numerous neutrophils in the corneal layer [(A), arrow]. (B) Transepidermal migration of neutrophils from the dermis to the corneal layer (arrows).<ref>{{cite journal | vauthors = Giang J, Seelen MA, van Doorn MB, Rissmann R, Prens EP, Damman J | title = Complement Activation in Inflammatory Skin Diseases | journal = Frontiers in Immunology | volume = 9 | article-number = 639 | year = 2018 | pmid = 29713318 | pmc = 5911619 | doi = 10.3389/fimmu.2018.00639 | doi-access = free | title-link = doi }}</ref>]]

A [[medical diagnosis|diagnosis]] of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly, [[erythema]]tous plaques, papules, or patches of skin that may be painful and itch.<ref name="Weigle2013"/> No special [[blood test]]s or diagnostic procedures are usually required to make the diagnosis.<ref name="Raychaudhuri2014"/>

The [[differential diagnosis]] of psoriasis includes dermatological conditions similar in appearance such as [[discoid eczema]], [[seborrheic eczema]], [[pityriasis rosea]] (may be confused with guttate psoriasis), [[tinea unguium|nail fungus]] (may be confused with nail psoriasis) or [[cutaneous T cell lymphoma]] (50% of individuals with this cancer are initially [[misdiagnosis|misdiagnosed]] with psoriasis).<ref name=Weller2008 /> Dermatologic manifestations of systemic illnesses such as the rash of [[secondary syphilis]] may also be confused with psoriasis.<ref name=Weller2008/>

If the clinical diagnosis is uncertain, a skin [[biopsy]] or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy shows clubbed [[rete pegs|epidermal projections that interdigitate with dermis]] on microscopy. [[Acanthosis|Epidermal thickening]] is another characteristic [[Histology|histologic]] finding of psoriasis lesions.<ref name="Raychaudhuri2014"/><ref name="Kunz2009">{{cite journal | vauthors = Kunz M, Ibrahim SM | title = Cytokines and cytokine profiles in human autoimmune diseases and animal models of autoimmunity | journal = Mediators of Inflammation | volume = 2009 | article-number = 979258 | year = 2009 | pmid = 19884985 | pmc = 2768824 | doi = 10.1155/2009/979258 | doi-access = free | title-link = doi }}</ref> The [[stratum granulosum]] layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the [[stratum corneum|most superficial layer of skin]] are also abnormal as they never fully mature. Unlike their mature counterparts, [[parakeratosis|these superficial cells]] keep their [[Cell nucleus|nuclei]].<ref name="Raychaudhuri2014"/> Inflammatory infiltrates can typically be seen on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells, while a predominance of CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and joints.<ref name="Raychaudhuri2014"/>

===Classification===

====Morphological====
{| class="wikitable" style = "float: right; margin-left:15px; text-align:center"
! Psoriasis Type
! ICD-10 Code
|-
| Psoriasis Vulgaris
| L40.0
|-
| [[Generalized pustular psoriasis]]
| L40.1
|-
| [[Acrodermatitis continua]]
| L40.2
|-
| [[Pustulosis palmaris et plantaris]]
| L40.3
|-
| [[Guttate psoriasis]]
| L40.4
|-
| [[Psoriatic arthritis]]
| L40.50
|-
| Psoriatic spondylitis
| L40.53
|-
| [[Inverse psoriasis]]
| L40.8
|}

Psoriasis is classified as a [[papulosquamous disorder]] and is most commonly subdivided into different categories based on histological characteristics.<ref name=Menter2008 /><ref name=Jain2012/> Variants include plaque, pustular, guttate, and flexural psoriasis. Each form has a dedicated [[ICD-10]] code.<ref>{{cite web |title=Application to Dermatology of International Classification of Disease (ICD-10) |publisher=The International League of Dermatological Societies |url=http://web.ilds.org/icd10_list.php?VIEW=1&START_CODE=L40.0&START_EXT=00 |archive-url=https://web.archive.org/web/20060709183301/http://web.ilds.org/icd10_list.php?VIEW=1&START_CODE=L40.0&START_EXT=00 |archive-date=9 July 2006 }}</ref> Psoriasis can also be classified into nonpustular and [[pustule|pustular]] types.<ref name="Fitz2">{{cite book | vauthors = Freedberg IM, Fitzpatrick TB |title=Fitzpatrick's dermatology in general medicine |publisher=McGraw-Hill |year=2003 |isbn=978-0-07-138076-8 |edition=6th |page=414 }}</ref>

====Pathogenetic====
Another classification scheme considers genetic and demographic factors. Type 1 has a positive family history, starts before the age of 40, and is associated with the [[human leukocyte antigen]], [[HLA-C|''HLA-Cw6'']]. Conversely, type 2 does not show a family history, presents after age 40, and is not associated with ''HLA-Cw6''.<ref name=Kupetsky2013 /> Type 1 accounts for about 75% of persons with psoriasis.<ref>{{cite journal | vauthors = Griffiths CE, Christophers E, Barker JN, Chalmers RJ, Chimenti S, Krueger GG, Leonardi C, Menter A, Ortonne JP, Fry L | title = A classification of psoriasis vulgaris according to phenotype | journal = The British Journal of Dermatology | volume = 156 | issue = 2 | pages = 258–62 | date = February 2007 | pmid = 17223864 | doi = 10.1111/j.1365-2133.2006.07675.x | s2cid = 45917573 }}</ref>

The classification of psoriasis as an autoimmune disease has sparked considerable debate. Researchers have proposed differing descriptions of psoriasis and psoriatic arthritis; some authors have classified them as autoimmune diseases<ref name="Raychaudhuri2014"/><ref name="Prieto2013"/><ref name="Weidemann2013">{{cite journal | vauthors = Weidemann AK, Crawshaw AA, Byrne E, Young HS | title = Vascular endothelial growth factor inhibitors: investigational therapies for the treatment of psoriasis | journal = Clinical, Cosmetic and Investigational Dermatology | volume = 6 | pages = 233–44 | date = September 2013 | pmid = 24101875 | pmc = 3790838 | doi = 10.2147/CCID.S35312 | doi-access = free }}</ref> while others have classified them as distinct from autoimmune diseases and referred to them as [[immune-mediated inflammatory diseases]].<ref name=Nestle/><ref name="Han2012">{{cite journal | vauthors = Han R, Rostami-Yazdi M, Gerdes S, Mrowietz U | title = Triptolide in the treatment of psoriasis and other immune-mediated inflammatory diseases | journal = British Journal of Clinical Pharmacology | volume = 74 | issue = 3 | pages = 424–36 | date = September 2012 | pmid = 22348323 | pmc = 3477344 | doi = 10.1111/j.1365-2125.2012.04221.x }}</ref><ref name="Quatresooz">{{cite journal | vauthors = Quatresooz P, Hermanns-Lê T, Piérard GE, Humbert P, Delvenne P, Piérard-Franchimont C | title = Ustekinumab in psoriasis immunopathology with emphasis on the Th17-IL23 axis: a primer | journal = Journal of Biomedicine & Biotechnology | volume = 2012 | article-number = 147413 | date = June 2012 | pmid = 22754278 | pmc = 3384985 | doi = 10.1155/2012/147413 | doi-access = free | title-link = doi }}</ref>

====Severity====
[[Image:Distribution of psoriasis severity.svg|thumb|Distribution of severity]]
No consensus exists about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)≤10, a [[Psoriasis Area and Severity Index]] (PASI) score ≤10, and a [[Dermatology Life Quality Index]] (DLQI) score ≤10.<ref name="Mrowietz2011">{{cite journal | vauthors = Mrowietz U, Kragballe K, Reich K, Spuls P, Griffiths CE, Nast A, Franke J, Antoniou C, Arenberger P, Balieva F, Bylaite M, Correia O, Daudén E, Gisondi P, Iversen L, Kemény L, Lahfa M, Nijsten T, Rantanen T, Reich A, Rosenbach T, Segaert S, Smith C, Talme T, Volc-Platzer B, Yawalkar N | title = Definition of treatment goals for moderate to severe psoriasis: a European consensus | journal = Archives of Dermatological Research | volume = 303 | issue = 1 | pages = 1–10 | date = January 2011 | pmid = 20857129 | pmc = 3016217 | doi = 10.1007/s00403-010-1080-1 }}</ref> Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.<ref name="Mrowietz2011"/>

The DLQI is a 10-question tool used to measure the impact of several dermatologic diseases on daily functioning. The DLQI score ranges from 0 (minimal impairment) to 30 (maximal impairment) and is calculated with each answer being assigned 0–3 points, with higher scores indicating greater social or occupational impairment.<ref name="Mease2011">{{cite journal | vauthors = Mease PJ | title = Measures of psoriatic arthritis: Tender and Swollen Joint Assessment, Psoriasis Area and Severity Index (PASI), Nail Psoriasis Severity Index (NAPSI), Modified Nail Psoriasis Severity Index (mNAPSI), Mander/Newcastle Enthesitis Index (MEI), Leeds Enthesitis Index (LEI), Spondyloarthritis Research Consortium of Canada (SPARCC), Maastricht Ankylosing Spondylitis Enthesis Score (MASES), Leeds Dactylitis Index (LDI), Patient Global for Psoriatic Arthritis, Dermatology Life Quality Index (DLQI), Psoriatic Arthritis Quality of Life (PsAQOL), Functional Assessment of Chronic Illness Therapy-Fatigue (FACIT-F), Psoriatic Arthritis Response Criteria (PsARC), Psoriatic Arthritis Joint Activity Index (PsAJAI), Disease Activity in Psoriatic Arthritis (DAPSA), and Composite Psoriatic Disease Activity Index (CPDAI) | journal = Arthritis Care & Research | volume = 63 | issue = Supplement 11 | pages = S64–85 | date = November 2011 | pmid = 22588772 | doi = 10.1002/acr.20577 }}</ref>

The PASI is the most widely used measurement tool for psoriasis. It assesses the severity of lesions and the area affected and combines these two factors into a single score from 0 (no disease) to 72 (maximal disease).<ref>{{cite journal|url=http://www.skinandaging.com/article/5394|archive-url=https://web.archive.org/web/20110302031858/http://www.skinandaging.com/article/5394|archive-date=2 March 2011|title=Psoriasis Update |journal=Skin & Aging |volume=14 |issue=3|year=2006 |pages=46–50}}</ref> Nevertheless, the PASI can be too unwieldy to use outside of research settings, which has led to attempts to simplify the index for clinical use.<ref name="pmid15530297">{{cite journal | vauthors = Louden BA, Pearce DJ, Lang W, Feldman SR | title = A Simplified Psoriasis Area Severity Index (SPASI) for rating psoriasis severity in clinic patients | journal = Dermatology Online Journal | volume = 10 | issue = 2 | page = 7 | date = October 2004 | doi = 10.5070/D318W9J736 | pmid = 15530297 }}</ref>

== Co-morbidities ==
Psoriasis is not just a skin disease. The symptoms of psoriasis can sometimes go beyond the skin and can hurt the [[quality of life]] of the affected individuals.<ref name=":1" /> Additionally, the co-morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition.<ref name=":1">{{cite journal | vauthors = Lønnberg AS, Skov L | title = Co-morbidity in psoriasis: mechanisms and implications for treatment | journal = Expert Review of Clinical Immunology | volume = 13 | issue = 1 | pages = 27–34 | date = January 2017 | pmid = 27426230 | doi = 10.1080/1744666X.2016.1213631 | s2cid = 21793052 }}</ref>

=== Cardiovascular complications ===
There is a 2.2 times increased risk of cardiovascular complications in people with psoriasis.<ref name=":2" /> Also, people with psoriasis are more susceptible to [[myocardial infarction]] (heart attack) and [[stroke]].<ref name=":2" /> It has been speculated that there is systemic inflammation in psoriasis, which drives "psoriatic march" and can cause other inflammatory complications including [[Cardiovascular disease|cardiovascular complications]].<ref name=":2">{{cite journal | vauthors = Masson W, Lobo M, Molinero G | title = Psoriasis and Cardiovascular Risk: A Comprehensive Review | journal = Advances in Therapy | volume = 37 | issue = 5 | pages = 2017–2033 | date = May 2020 | pmid = 32314303 | pmc = 7467489 | doi = 10.1007/s12325-020-01346-6 }}</ref> A study used [[Fluorodeoxyglucose (18F)|fluorodeoxyglucose F-18]] positron emission tomography-computed tomography (FDG PET/CT) to measure aortic vascular inflammation in psoriasis patients, and found increased [[Coronary arteries|coronary artery]] disease indices, including total plaque burden, luminal stenosis, and high-risk plaques in people with psoriasis. Similarly, it was found that there is an 11% reduction in aortic vascular inflammation when there is a 75% reduction in the PASI score.<ref>{{cite journal | vauthors = Amin M, Lee EB, Tsai TF, Wu JJ | title = Psoriasis and Co-morbidity | journal = Acta Dermato-Venereologica | volume = 100 | issue = 3 | pages = 81–87 | date = January 2020 | pmid = 31971602 | pmc = 9128942 | doi = 10.2340/00015555-3387 }}</ref>

=== Depression ===
[[Depression (mood)|Depression]] or depressive symptoms are present in 28–55% of people with psoriasis.<ref name=":3" /> People with psoriasis are often stigmatized due to visible disfigurement of the skin. [[Social stigma]]tization is a risk factor for depression; however, other immune system factors may also be related to the observed increased incidence of depression in people with psoriasis.<ref name=":3" /> There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases, including psoriasis.<ref name=":3">{{cite journal | vauthors = Hölsken S, Krefting F, Schedlowski M, Sondermann W | title = Common Fundamentals of Psoriasis and Depression | journal = Acta Dermato-Venereologica | volume = 101 | issue = 11 | pages = adv00609 | date = November 2021 | pmid = 34806760 | pmc = 9455336 | doi = 10.2340/actadv.v101.565 }}</ref>

=== Type 2 diabetes ===
People with psoriasis are at increased risk of developing [[type 2 diabetes]] (~1.5 odds ratio).<ref name=":4" /> A [[genome]]-wide genetic study found that psoriasis and type 2 diabetes share four loci, namely, ACTR2, ERLIN1, TRMT112, and BECN1, which are connected via the inflammatory NF-κB pathway.<ref name=":4">{{cite journal | vauthors = Patrick MT, Stuart PE, Zhang H, Zhao Q, Yin X, He K, Zhou XJ, Mehta NN, Voorhees JJ, Boehnke M, Gudjonsson JE, Nair RP, Handelman SK, Elder JT, Liu DJ, Tsoi LC | title = Causal Relationship and Shared Genetic Loci between Psoriasis and Type 2 Diabetes through Trans-Disease Meta-Analysis | journal = The Journal of Investigative Dermatology | volume = 141 | issue = 6 | pages = 1493–1502 | date = June 2021 | pmid = 33385400 | pmc = 8154633 | doi = 10.1016/j.jid.2020.11.025 }}</ref>

==Management==
[[Image:Psoriasis treatment ladder.svg|thumb|upright=1.3|Schematic of psoriasis treatment ladder]]
While no cure is available for psoriasis,<ref name=Weller2008 /> many treatment options exist. [[Topical medication|Topical agents]] are typically used for mild disease, [[Light therapy|phototherapy]] for moderate disease, and systemic agents for severe disease.<ref name=Lancet07>{{cite journal | vauthors = Menter A, Griffiths CE | title = Current and future management of psoriasis | journal = Lancet | volume = 370 | issue = 9583 | pages = 272–284 | date = July 2007 | pmid = 17658398 | doi = 10.1016/S0140-6736(07)61129-5 | s2cid = 7907468 }}</ref> There is no evidence to support the effectiveness of conventional topical and systemic drugs, biological therapy, or phototherapy for acute guttate psoriasis or an acute guttate flare of chronic psoriasis.<ref>{{cite journal | vauthors = Maruani A, Samimi M, Stembridge N, Abdel Hay R, Tavernier E, Hughes C, Le Cleach L | title = Nonantistreptococcal interventions for acute guttate psoriasis or an acute guttate flare of chronic psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | article-number = CD011541 | date = April 2019 | issue = 4 | pmid = 30958563 | pmc = 6452774 | doi = 10.1002/14651858.CD011541.pub2 | collaboration = Cochrane Skin Group }}</ref>

===Topical agents===
Topical [[corticosteroid]] preparations are the most effective agents when used continuously for eight weeks; [[retinoid]]s and [[coal tar]] were found to be of limited benefit and may be no better than [[placebo]].<ref name="Samarasekera2013">{{cite journal | vauthors = Samarasekera EJ, Sawyer L, Wonderling D, Tucker R, Smith CH | title = Topical therapies for the treatment of plaque psoriasis: systematic review and network meta-analyses | journal = The British Journal of Dermatology | volume = 168 | issue = 5 | pages = 954–967 | date = May 2013 | pmid = 23413913 | doi = 10.1111/bjd.12276 | s2cid = 21979785 }}</ref> Very potent topical corticosteroids may be helpful in some cases; however, it is suggested to only use them for four weeks at a time and only if other less potent topical treatment options are not working.<ref>{{cite journal | vauthors = Kleyn EC, Morsman E, Griffin L, Wu JJ, Cm van de Kerkhof P, Gulliver W, van der Walt JM, Iversen L | title = Review of international psoriasis guidelines for the treatment of psoriasis: recommendations for topical corticosteroid treatments | journal = The Journal of Dermatological Treatment | volume = 30 | issue = 4 | pages = 311–319 | date = June 2019 | pmid = 31138038 | doi = 10.1080/09546634.2019.1620502 | s2cid = 169036303 | doi-access = free }}</ref>

[[Vitamin D analogue]]s (such as [[paricalcitol]], [[calcipotriol]], [[tacalcitol]], and [[calcitriol]]) are superior to placebo. Combination therapy with vitamin D and a corticosteroid is superior to either treatment alone and [[vitamin D]] is superior to coal tar for chronic plaque psoriasis.<ref name="Mason2013">{{cite journal | vauthors = Mason AR, Mason J, Cork M, Dooley G, Hancock H | title = Topical treatments for chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 3 | article-number = CD005028 | date = March 2013 | volume = 2015 | pmid = 23543539 | doi = 10.1002/14651858.CD005028.pub3 | pmc = 11227123 | url = http://dro.dur.ac.uk/20582/1/20582.pdf | id = CD005028 | access-date = 6 November 2019 | archive-date = 28 April 2021 | archive-url = https://web.archive.org/web/20210428101001/https://dro.dur.ac.uk/20582/1/20582.pdf | url-status = live }}</ref>

For psoriasis of the scalp, a 2016 review found dual therapy (vitamin D analogs and topical corticosteroids) or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogs alone.<ref name=Schlager2016>{{cite journal | vauthors = Schlager JG, Rosumeck S, Werner RN, Jacobs A, Schmitt J, Schlager C, Nast A | title = Topical treatments for scalp psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2016 | issue = 2 | article-number = CD009687 | date = February 2016 | pmid = 26915340 | doi = 10.1002/14651858.CD009687.pub2 | pmc = 8697570 | id = CD009687 }}</ref> Due to their similar safety profiles and minimal benefit of dual therapy over monotherapy, corticosteroid monotherapy appears to be an acceptable treatment for short-term treatment.<ref name=Schlager2016 />

[[Moisturizer]]s and emollients such as [[mineral oil]], [[petroleum jelly]], and [[decubal]] (an oil-in-water emollient) were found to increase the clearance of psoriatic plaques. Some emollients are even more effective at clearing psoriatic plaques when combined with [[Light therapy|phototherapy]].<ref name="Asztalos2013">{{cite journal | vauthors = Asztalos ML, Heller MM, Lee ES, Koo J | title = The impact of emollients on phototherapy: a review | journal = Journal of the American Academy of Dermatology | volume = 68 | issue = 5 | pages = 817–24 | date = May 2013 | pmid = 23399460 | doi = 10.1016/j.jaad.2012.05.034 | url = https://zenodo.org/record/897997 | access-date = 30 June 2019 | archive-date = 29 August 2021 | archive-url = https://web.archive.org/web/20210829015357/https://zenodo.org/record/897997/preview/article.pdf | url-status = live }}</ref> Certain emollients, though, have no impact on psoriasis plaque clearance or may even decrease the clearance achieved with phototherapy, e.g., the emollient [[salicylic acid]] is structurally similar to [[para-aminobenzoic acid]], commonly found in [[sunscreen]], and is known to interfere with phototherapy in psoriasis. [[Coconut oil]], when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy.<ref name="Asztalos2013"/> Medicated creams and ointments applied directly to psoriatic plaques can help reduce inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques. Ointment and creams containing coal tar, [[dithranol]], corticosteroids (i.e. [[desoximetasone]]), [[fluocinonide]], vitamin D<sub>3</sub> analogues (for example, calcipotriol), and [[retinoid]]s are routinely used. (The use of the [[finger tip unit]] may help guide how much topical treatment to use.)<ref name="Clarke2011"/><ref>{{cite journal | vauthors = Menter A, Korman NJ, Elmets CA, Feldman SR, Gelfand JM, Gordon KB, Gottlieb A, Koo JY, Lebwohl M, Lim HW, Van Voorhees AS, Beutner KR, Bhushan R | title = Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies | journal = Journal of the American Academy of Dermatology | volume = 60 | issue = 4 | pages = 643–59 | date = April 2009 | pmid = 19217694 | doi = 10.1016/j.jaad.2008.12.032 }}</ref>

Vitamin D analogs may be useful with [[steroid]]s; steroids alone have a higher rate of side effects.<ref name="Mason2013" /> Vitamin D analogs may allow lower doses of steroids to be used.<ref>{{cite journal | vauthors = Soleymani T, Hung T, Soung J | title = The role of vitamin D in psoriasis: a review | journal = International Journal of Dermatology | volume = 54 | issue = 4 | pages = 383–92 | date = April 2015 | pmid = 25601579 | doi = 10.1111/ijd.12790 | s2cid = 1688553 }}</ref>

Another topical therapy used to treat psoriasis is a form of [[balneotherapy]], which involves daily baths in [[Saline water|saltwater]], such as the [[Dead Sea]], combined with sun exposure. This is usually done for four weeks, in which exposure time is gradually increased. The primary benefit is attributed to sun exposure and specifically [[UVB]] light. This is cost-effective, and it has been propagated as an effective way to treat psoriasis without medication.<ref name="Halverstam2008">{{cite journal | vauthors = Halverstam CP, Lebwohl M | title = Nonstandard and off-label therapies for psoriasis | journal = Clinics in Dermatology | volume = 26 | issue = 5 | pages = 546–53 | date = September–October 2008 | pmid = 18755374 | doi = 10.1016/j.clindermatol.2007.10.023 }}</ref> Decreases of PASI scores greater than 75% and [[Remission (medicine)|remission]] for several months have commonly been observed.<ref name="Halverstam2008"/> Side effects may be mild, such as itchiness, [[folliculitis]], [[sunburn]], [[poikiloderma]], and a theoretical risk of nonmelanoma cancer or melanoma has been suggested.<ref name="Halverstam2008"/> Some studies indicate no increased risk of melanoma in the long term.<ref name="Katz2012"/> Data are inconclusive concerning nonmelanoma skin cancer risk, but support the idea that the therapy is associated with an increased risk of benign forms of sun-induced skin damage such as, but not limited to, [[actinic elastosis]] or [[solar lentigines|liver spots]].<ref name="Katz2012">{{cite journal | vauthors = Katz U, Shoenfeld Y, Zakin V, Sherer Y, Sukenik S | title = Scientific evidence of the therapeutic effects of dead sea treatments: a systematic review | journal = Seminars in Arthritis and Rheumatism | volume = 42 | issue = 2 | pages = 186–200 | date = October 2012 | pmid = 22503590 | doi = 10.1016/j.semarthrit.2012.02.006 }}</ref> Dead Sea balneotherapy is also effective for psoriatic arthritis.<ref name="Katz2012"/> Tentative evidence indicates that balneophototherapy, a combination of [[balneotherapy|salt bath]]es and exposure to [[ultraviolet]] B-light (UVB), in chronic plaque psoriasis is better than UVB alone.<ref>{{cite journal | vauthors = Peinemann F, Harari M, Peternel S, Chan T, Chan D, Labeit AM, Gambichler T | title = Indoor salt water baths followed by artificial ultraviolet B light for chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2020 | issue = 5 | article-number = CD011941 | date = May 2020 | pmid = 32368795 | doi = 10.1002/14651858.CD011941.pub2| pmc = 7199317 }}</ref> [[Glycerin]] is also an effective treatment for Psoriasis.<ref>Medical College of Georgia at Augusta University. "Glycerin is safe, effective in psoriasis model." ScienceDaily. [www.sciencedaily.com/releases/2021/10/211004104229.htm] (accessed 9 July 2023).</ref>

===UV phototherapy===
[[Phototherapy]] in the form of [[sunlight]] has long been used for psoriasis.<ref name=Lancet07/> UVB [[wavelength]]s of 311–313&nbsp;[[nanometer]]s are most common. [[UV-B lamps]] have been developed for this treatment.<ref name=Lancet07/> The exposure time should be controlled to avoid overexposure and burning of the skin. The UVB lamps should have a timer that turns off the lamp when the time ends. The dose is increased in every treatment to let the skin get used to the light.<ref name=Lancet07/> Increased rates of cancer from treatment appear to be small.<ref name=Lancet07/> [[Narrowband UVB therapy]] has been demonstrated to have similar efficacy to [[psoralen and ultraviolet A phototherapy]] (PUVA).<ref name="Dogra2010"/> A 2013 meta-analysis found no difference in efficacy between NB-UVB and PUVA in the treatment of psoriasis, but NB-UVB is usually more convenient.<ref>{{cite journal | vauthors = Chen X, Yang M, Cheng Y, Liu GJ, Zhang M | title = Narrow-band ultraviolet B phototherapy versus broad-band ultraviolet B or psoralen-ultraviolet A photochemotherapy for psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 10 | article-number = CD009481 | date = October 2013 | volume = 2016 | pmid = 24151011 | doi = 10.1002/14651858.CD009481.pub2 | pmc = 11076274 }}</ref>

<!-- Tanning bed benefits and limited effectiveness with UVA -->
One of the problems with clinical phototherapy is the difficulty many people have gaining access to a facility. [[Indoor tanning]] resources are almost ubiquitous today and could be considered as a means for people to get UV exposure when dermatologist-provided phototherapy is not available. Indoor tanning is already used by many people as a treatment for psoriasis; one indoor facility reported that 50% of its clients were using the center for psoriasis treatment, and another reported 36% were doing the same thing. However, a concern with the use of commercial tanning is that tanning beds that primarily emit UVA might not effectively treat psoriasis. One study found that plaque psoriasis is responsive to [[erythema|erythemogenic]] doses of either UVA or UVB, as exposure to either can cause dissipation of psoriatic plaques. It does require more energy to reach erythemogenic dosing with UVA.<ref name="radack">{{cite journal | vauthors = Radack KP, Farhangian ME, Anderson KL, Feldman SR | title = A review of the use of tanning beds as a dermatological treatment | journal = Dermatology and Therapy | volume = 5 | issue = 1 | pages = 37–51 | date = March 2015 | pmid = 25735439 | pmc = 4374067 | doi = 10.1007/s13555-015-0071-8 }}</ref>

<!-- Risks of UV light therapy -->
UV light therapies all have risks; tanning beds are no exception, being listed by the [[World Health Organization]] as [[carcinogen]]s.<ref>{{cite book | vauthors=((World Health Organization)) | title=Artificial tanning devices: public health interventions to manage sunbeds | publisher=[[World Health Organization]] (WHO) | date=15 June 2017 | hdl=10665/255695 | isbn=978-92-4-151259-6 }}</ref> Exposure to UV light is known to increase the risks of melanoma and squamous cell and basal cell carcinomas; younger people with psoriasis, particularly those under age 35, are at increased risk from melanoma from UV light treatment. A review of studies recommends that people who are susceptible to skin cancers exercise caution when using UV light therapy as a treatment.<ref name="radack" />

A major mechanism of NB-UVB is the induction of [[DNA]] damage in the form of [[pyrimidine dimer]]s. This type of phototherapy is useful in the treatment of psoriasis because the formation of these dimers interferes with the [[cell cycle]] and stops it. The interruption of the cell cycle induced by NB-UVB opposes the characteristic rapid division of skin cells seen in psoriasis.<ref name="Dogra2010">{{cite journal | vauthors = Dogra S, De D | title = Narrowband ultraviolet B in the treatment of psoriasis: the journey so far! | journal = Indian Journal of Dermatology, Venereology and Leprology | volume = 76 | issue = 6 | pages = 652–61 | date = November–December 2010 | pmid = 21079308 | doi = 10.4103/0378-6323.72461 | doi-access = free | title-link = doi }}</ref> The activity of many types of immune cells found in the skin is also effectively suppressed by NB-UVB phototherapy treatments.<ref>{{cite journal | vauthors = Rácz E, Prens EP, Kurek D, Kant M, de Ridder D, Mourits S, Baerveldt EM, Ozgur Z, van IJcken WF, Laman JD, Staal FJ, van der Fits L | title = Effective treatment of psoriasis with narrow-band UVB phototherapy is linked to suppression of the IFN and Th17 pathways | journal = The Journal of Investigative Dermatology | volume = 131 | issue = 7 | pages = 1547–1558 | date = July 2011 | pmid = 21412260 | doi = 10.1038/jid.2011.53 | doi-access = free | title-link = doi | oclc = 6757253389 }}</ref> The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NB-UVB phototherapy are itching and [[blister]]ing of the treated skin, irritation of the eyes in the form of [[conjunctivitis|conjunctival inflammation]] or [[keratitis|inflammation of the cornea]], or [[Herpes labialis|cold sores]] due to reactivation of the [[herpes simplex virus]] in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments.<ref name="Dogra2010"/>

PUVA combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. The [[mechanism of action]] of PUVA is unknown but probably involves activation of psoralen by UVA light, which inhibits the abnormally rapid production of cells in psoriatic skin. There are multiple mechanisms of action associated with PUVA, including effects on the skin's immune system. PUVA is associated with [[nausea]], [[headache]], [[Fatigue (physical)|fatigue]], burning, and itching. Long-term treatment is associated with [[squamous cell carcinoma]] (but not with [[melanoma]]).<ref name="Richard2013"/><ref name="Lapolla2011">{{cite journal | vauthors = Lapolla W, Yentzer BA, Bagel J, Halvorson CR, Feldman SR | title = A review of phototherapy protocols for psoriasis treatment | journal = Journal of the American Academy of Dermatology | volume = 64 | issue = 5 | pages = 936–49 | date = May 2011 | pmid = 21429620 | doi = 10.1016/j.jaad.2009.12.054 }}</ref> A combination therapy for moderate to severe psoriasis using PUVA plus [[acitretin]] resulted in benefit, but acitretin use has been associated with [[birth defect]]s and [[hepatotoxicity|liver damage]].<ref name="Dunn2011">{{cite journal | vauthors = Dunn LK, Gaar LR, Yentzer BA, O'Neill JL, Feldman SR | title = Acitretin in dermatology: a review | journal = Journal of Drugs in Dermatology | volume = 10 | issue = 7 | pages = 772–82 | date = July 2011 | pmid = 21720660 }}</ref>

===Systemic agents===
[[Image:Psoriasis infliximab ar1182-2.gif|thumb|Pictures of a person with psoriasis (and [[psoriatic arthritis]]) at baseline and eight weeks after initiation of [[infliximab]] therapy]]
Psoriasis resistant to [[topical|topical treatment]] and [[light therapy|phototherapy]] may be treated with systemic therapies including [[medication]]s by mouth or [[Injection (medicine)|injectable treatments]].<ref name="Dogra2013">{{cite journal | vauthors = Dogra S, Mahajan R | title = Systemic methotrexate therapy for psoriasis: past, present and future | journal = Clinical and Experimental Dermatology | volume = 38 | issue = 6 | pages = 573–88 | date = August 2013 | pmid = 23837932 | doi = 10.1111/ced.12062 | s2cid = 11207097 }}</ref> People undergoing systemic treatment must have regular [[Blood test|blood]] and [[liver function tests]] to check for medication toxicities.<ref name="Dogra2013"/> [[Pregnancy]] must be avoided for most of these treatments.{{medical citation needed|date=July 2023}} The majority of people experience a [[Recrudescence|recurrence]] of psoriasis after systemic treatment is discontinued.{{medical citation needed|date=July 2023}}

<!-- First line treatments -->
Non-biologic systemic treatments frequently used for psoriasis include [[methotrexate]], [[ciclosporin]], [[hydroxycarbamide]], [[fumarate]]s such as [[dimethyl fumarate]], and [[retinoids]].<ref name="Rustin2012">{{cite journal | vauthors = Rustin MH | title = Long-term safety of biologics in the treatment of moderate-to-severe plaque psoriasis: review of current data | journal = The British Journal of Dermatology | volume = 167 | issue = Suppl 3 | pages = 3–11 | date = November 2012 | pmid = 23082810 | doi = 10.1111/j.1365-2133.2012.11208.x | s2cid = 22462278 }}</ref> Methotrexate and ciclosporin are [[immunosuppressive drug|medications that suppress the immune system]]; retinoids are synthetic forms of [[vitamin A]]. These agents are also regarded as first-line treatments for [[psoriatic erythroderma]].<ref name="Zattra2012"/> Oral [[corticosteroid]]s should not be used as they can severely flare psoriasis upon their discontinuation.<ref>{{cite web|url=https://www.aad.org/education/basic-derm-curriculum/suggested-order-of-modules/psoriasis|title=Learning module: Psoriasis {{!}} American Academy of Dermatology|website=www.aad.org|access-date=26 March 2017|url-status=live|archive-url=https://web.archive.org/web/20170327075847/https://www.aad.org/education/basic-derm-curriculum/suggested-order-of-modules/psoriasis|archive-date=27 March 2017}}</ref>

<!-- Biologics -->
[[biologic medical product|Biologics]] are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalized immunosuppressive medical therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis.<ref name="Rustin2012"/> These medications are generally well-tolerated, and limited long-term outcome data have demonstrated biologics to be safe for long-term use in moderate to severe plaque psoriasis.<ref name="Rustin2012"/><ref name="Griffiths2012"/> However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.<ref name="Rustin2012"/>

Guidelines regard biologics as a third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.<ref name="Griffiths2012">{{cite journal | vauthors = Griffiths CE | title = Biologics for psoriasis: current evidence and future use | journal = The British Journal of Dermatology | volume = 167 | issue = Suppl 3 | pages = 1–2 | date = November 2012 | pmid = 23082809 | doi = 10.1111/j.1365-2133.2012.11207.x | s2cid = 42598571 }}</ref> The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; [[TNF inhibitor|anti-TNF]] therapies such as infliximab are not recommended for use in chronic carriers of the [[hepatitis B virus]] or individuals infected with [[HIV]].<ref name="Rustin2012"/>

<!-- Monoclonal antibiodies -->
Several monoclonal [[Antibody|antibodies]] target cytokines, the molecules that cells use to send inflammatory signals to each other. [[tumor necrosis factor α|TNF-α]] is one of the main executor inflammatory cytokines. Four [[monoclonal antibody|monoclonal antibodies]] (MAbs) ([[infliximab]], [[adalimumab]], [[golimumab]], and [[certolizumab pegol]]) and one recombinant TNF-α [[decoy receptor]], [[etanercept]], have been developed to inhibit TNF-α signaling. Additional monoclonal antibodies, such as [[ixekizumab]],<ref>{{cite journal | vauthors = Farahnik B, Beroukhim K, Zhu TH, Abrouk M, Nakamura M, Singh R, Lee K, Bhutani T, Koo J | title = Ixekizumab for the Treatment of Psoriasis: A Review of Phase III Trials | journal = Dermatology and Therapy | volume = 6 | issue = 1 | pages = 25–37 | date = March 2016 | pmid = 26910853 | pmc = 4799032 | doi = 10.1007/s13555-016-0102-0 }}</ref> have been developed against pro-inflammatory cytokines<ref>{{cite journal | vauthors = Hueber W, Patel DD, Dryja T, Wright AM, Koroleva I, Bruin G, Antoni C, Draelos Z, Gold MH, Durez P, Tak PP, Gomez-Reino JJ, Foster CS, Kim RY, Samson CM, Falk NS, Chu DS, Callanan D, Nguyen QD, Rose K, Haider A, Di Padova F | title = Effects of AIN457, a fully human antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis | journal = Science Translational Medicine | volume = 2 | issue = 52 | pages = 52ra72 | date = October 2010 | pmid = 20926833 | doi = 10.1126/scitranslmed.3001107 | doi-access =  | title-link = doi | s2cid = 10132276 }}</ref> and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies.<ref name=Nestle/> IL-12 and IL-23 share a common domain, [[interleukin-12 subunit beta|p40]], which is the target of the [[Food and Drug Administration|FDA-approved]] [[ustekinumab]].<ref name="Prieto2013">{{cite journal | vauthors = Prieto-Pérez R, Cabaleiro T, Daudén E, Ochoa D, Roman M, Abad-Santos F | title = Genetics of psoriasis and pharmacogenetics of biological drugs | journal = Autoimmune Diseases | volume = 2013 | article-number = 613086 | date = August 2013 | pmid = 24069534 | pmc = 3771250 | doi = 10.1155/2013/613086 | doi-access = free | title-link = doi }}</ref> In 2017 the [[US FDA]] approved [[guselkumab]] for plaque psoriasis.<ref name=FDA-n-2017>[https://www.fda.gov/drugs/developmentapprovalprocess/druginnovation/ucm537040.htm Novel Drug Approvals for 2017] {{webarchive|url=https://web.archive.org/web/20170629124028/https://www.fda.gov/Drugs/DevelopmentApprovalProcess/DrugInnovation/ucm537040.htm |date=29 June 2017 }}</ref> There have been few studies of the efficacy of anti-TNF medications for psoriasis in children. One randomized controlled study suggested that 12 weeks of etanercept treatment reduced the extent of psoriasis in children with no lasting adverse effects.<ref>{{cite journal | vauthors = Sanclemente G, Murphy R, Contreras J, García H, Bonfill Cosp X | title = Anti-TNF agents for paediatric psoriasis | journal = The Cochrane Database of Systematic Reviews | issue = 11 | article-number = CD010017 | date = November 2015 | volume = 2019 | pmid = 26598969 | pmc = 6493213 | doi = 10.1002/14651858.CD010017.pub2 }}</ref>

<!-- Others -->
Two medications that target T cells are [[efalizumab]] and [[alefacept]]. Efalizumab is a monoclonal antibody that specifically targets the [[CD11a]] subunit of [[LFA-1]].<ref name="Rustin2012"/> It also blocks the adhesion molecules on the [[endothelial]] cells that line blood vessels, which attract T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009, and from the U.S. market in June 2009, by the manufacturer due to the medication's association with cases of [[progressive multifocal leukoencephalopathy]].<ref name="Rustin2012"/> Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes [[natural killer cell]]s to kill T cells as a way of controlling inflammation.<ref name=Nestle/> [[Apremilast]] may also be used.<ref name="Palfreeman2013"/>

Individuals with psoriasis may develop [[neutralizing antibodies]] against monoclonal antibodies. Neutralization occurs when an antidrug antibody prevents a monoclonal antibody, such as infliximab, from binding [[antigen]] in a laboratory test. Specifically, neutralization occurs when the anti-drug antibody binds to infliximab's antigen-binding site instead of TNF-α. When infliximab no longer binds [[tumor necrosis factor alpha]], it no longer decreases inflammation, and psoriasis may worsen. Neutralizing antibodies have not been reported against [[etanercept]], a biologic medication that is a fusion protein composed of two TNF-α receptors. The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF-α receptor and the development of [[immune tolerance]].<ref>{{cite journal | vauthors = Harding FA, Stickler MM, Razo J, DuBridge RB | title = The immunogenicity of humanized and fully human antibodies: residual immunogenicity resides in the CDR regions | journal = mAbs | volume = 2 | issue = 3 | pages = 256–65 | date = 2010 | pmid = 20400861 | pmc = 2881252 | doi = 10.4161/mabs.2.3.11641 }}</ref>

There is strong evidence to indicate that infliximab, [[bimekizumab]], ixekizumab, and [[risankizumab]] are the most effective biologics for treating moderate to severe cases of psoriasis.<ref name=":5">{{cite journal | vauthors = Sbidian E, Chaimani A, Guelimi R, Garcia-Doval I, Hua C, Hughes C, Naldi L, Kinberger M, Afach S, Le Cleach L | title = Systemic pharmacological treatments for chronic plaque psoriasis: a network meta-analysis | journal = The Cochrane Database of Systematic Reviews | volume = 2023 | issue = 7 | article-number = CD011535 | date = July 2023 | pmid = 37436070 | pmc = 10337265 | doi = 10.1002/14651858.CD011535.pub6 }}</ref> There is also some evidence to support use of [[secukinumab]], [[brodalumab]], [[guselkumab]], certolizumab, and ustekinumab.<ref name="pmid26714681">{{cite journal | vauthors = Campa M, Mansouri B, Warren R, Menter A | title = A Review of Biologic Therapies Targeting IL-23 and IL-17 for Use in Moderate-to-Severe Plaque Psoriasis | journal = Dermatology and Therapy | volume = 6 | issue = 1 | pages = 1–12 | date = March 2016 | pmid = 26714681 | pmc = 4799039 | doi = 10.1007/s13555-015-0092-3 }}</ref><ref name=":5" /> In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNF alpha biologics were found to be more effective than traditional systemic treatments.<ref name=":5" /> The [[Immunology|immunologic]] pathways of psoriasis involve [[Th 9 cell|Th9]], [[Th17]], [[Th1 cell|Th1]] lymphocytes, and [[Interleukin 22|IL-22]]. The aforementioned biologic agents hinder different aspects of these pathways.{{citation needed|date=January 2020}}

Another set of treatments for moderate to severe psoriasis are [[fumaric acid esters]] (FAE), which may be similar in effectiveness to [[methotrexate]].<ref>{{cite journal | vauthors = Atwan A, Ingram JR, Abbott R, Kelson MJ, Pickles T, Bauer A, Piguet V | title = Oral fumaric acid esters for psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2015 | issue = 8 | article-number = CD010497 | date = August 2015 | pmid = 26258748 | pmc = 6464505 | doi = 10.1002/14651858.CD010497.pub2 }}</ref>

[[Apremilast]] (Otezla, Celgene) is an oral small-molecule inhibitor of the enzyme [[phosphodiesterase 4]], which plays an important role in chronic inflammation associated with psoriasis.<ref>{{cite journal |last1=Papp |first1=K |last2=Reich |first2=K |last3=Leonardi |first3=CL |last4=Kircik |first4=L |last5=Chimenti |first5=S |last6=Langley |first6=RG |last7=Hu |first7=C |last8=Stevens |first8=RM |last9=Day |first9=RM |last10=Gordon |first10=KB |last11=Korman |first11=NJ |last12=Griffiths |first12=CE |title=Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor, in patients with moderate to severe plaque psoriasis: Results of a phase III, randomized, controlled trial (Efficacy and Safety Trial Evaluating the Effects of Apremilast in Psoriasis [ESTEEM] 1). |journal=Journal of the American Academy of Dermatology |date=July 2015 |volume=73 |issue=1 |pages=37–49 |doi=10.1016/j.jaad.2015.03.049 |pmid=26089047 |doi-access=free }}</ref>

It has been theorized that [[Streptococcus|antistreptococcal]] medications may improve guttate and chronic plaque psoriasis; however, limited studies do not show that [[antibiotic]]s are effective.<ref>{{cite journal | vauthors = Dupire G, Droitcourt C, Hughes C, Le Cleach L | title = Antistreptococcal interventions for guttate and chronic plaque psoriasis | journal = The Cochrane Database of Systematic Reviews | volume = 2019 | article-number = CD011571 | date = March 2019 | issue = 3 | pmid = 30835819 | pmc = 6400423 | doi = 10.1002/14651858.cd011571.pub2 }}</ref>

===Surgery===
Limited evidence suggests [[tonsillectomy|removal of the tonsils]] may benefit people with chronic plaque psoriasis, guttate psoriasis, and [[Pustulosis palmaris et plantaris|palmoplantar pustulosis]].<ref name="Wu2014">{{cite journal | vauthors = Wu W, Debbaneh M, Moslehi H, Koo J, Liao W | title = Tonsillectomy as a treatment for psoriasis: a review | journal = The Journal of Dermatological Treatment | volume = 25 | issue = 6 | pages = 482–6 | date = December 2014 | pmid = 24283892 | pmc = 4620715 | doi = 10.3109/09546634.2013.848258 }}</ref><ref>{{cite journal | vauthors = Sigurdardottir SL, Thorleifsdottir RH, Valdimarsson H, Johnston A | title = The role of the palatine tonsils in the pathogenesis and treatment of psoriasis | journal = The British Journal of Dermatology | volume = 168 | issue = 2 | pages = 237–42 | date = February 2013 | pmid = 22901242 | doi = 10.1111/j.1365-2133.2012.11215.x | url = https://deepblue.lib.umich.edu/bitstream/2027.42/96289/1/bjd11215.pdf | hdl = 2027.42/96289 | s2cid = 11572308 | hdl-access = free | access-date = 3 September 2019 | archive-date = 29 August 2021 | archive-url = https://web.archive.org/web/20210829015354/https://deepblue.lib.umich.edu/bitstream/handle/2027.42/96289/bjd11215.pdf;jsessionid=582C9DAE0038517119D12BA23A3404DF?sequence=1 | url-status = live }}</ref>

===Diet===
Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented with [[fish oil]] rich in [[eicosapentaenoic acid]] (EPA) and [[docosahexaenoic acid]] (DHA).<ref name="Kaimal2010">{{cite journal | vauthors = Kaimal S, Thappa DM | title = Diet in dermatology: revisited | journal = Indian Journal of Dermatology, Venereology and Leprology | volume = 76 | issue = 2 | pages = 103–15 | year = 2010 | pmid = 20228538 | doi = 10.4103/0378-6323.60540 | doi-access = free | title-link = doi }}</ref> A low-calorie diet appears to reduce the severity of psoriasis.<ref name=Shu2019/> Diet recommendations include consumption of cold water fish (preferably wild fish, not [[Fish farming|farmed]]) such as [[salmon]], [[herring]], and [[mackerel]]; extra virgin olive oil; legumes; vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products (due to their saturated fat). The effect of caffeine consumption (including from coffee, [[black tea]], mate, and dark chocolate) remains to be determined.<ref name=BarreaNappi2016>{{cite journal | vauthors = Barrea L, Nappi F, Di Somma C, Savanelli MC, Falco A, Balato A, Balato N, Savastano S | title = Environmental Risk Factors in Psoriasis: The Point of View of the Nutritionist | journal = International Journal of Environmental Research and Public Health | volume = 13 | issue = 5 | page = 743 | date = July 2016 | pmid = 27455297 | pmc = 4962284 | doi = 10.3390/ijerph13070743 | doi-access = free | title-link = doi }}</ref>

Many patients report improvements after consuming less tobacco, caffeine, sugar, [[nightshades]] (tomatoes, eggplant, peppers, [[paprika]] and white potatoes) and taking [[probiotic]]s and oral Vitamin D.<ref name=AfifiDanesh2017>{{cite journal | vauthors = Afifi L, Danesh MJ, Lee KM, Beroukhim K, Farahnik B, Ahn RS, Yan D, Singh RK, Nakamura M, Koo J, Liao W | title = Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey | journal = Dermatology and Therapy | volume = 7 | issue = 2 | pages = 227–242 | date = 19 May 2017 | pmid = 28526915 | pmc = 5453925 | doi = 10.1007/s13555-017-0183-4 | doi-access = free | title-link = doi }}</ref>

There is a higher rate of [[celiac disease]] among people with psoriasis.<ref name=BarreaNappi2016 /><ref name=NiChiu2014>{{cite journal | vauthors = Ni C, Chiu MW | title = Psoriasis and comorbidities: links and risks | journal = Clinical, Cosmetic and Investigational Dermatology | volume = 7 | pages = 119–32 | year = 2014 | pmid = 24790463 | pmc = 4000177 | doi = 10.2147/CCID.S44843 | type = Review | doi-access = free }}</ref> When adopting a [[gluten-free diet]], disease severity generally decreases in people with celiac disease and those with [[anti-gliadin antibodies]].<ref name="Kaimal2010"/><ref name=LefflerGreen2015>{{cite journal | vauthors = Leffler DA, Green PH, Fasano A | title = Extraintestinal manifestations of coeliac disease | journal = Nature Reviews. Gastroenterology & Hepatology | volume = 12 | issue = 10 | pages = 561–71 | date = October 2015 | pmid = 26260366 | doi = 10.1038/nrgastro.2015.131 | s2cid = 15561525 | type = Review }}</ref><ref name=BhatiaMillsop2014>{{cite journal | vauthors = Bhatia BK, Millsop JW, Debbaneh M, Koo J, Linos E, Liao W | title = Diet and psoriasis, part II: celiac disease and role of a gluten-free diet | journal = Journal of the American Academy of Dermatology | volume = 71 | issue = 2 | pages = 350–8 | date = August 2014 | pmid = 24780176 | pmc = 4104239 | doi = 10.1016/j.jaad.2014.03.017 }}</ref>

==Prognosis==
Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies.<ref name="Samarasekera2013"/> Depending on the severity and location of outbreaks, people may experience significant physical discomfort and some disability, affecting the person's [[Quality of life (healthcare)|quality of life]].<ref name="Prieto2013" /> Itching and pain can interfere with basic functions, such as self-care and sleep.<ref name="Parrish2012" /> Participation in sporting activities, certain occupations, and caring for family members can become difficult activities for those with plaques located on their hands and feet.<ref name="Parrish2012" /> Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for [[dandruff]].<ref name="Dessinioti2013">{{cite journal | vauthors = Dessinioti C, Katsambas A | title = Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies | journal = Clinics in Dermatology | volume = 31 | issue = 4 | pages = 343–351 | year = 2013 | pmid = 23806151 | doi = 10.1016/j.clindermatol.2013.01.001 }}</ref>
[[ File:Women_with_vitiligo_Psoriasis2.jpg|thumb|100px|[[Women in the Philippines|Filipina]] with psoriasis]]
Individuals with psoriasis may feel self-conscious about their appearance and have a poor self-image that stems from fear of public rejection and [[Psychosexual disorder|psychosexual concerns]]. Psoriasis has been associated with low self-esteem, and [[Depression (mood)|depression]] is more common among those with the condition.<ref name=Menter2008 /> People with psoriasis often feel prejudiced against due to the commonly held incorrect belief that psoriasis is contagious.<ref name="Parrish2012">{{cite journal | vauthors = Parrish L | title = Psoriasis: symptoms, treatments and its impact on quality of life | journal = British Journal of Community Nursing | volume = 17 | issue = 11 | pages = 524–528 | date = November 2012 | pmid = 23124421 | doi = 10.12968/bjcn.2012.17.11.524 }}</ref> Psychological distress can lead to significant [[clinical depression|depression]] and [[social isolation]]; a high rate of [[Suicidal ideation|thoughts about suicide]] has been associated with psoriasis.<ref name="Gelmetti2009"/> Many tools exist to measure the quality of life of people with psoriasis and other dermatological disorders. Clinical research has indicated that individuals often experience a diminished quality of life.<ref name=Bhosle>{{cite journal | vauthors = Bhosle MJ, Kulkarni A, Feldman SR, Balkrishnan R | title = Quality of life in patients with psoriasis | journal = Health and Quality of Life Outcomes | volume = 4 | article-number = 35 | date = June 2006 | pmid = 16756666 | pmc = 1501000 | doi = 10.1186/1477-7525-4-35 | doi-access = free }}</ref> Children with psoriasis may encounter [[bullying]].<ref>{{cite journal | vauthors = Magin P | title = Appearance-related bullying and skin disorders | journal = Clinics in Dermatology | volume = 31 | issue = 1 | pages = 66–71 | date = Jan–Feb 2013 | pmid = 23245976 | doi = 10.1016/j.clindermatol.2011.11.009 }}</ref>

Several conditions are associated with psoriasis, including [[obesity]], [[Cardiovascular disease|cardiovascular]], and [[Metabolic disorder|metabolic disturbances]]. These occur more frequently in older people. Nearly half of individuals with psoriasis over the age of 65 have at least three [[Comorbidity|comorbidities]] (concurrent conditions), and two-thirds have at least two comorbidities.<ref name=Habif2010>{{cite book|vauthors=Habif TP|title=Clinical dermatology a color guide to diagnosis and therapy|year=2010|publisher=Mosby Elsevier|location=Edinburgh|isbn=978-0-323-08037-8|chapter-url=https://books.google.com/books?id=kDWlWR5UbqQC|edition=5th|chapter=8|access-date=8 May 2020|archive-date=14 January 2023|archive-url=https://web.archive.org/web/20230114005622/https://books.google.com/books?id=kDWlWR5UbqQC|url-status=live}}</ref>

===Cardiovascular disease===
Psoriasis has been associated with [[obesity]]<ref name=Menter2008 /> and several other cardiovascular and metabolic disturbances. The [[Incidence (epidemiology)|number of new cases per year]] of diabetes is 27% higher in people affected by psoriasis than in those without the condition.<ref name=Sh2014>{{cite journal | vauthors = Shlyankevich J, Mehta NN, Krueger JG, Strober B, Gudjonsson JE, Qureshi AA, Tebbey PW, Kimball AB | title = Accumulating evidence for the association and shared pathogenic mechanisms between psoriasis and cardiovascular-related comorbidities | journal = The American Journal of Medicine | volume = 127 | issue = 12 | pages = 1148–53 | date = December 2014 | pmid = 25149424 | pmc = 4259841 | doi = 10.1016/j.amjmed.2014.08.008 }}</ref> Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis.<ref name=Sh2014/> Younger people with psoriasis may also be at increased risk for developing diabetes.<ref name=Habif2010 /> Individuals with psoriasis or psoriatic arthritis have a slightly higher risk of heart disease and [[Myocardial infarction|heart attacks]] when compared to the general population. Cardiovascular disease risk appeared to be correlated with the severity of psoriasis and its duration. There is no strong evidence to suggest that psoriasis is associated with an increased risk of death from cardiovascular events. [[Methotrexate]] may provide a degree of protection for the heart.<ref name="Richard2013">{{cite journal | vauthors = Richard MA, Barnetche T, Horreau C, Brenaut E, Pouplard C, Aractingi S, Aubin F, Cribier B, Joly P, Jullien D, Le Maître M, Misery L, Ortonne JP, Paul C | title = Psoriasis, cardiovascular events, cancer risk and alcohol use: evidence-based recommendations based on systematic review and expert opinion | journal = Journal of the European Academy of Dermatology and Venereology | volume = 27 | issue = Supplement 3 | pages = 2–11 | date = August 2013 | pmid = 23845148 | doi = 10.1111/jdv.12162 | s2cid = 2766931 | doi-access = free }}</ref><ref name=Habif2010 />

The odds of having [[hypertension]] are 1.58 times {{nowrap|( ''i.e.'' 58%)}} higher in people with psoriasis than those without the condition; these odds are even higher with severe cases of psoriasis. A similar association was noted in people who have psoriatic arthritis—the odds of having hypertension were found to be 2.07 times {{nowrap|( ''i.e.,'' 107%)}} greater when compared to the odds of the general population. The link between psoriasis and hypertension is not currently{{when|date=October 2019}} understood. Mechanisms hypothesized to be involved in this relationship include the following: dysregulation of the [[renin–angiotensin system]], elevated levels of [[endothelin 1]] in the blood, and increased [[oxidative stress]]. The number of new cases of the heart rhythm abnormality [[atrial fibrillation]] is 1.31 times {{nowrap|( ''i.e.'' 31%)}} higher in people with mild psoriasis and 1.63 times {{nowrap|( ''i.e.'' 63%)}} higher in people with severe psoriasis.<ref name="Tablazon2013"/> There may be a slightly increased risk of [[stroke]] associated with psoriasis, especially in severe cases.<ref name="Richard2013"/><ref>{{cite news|title=Psoriasis Linked to Stroke Risk|publisher=BBC|url=https://www.bbc.co.uk/news/health-14559523|date=August 2011|url-status=live|archive-url=https://web.archive.org/web/20110828171242/http://www.bbc.co.uk/news/health-14559523|archive-date=28 August 2011}}</ref> Treating [[hypercholesterolemia|high levels of cholesterol]] with [[statin]]s has been associated with decreased psoriasis severity, as measured by PASI score, and has also been associated with improvements in other cardiovascular disease risk factors such as markers of [[inflammation]].<ref name="Ghazizadeh2011">{{cite journal | vauthors = Ghazizadeh R, Tosa M, Ghazizadeh M | title = Clinical improvement in psoriasis with treatment of associated hyperlipidemia | journal = The American Journal of the Medical Sciences | volume = 341 | issue = 5 | pages = 394–8 | date = May 2011 | pmid = 21233693 | doi = 10.1097/MAJ.0b013e3181ff8eeb | s2cid = 12519829 }}</ref> These [[Cardioprotection|cardioprotective]] effects are attributed to ability of statins to improve blood [[lipid]] profile and because of their anti-inflammatory effects. Statin use in those with psoriasis and [[hyperlipidemia]] was associated with decreased levels of [[high-sensitivity C-reactive protein]] and [[TNFα]] as well as decreased activity of the immune protein [[Lymphocyte function-associated antigen 1|LFA-1]].<ref name="Ghazizadeh2011"/> Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for [[metabolic syndrome]].<ref name="Raychaudhuri2014">{{cite journal | vauthors = Raychaudhuri SK, Maverakis E, Raychaudhuri SP | title = Diagnosis and classification of psoriasis | journal = Autoimmunity Reviews | volume = 13 | issue = 4–5 | pages = 490–5 | date = January 2014 | pmid = 24434359 | doi = 10.1016/j.autrev.2014.01.008 }}</ref><ref name="Tablazon2013">{{cite journal | vauthors = Tablazon IL, Al-Dabagh A, Davis SA, Feldman SR | title = Risk of cardiovascular disorders in psoriasis patients: current and future | journal = American Journal of Clinical Dermatology | volume = 14 | issue = 1 | pages = 1–7 | date = February 2013 | pmid = 23329076 | doi = 10.1007/s40257-012-0005-5 | s2cid = 207482092 }}</ref>

===Other diseases===
The rates of [[Crohn's disease]] and [[ulcerative colitis]] are increased when compared with the general population by a factor of 3.8 and 7.5, respectively.<ref name=Menter2008 /> People with psoriasis also have a higher risk of [[celiac disease]].<ref name=BarreaNappi2016 /><ref name=BhatiaMillsop2014 /> Few studies have evaluated the association of [[multiple sclerosis]] with psoriasis, and the relationship has been questioned.<ref name=Menter2008 /> Psoriasis has been associated with a 16% increase in overall relative risk for non-skin cancer, thought to be attributed to systemic therapy, particularly methotrexate.<ref name="Richard2013"/> People treated with long-term systemic therapy for psoriasis have a 52% increased risk [[lung cancer|cancers of the lung and bronchus]], a 205% increase in the risk of developing [[esophageal cancer|cancers of the upper gastrointestinal tract]], a 31% increase in the risk of developing [[Urologic disease|cancers of the urinary tract]], a 90% increase in the risk of developing [[liver cancer]], and a 46% increase in the risk of developing [[pancreatic cancer]].<ref name="Richard2013"/> The risk for the development of non-melanoma skin cancers is also increased. Psoriasis increases the risk of developing [[Squamous cell skin cancer|squamous cell carcinoma of the skin]] by 431% and increases the risk of [[basal cell carcinoma]] by 100%.<ref name="Richard2013"/> There is no increased risk of [[melanoma]] associated with psoriasis.<ref name="Richard2013"/> People with psoriasis have a higher risk of developing cancer.<ref>{{cite journal | vauthors = Trafford AM, Parisi R, Kontopantelis E, Griffiths CE, Ashcroft DM | title = Association of Psoriasis With the Risk of Developing or Dying of Cancer: A Systematic Review and Meta-analysis | journal = JAMA Dermatology | date = October 2019 | volume = 155 | issue = 12 | pages = 1390–1403 | pmid = 31617868 | pmc = 6802036 | doi = 10.1001/jamadermatol.2019.3056 }}
*{{lay source |template = cite news|vauthors = Bakalar N |url= https://www.nytimes.com/2019/10/16/well/live/psoriasis-tied-to-increased-cancer-risk.html|title= Psoriasis Tied to Increased Cancer Risk|date = 16 October 2019 |website= The New York Times }}</ref>

==Epidemiology==
Psoriasis is estimated to affect 2–4% of the population of the Western world.<ref name="Parisi2013" /> The rate of psoriasis varies according to age, region, and ethnicity; a combination of environmental and genetic factors is thought to be responsible for these differences.<ref name=Parisi2013/> Psoriasis is about five times more common in people of European descent than in people of Asian descent,<ref>{{cite web |title=Psoriasis affects more than 8 million people in the U.S. |url=https://www.psoriasis.org/advance/why-psoriasis-less-common-asians |access-date=12 July 2021 |publisher=National Psoriasis Foundation |archive-date=24 February 2024 |archive-url=https://web.archive.org/web/20240224040820/https://www.psoriasis.org/about-psoriasis/ |url-status=live }}</ref> more common in countries farther from the [[equator]],<ref name="Guerra2013" /> relatively uncommon in African Americans, and extremely uncommon in Native Americans.<ref name="Weller2008" /> Psoriasis has been estimated to affect about 6.7{{Spaces}}million Americans.<ref name="NIH2015" />

Psoriasis can occur at any age, although it is more frequent in adults and commonly appears for the first time between the ages of 15 and 25 years.<ref name="NIH2015" /> Approximately one-third of people with psoriasis report being diagnosed before age 20.<ref>{{cite journal | vauthors = Benoit S, Hamm H | title = Childhood psoriasis | journal = Clinics in Dermatology | volume = 25 | issue = 6 | pages = 555–62 | year = 2007 | pmid = 18021892 | doi = 10.1016/j.clindermatol.2007.08.009 }}</ref> Psoriasis affects both [[sex]]es equally.<ref name="Kupetsky2013">{{cite journal | vauthors = Kupetsky EA, Keller M | title = Psoriasis vulgaris: an evidence-based guide for primary care | journal = Journal of the American Board of Family Medicine | volume = 26 | issue = 6 | pages = 787–801 | date = November–December 2013 | pmid = 24204077 | doi = 10.3122/jabfm.2013.06.130055 | doi-access = free | title-link = doi }}</ref>

People with [[inflammatory bowel disease]], such as Crohn's disease or ulcerative colitis, are at an increased risk of developing psoriasis.<ref name="Guerra2013" />

==History==
Scholars believe psoriasis to have been included among the various skin conditions called ''[[tzaraath]]'' (translated as [[leprosy]]) in the [[Hebrew Bible]].<ref>E. V. Hulse, "The Nature of Biblical 'Leprosy' and the Use of Alternative Medical Terms in Modern Translations of the Bible," ''Palestine Exploration Quarterly'' 107.2 (1975): 87-105.</ref> The person was deemed "impure" (see [[tumah and taharah]]) during their affected phase and is ultimately treated by the [[kohen]].<ref name="Gruber2004">{{cite journal | vauthors = Gruber F, Kastelan M, Brajac I | title = Psoriasis treatment--yesterday, today, and tomorrow | journal = Acta Dermatovenerologica Croatica | volume = 12 | issue = 1 | pages = 30–4 | year = 2004 | pmid = 15072746 }}</ref> However, it is more likely that this confusion arose from the use of the same Greek term for both conditions. The Greeks used the term {{Transliteration|grc|lepra}} ({{lang|grc|λέπρα}}) for scaly skin conditions. They used the term {{Transliteration|grc|psora}} ({{lang|grc|ψώρα}}) to describe itchy skin conditions.<ref name="Gruber2004"/> It became known as ''Willan's lepra'' in the late 18th century when English [[dermatologist]]s [[Robert Willan]] and Thomas Bateman differentiated it from other skin diseases. [[Leprosy]], they said, is distinguished by the regular, circular form of patches, while psoriasis is always irregular. Willan identified two categories: {{lang|la|leprosa graecorum}} and {{lang|la|psora leprosa}}.<ref>{{cite journal | vauthors = Meenan FO | title = A note on the history of psoriasis | journal = Irish Journal of Medical Science | volume = 30 | issue = 351 | pages = 141–2 | date = March 1955 | pmid = 14353580 | doi = 10.1007/bf02949688 | s2cid = 27467338 }}</ref>

Psoriasis is thought to have first been described in [[Ancient Rome]] by [[Cornelius Celsus]].<ref name="Benedek2013"/> The British dermatologist [[Thomas Bateman (physician)|Thomas Bateman]] described a possible link between psoriasis and arthritic symptoms in 1813.<ref name="Benedek2013">{{cite journal | vauthors = Benedek TG | title = Psoriasis and psoriatic arthropathy, historical aspects: part I | journal = Journal of Clinical Rheumatology | volume = 19 | issue = 4 | pages = 193–8 | date = June 2013 | pmid = 23669809 | doi = 10.1097/RHU.0b013e318293eaeb | s2cid = 5813486 }}</ref> Admiral [[William Halsey Jr.|William Halsey]] missed out on the [[Battle of Midway]] because he contracted psoriasis while out at sea in the early months of American participation of [[World War II]]. Admiral [[Chester W. Nimitz|Chester Nimitz]] medically ordered Halsey to recover at a hospital in [[Hawaii]].

The history of psoriasis is littered with treatments of dubious effectiveness and high toxicity. In the 18th and 19th centuries, [[Fowler's solution]], which contains a [[poisonous]] and [[carcinogenic]] [[arsenic]] compound, was used by dermatologists as a treatment for psoriasis.<ref name="Gruber2004"/> [[Mercury (element)|Mercury]] was also used for psoriasis treatment during this time.<ref name="Gruber2004"/> [[Sulfur]], [[iodine]], and [[phenol]] were also commonly used treatments for psoriasis during this era, when it was incorrectly believed that psoriasis was an infectious disease.<ref name="Gruber2004"/> [[Coal tar]]s were widely used with [[ultraviolet]] light irradiation as a topical treatment approach in the early 1900s.<ref name="Gruber2004"/><ref name="Benedek2013 Part 2"/> During the same time, psoriatic arthritis cases were treated with [[Intravenous therapy|intravenously]] administered gold preparations in the same manner as [[rheumatoid arthritis]].<ref name="Benedek2013 Part 2">{{cite journal | vauthors = Benedek TG | title = Psoriasis and psoriatic arthropathy: historical aspects: part II | journal = Journal of Clinical Rheumatology | volume = 19 | issue = 5 | pages = 267–71 | date = August 2013 | pmid = 23872545 | doi = 10.1097/RHU.0b013e31829d4ad4 | s2cid = 199596315 }}</ref>

== Society and culture ==
The International Federation of Psoriasis Associations (IFPA) is the global umbrella organization for national and regional psoriasis associations and also gathers the leading experts in psoriasis and psoriatic arthritis research for scientific conferences every three years.<ref>[http://www.ifpa-pso.org/ International Federation of Psoriasis Associations] {{webarchive|url=https://web.archive.org/web/20081121043918/http://www.ifpa-pso.org/ |date=21 November 2008 }}. Ifpa-pso.org. Retrieved on 8 June 2013.</ref> The Psoriasis International Network, a program of the Fondation René Touraine, gathers dermatologists, [[rheumatologist]]s, and other caregivers involved in the management of psoriasis. Non-profit organizations like the [[National Psoriasis Foundation]] in the United States, the Psoriasis Association in the United Kingdom, Association France Psoriasis<ref>{{cite web |author=<!-- not stated --> |date= |title=Tous unis face au psoriasis et au rhumatisme psoriasique ! - Association France Psoriasis |url=https://francepsoriasis.org/ |website=France Psoriasis |location=Paris |publisher= |access-date=April 2, 2025}}</ref> and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries. October 29 is World Psoriasis Day.<ref>{{cite web |author=<!-- not stated --> |date=2021-09-22 |title=IFPA, World Psoriasis Day |url=https://www.ifpa-pso.com/global-actions-overview/world-psoriasis-day |website=IFPA |location= |access-date=2025-08-06}}</ref>

===Cost===
The annual cost of treating psoriasis in the United States is estimated as high as $32.5{{Spaces}}billion, including $12.2{{Spaces}}billion in direct costs. Pharmacy costs are the main source of direct expense, with biologic therapy the most prevalent. These costs increase significantly when co-morbid conditions such as heart disease, hypertension, diabetes, lung disease, and [[Mental disorder|psychiatric disorders]] are factored in. Expenses linked to co-morbidities are estimated at an additional $23,000 per person per year.<ref>{{cite journal | vauthors = Evans C | title = Managed care aspects of psoriasis and psoriatic arthritis | journal = The American Journal of Managed Care | volume = 22 | issue = 8 Suppl | pages = s238–43 | date = June 2016 | pmid = 27356195 | url = http://www.ajmc.com/journals/supplement/2016/Easing_the_Economic_Clinical_Burden_Psoriasis_Psoriatic_Arthritis_The_Role_Managed_Care/Managed-Care-Aspects-of-Psoriasis-and-Psoriatic-Arthritis/ | url-status = live | archive-url = https://web.archive.org/web/20170202134534/http://www.ajmc.com/journals/supplement/2016/Easing_the_Economic_Clinical_Burden_Psoriasis_Psoriatic_Arthritis_The_Role_Managed_Care/Managed-Care-Aspects-of-Psoriasis-and-Psoriatic-Arthritis/ | archive-date = 2 February 2017 }}</ref>

==Research==
The role of [[insulin resistance]] in the pathogenesis of psoriasis is under investigation. Preliminary research has suggested that [[antioxidant]]s such as [[polyphenol]]s may have beneficial effects on the inflammation characteristic of psoriasis.<ref name="Dubois2013"/>

Many novel medications being researched during the 2010s target the [[Th17]]/[[Interleukin 23 subunit alpha|IL-23]] axis,<ref name="Dubois2013"/> particularly [[Interleukin 23 subunit alpha|IL-23p19]] inhibitors, as IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections.<ref name=Patel2012>{{cite journal | vauthors = Patel M, Day A, Warren RB, Menter A | title = Emerging therapies for the treatment of psoriasis | journal = Dermatology and Therapy | volume = 2 | issue = 1 | article-number = 16 | date = December 2012 | pmid = 23205338 | pmc = 3510410 | doi = 10.1007/s13555-012-0016-4 }}</ref> Other [[cytokine]]s such as [[Interleukin 17|IL-17]] and [[Interleukin 22|IL-22]] also have been targets for inhibition as they play important roles in the pathogenesis of psoriasis.<ref name=Patel2012 /> Another avenue of research has focused on the use of [[vascular endothelial growth factor receptor tyrosine kinase inhibitor|vascular endothelial growth factor inhibitors]] to treat psoriasis.<ref name="Weidemann2013"/> Oral agents being investigated during the 2010s as alternatives to medications administered by injection include [[Janus kinase inhibitor]]s, [[protein kinase C]] inhibitors, [[mitogen-activated protein kinase]] inhibitors, and [[PDE4 inhibitor|phosphodiesterase 4 inhibitors]], all of which have proven effective in various phase 2 and 3 [[clinical trial]]s.<ref name="Dubois2013">{{cite journal | vauthors = Dubois Declercq S, Pouliot R | title = Promising new treatments for psoriasis | journal = TheScientificWorldJournal | volume = 2013 | article-number = 980419 | date = July 2013 | pmid = 23935446 | pmc = 3713318 | doi = 10.1155/2013/980419 | doi-access = free | title-link = doi }}</ref><ref name=Patel2012/> These agents have potentially severe side-effects due to their [[Immunosuppression|immunosuppressive]] mechanisms.<ref name=Patel2012/>

== References ==
{{Reflist}}

== Further reading ==
{{refbegin}}
*{{cite book |title=From Arsenic to Biologicals: A 200 Year History of Psoriasis | vauthors = Baker BS |location=Beckenham UK |publisher=Garner |year=2008 |isbn=978-0-9551603-2-5 |url=https://books.google.com/books?id=W8HZtSkDhXgC&pg=PP1 }}
* {{cite web |title=Guidelines for the assessment and management of psoriasis |publisher=U.S. [[National Guideline Clearinghouse]] |url=http://www.guideline.gov/content.aspx?id=38575 |access-date=26 July 2013 |archive-url=https://web.archive.org/web/20130927041156/http://www.guideline.gov/content.aspx?id=38575 |archive-date=27 September 2013 }}
* {{cite book | vauthors=((World Health Organization)) | title=Global report on psoriasis | publisher=[[World Health Organization]] (WHO) | year=2016 | isbn=978-92-4-156518-9 | url=https://www.who.int/ncds/management/psoriasis/en/ | archive-url=https://web.archive.org/web/20160229000322/http://www.who.int/ncds/management/psoriasis/en/ | archive-date=29 February 2016 | hdl=10665/204417 }}
{{refend}}

== External links ==
{{Commons category}}
<!-- Please read http://en.wikipedia.org/wiki/WP:EL before adding links. Specifically, links to commercial sites and forums are strongly discouraged. Wikipedia is not a collection of links, no matter how useful/helpful. -->
* {{cite web | title=Psoriatic arthritis | website=Genetics Home Reference | url=https://medlineplus.gov/genetics/condition/psoriatic-arthritis/ }}
* {{cite web | url = https://medlineplus.gov/psoriasis.html | publisher = U.S. National Library of Medicine | work = MedlinePlus | title = Psoriasis }}

{{Medical resources
 | DiseasesDB     = 10895
 | ICD10          = {{ICD10|L|40||l|40}}
 | ICD9           = {{ICD9|696}}
 | ICDO           =
 | OMIM           = 177900
 | MedlinePlus    = 000434
 | eMedicineSubj  = emerg
 | eMedicineTopic = 489
 | eMedicine_mult = plaque {{eMedicine2|derm|365}}, guttate {{eMedicine2|derm|361}}, nails {{eMedicine2|derm|363}}, pustular {{eMedicine2|derm|366}}
 | MeshID         = D011565
}}
{{Diseases of the skin and appendages by morphology}}
{{Papulosquamous disorders}}
{{Portal bar | Medicine}}
{{Authority control}}

[[Category:Autoimmune diseases]]
[[Category:Cutaneous conditions]]
[[Category:Psoriasis| ]]
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[[Category:Wikipedia medicine articles ready to translate]]