psoriasis

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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. Plaque psoriasis typically appears as raised areas of 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.{{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 }}

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

Additional types of psoriasis comprise about 10% of cases. They include pustular, inverse, napkin, guttate, oral, and seborrheic-like forms.{{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 }}

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Pustular psoriasis appears as raised bumps filled with noninfectious pus (pustules).{{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 }} The skin under and surrounding the pustules is red and tender. Pustular psoriasis can either be localized or more widespread throughout the body. Two types of localized pustular psoriasis include psoriasis pustulosa palmoplantaris and acrodermatitis continua of Hallopeau; both forms are localized to the hands and feet.

Inverse psoriasis (also known as flexural psoriasis) appears as smooth, inflamed patches of skin. The patches frequently affect skin folds, particularly around the genitals (between the thigh and groin), the armpits, 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.

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.{{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}} Napkin psoriasis is often misdiagnosed as napkin dermatitis (diaper rash).{{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 }} It typically improves as children age and may later present in more common forms as plaque psoriasis or inverse psoriasis.{{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}}

File:Psoriasis en gouttes enfant 2.jpg]]

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 trunk, limbs, and scalp, but typically spare the palms and soles. Guttate psoriasis is often triggered by a streptococcal infection (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.{{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}} Skin biopsy can also be performed which typically shows a psoriasiform reaction pattern characterized by epidermal hyperplasia with elongation of the rete ridges.

There is no firm evidence regarding the best management for guttate psoriasis; however, first-line therapy for mild guttate psoriasis typically includes topical corticosteroids.{{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 }} Phototherapy can be used for moderate or severe guttate psoriasis. Biologic treatments have not been well studied in the treatment of guttate psoriasis.

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.{{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 }}

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.{{cite journal | vauthors = Rendon A, Schäkel K | title = Psoriasis Pathogenesis and Treatment | journal = International Journal of Molecular Sciences | volume = 20 | issue = 6 | pages = 1475 | date = March 2019 | pmid = 30909615 | doi = 10.3390/ijms20061475 | pmc = 6471628 | doi-access = free | title-link = doi }} It may be accompanied by severe dryness, itching, swelling, and pain. It can develop from any type of psoriasis. It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic glucocorticoids.{{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 }} This form of psoriasis can be fatal as the extreme inflammation and exfoliation disrupt the body's ability to regulate temperature and perform barrier functions.{{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 }}

Psoriasis in the mouth is very rare, in contrast to lichen planus, another common papulosquamous disorder that commonly involves both the skin and mouth.{{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 }} When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic, but it may appear as white or grey-yellow plaques. 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.{{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 }} A recent study found an association between the two conditions, and it suggests that geographic tongue might be a predictor for psoriasis.{{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 |url=https://pubmed.ncbi.nlm.nih.gov/30739339/ |journal=Journal of Oral Pathology & Medicine|volume=48 |issue=5 |pages=365–372 |doi=10.1111/jop.12840 |issn=1600-0714 |pmid=30739339}}

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, skin folds next to the nose, the skin surrounding the mouth, skin on the chest above the sternum, and in skin folds.

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.{{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 }} It typically involves painful inflammation of the joints and 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. Psoriatic arthritis can also affect the hips, knees, spine (spondylitis), and sacroiliac joint (sacroiliitis).{{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 }} About 30% of individuals with psoriasis will develop psoriatic arthritis.{{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 }} Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.{{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 }}

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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.{{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 }} These changes include pitting of the nails (pinhead-sized depressions in the nail is seen in 70% with nail psoriasis), whitening of the nail, 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.

In addition to the appearance and distribution of the rash, specific medical signs 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),{{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 }} and itching and pain localized to papules and plaques.

The cause of psoriasis is not fully understood. Genetics, seasonal changes, skin damage, climate, immunocompromised state, specific infections, and the use of some medications have been connected with different types of psoriasis.

{{See also|List of human leukocyte antigen alleles associated with cutaneous conditions}}

Around one-third of people with psoriasis report a family history of the disease, and researchers have identified genetic loci associated with the condition. 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.{{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 }}

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.{{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 }}

Classic genome-wide linkage analysis has identified nine loci on different chromosomes 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 (mutations) of those genes are commonly found in psoriasis. 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.

The major determinant is PSORS1, which probably accounts for 35–50% of psoriasis heritability.{{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 }} It controls genes that affect the immune system or encode skin proteins that are overabundant with 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, 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 layers of the epidermis and upregulated in psoriasis.

Two major immune system genes under investigation are interleukin-12 subunit beta (IL12B) on 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. T cells are involved in the inflammatory process that leads to psoriasis. These genes are on the pathway that upregulates tumor necrosis factor-α and nuclear factor κB, two genes involved in inflammation. 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).{{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 }}{{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 }}

Conditions reported as worsening the disease include chronic infections, stress, and changes in season and climate. Other factors that might worsen the condition include hot water, scratching psoriasis skin lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity.{{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 }}{{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 | pages = CD011972 | date = July 2019 | issue = 7 | pmid = 31309536 | pmc = 6629583 | doi = 10.1002/14651858.CD011972.pub2 | id = CD011972 }} The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019.

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. A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with psoriasis than in those without the infection. The immune response in those infected with HIV is typically characterized by cellular signals from T_h2 subset of CD4+ helper T cells,{{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 | pages = 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 }} whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of T_h1 subset of CD4+ helper T cells and T_h17 helper T cells.{{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 }}{{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 }} 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.{{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 }} 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}}

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.{{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 }} Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection (tonsillitis or pharyngitis).

Drug-induced psoriasis may occur with beta blockers, lithium, antimalarial medications, nonsteroidal anti-inflammatory drugs, terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor, interleukins, interferons, lipid-lowering medications,{{rp|197}} and paradoxically TNF inhibitors such as infliximab or adalimumab.{{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 }} Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect.{{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}}

Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin.{{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 }} Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis. 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. Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days. These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of immune cells).{{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 | pages = 5 | date = January 2011 | pmid = 21261982 | pmc = 3037296 | doi = 10.1186/1758-2652-14-5 | doi-access = free }} These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals (cytokines) such as interleukin-36γ, tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-22.{{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 }} These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate. One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10. 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.

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.{{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 }}{{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 }}

Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis{{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 }} and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α. 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.

Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions and induce the proliferation of T cells and type 1 helper T cells (T_h1). Targeted immunotherapy, as well as psoralen and ultraviolet A (PUVA) therapy, can reduce the number of dendritic cells and favors a T_H2 cell cytokine secretion pattern over a T_h1/T_h17 cell cytokine profile. Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17.{{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 | pages = 1 | date = October 2012 | doi = 10.5070/D33N39N8XM | pmid = 23122008 }} Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22. Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.

File:Micrograph of psoriasis vulgaris.jpg, 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).{{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 | pages = 639 | year = 2018 | pmid = 29713318 | pmc = 5911619 | doi = 10.3389/fimmu.2018.00639 | doi-access = free | title-link = doi }}]]

A diagnosis of psoriasis is usually based on the appearance of the skin. Skin characteristics typical for psoriasis are scaly, erythematous plaques, papules, or patches of skin that may be painful and itch. No special blood tests or diagnostic procedures are usually required to make the diagnosis.

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), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis). Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.

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 epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions.{{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 | pages = 979258 | year = 2009 | pmid = 19884985 | pmc = 2768824 | doi = 10.1155/2009/979258 | doi-access = free | title-link = doi }} The stratum granulosum layer of the epidermis is often missing or significantly decreased in psoriatic lesions; the skin cells from the most superficial layer of skin are also abnormal as they never fully mature. Unlike their mature counterparts, these superficial cells keep their nuclei. 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.

Psoriasis is classified as a papulosquamous disorder and is most commonly subdivided into different categories based on histological characteristics. Variants include plaque, pustular, guttate, and flexural psoriasis. Each form has a dedicated ICD-10 code.{{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 |url-status=dead |archive-date=9 July 2006 }} Psoriasis can also be classified into nonpustular and pustular types.{{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 }}

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-Cw6. Conversely, type 2 does not show a family history, presents after age 40, and is not associated with HLA-Cw6. Type 1 accounts for about 75% of persons with psoriasis.{{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 }}

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{{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 }} while others have classified them as distinct from autoimmune diseases and referred to them as immune-mediated inflammatory diseases.{{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 }}{{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 | issue = 147413 | pages = 147413 | date = June 2012 | pmid = 22754278 | pmc = 3384985 | doi = 10.1155/2012/147413 | doi-access = free | title-link = doi }}

Image:Distribution of psoriasis severity.svg

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.{{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 }} Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.

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.{{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 }}

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).{{cite journal|url=http://www.skinandaging.com/article/5394|archive-url=https://web.archive.org/web/20110302031858/http://www.skinandaging.com/article/5394|url-status=dead|archive-date=2 March 2011|title=Psoriasis Update |journal=Skin & Aging |volume=14 |issue=3|year=2006 |pages=46–50}} 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.{{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 | pages = 7 | date = October 2004 | doi = 10.5070/D318W9J736 | pmid = 15530297 }}

Psoriasis is not just a skin disease. The symptoms of psoriasis can sometimes go beyond the skin and can have a negative impact on the quality of life of the affected individuals. Additionally, the co-morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition.{{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 }}

There is 2.2 times increased risk of cardiovascular complications in people with psoriasis. Also, people with psoriasis are more susceptible to myocardial infarction (heart attack) and stroke. It has been speculated that there is systemic inflammation in psoriasis, which drives “psoriatic march” and can cause other inflammatory complications including cardiovascular complications.{{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 }} A study used fluorodeoxyglucose F-18 positron emission tomography-computed tomography (FDG PET/CT) to measure aortic vascular inflammation in psoriasis patients, and found increased 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.{{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 }}

Depression or depressive symptoms are present in 28–55% of people with psoriasis. People with psoriasis are often stigmatized due to visible disfigurement of the skin. Social stigmatization is a risk factor for depression, however, other immune system factors may also be related to this observed increased incidence of depression in people with psoriasis. There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases, including psoriasis.{{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 }}

People with psoriasis are at increased risk of developing type 2 diabetes (~1.5 odds ratio). 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 inflammatory NF-κB pathway.{{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 }}

Image:Psoriasis treatment ladder.svg

While no cure is available for psoriasis, many treatment options exist. Topical agents are typically used for mild disease, phototherapy for moderate disease, and systemic agents for severe disease.{{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 }} 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.{{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 | pages = CD011541 | date = April 2019 | issue = 4 | pmid = 30958563 | pmc = 6452774 | doi = 10.1002/14651858.CD011541.pub2 | collaboration = Cochrane Skin Group }}

Topical corticosteroid preparations are the most effective agents when used continuously for eight weeks; retinoids and coal tar were found to be of limited benefit and may be no better than placebo.{{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 }} 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.{{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 }}

Vitamin D analogues (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.{{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 | pages = 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 }}

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.{{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 | pages = CD009687 | date = February 2016 | pmid = 26915340 | doi = 10.1002/14651858.CD009687.pub2 | pmc = 8697570 | id = CD009687 }} 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.

Moisturizers 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 phototherapy.{{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 }} 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. 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 D₃ analogues (for example, calcipotriol), and retinoids are routinely used. (The use of the finger tip unit may be helpful in guiding how much topical treatment to use.){{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 }}

Vitamin D analogs may be useful with steroids; steroids alone have a higher rate of side effects. Vitamin D analogs may allow lower doses of steroids to be used.{{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 }}

Another topical therapy used to treat psoriasis is a form of balneotherapy, which involves daily baths in 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.{{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 }} Decreases of PASI scores greater than 75% and remission for several months have commonly been observed. Side effects may be mild such as itchiness, folliculitis, sunburn, poikiloderma, and a theoretical risk of nonmelanoma cancer or melanoma has been suggested. Some studies indicate no increased risk of melanoma in the long term. 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 liver spots.{{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 }} Dead Sea balneotherapy is also effective for psoriatic arthritis. Tentative evidence indicates that balneophototherapy, a combination of salt bathes and exposure to ultraviolet B-light (UVB), in chronic plaque psoriasis is better than UVB alone.{{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 | pages = CD011941 | date = May 2020 | pmid = 32368795 | doi = 10.1002/14651858.CD011941.pub2| pmc = 7199317 }} Glycerin is also an effective treatment for Psoriasis.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).

Phototherapy in the form of sunlight has long been used for psoriasis. UVB wavelengths of 311–313 nanometers are most common. UV-B lamps have been developed for this treatment. 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. Increased rates of cancer from treatment appear to be small. Narrowband UVB therapy has been demonstrated to have similar efficacy to psoralen and ultraviolet A phototherapy (PUVA). 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.{{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 | pages = CD009481 | date = October 2013 | volume = 2016 | pmid = 24151011 | doi = 10.1002/14651858.CD009481.pub2 | pmc = 11076274 }}

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; 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 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.{{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 }}

UV light therapies all have risks; tanning beds are no exception, being listed by the World Health Organization as carcinogens.{{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 }} 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.

A major mechanism of NB-UVB is the induction of DNA damage in the form of pyrimidine dimers. 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.{{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 }} The activity of many types of immune cells found in the skin is also effectively suppressed by NB-UVB phototherapy treatments.{{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 }} 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 blistering of the treated skin, irritation of the eyes in the form of conjunctival inflammation or inflammation of the cornea, or cold sores due to reactivation of the herpes simplex virus in the skin surrounding the lips. Eye protection is usually given during phototherapy treatments.

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 the 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, burning, and itching. Long-term treatment is associated with squamous cell carcinoma (but not with melanoma).{{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 }} A combination therapy for moderate to severe psoriasis using PUVA plus acitretin resulted in benefit, but acitretin use has been associated with birth defects and liver damage.{{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 }}

Image:Psoriasis infliximab ar1182-2.gif) at baseline and eight weeks after initiation of infliximab therapy]]

Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments.{{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 }} People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities. Pregnancy must be avoided for most of these treatments.{{medical citation needed|date=July 2023}} The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.{{medical citation needed|date=July 2023}}

Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids.{{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 }} Methotrexate and ciclosporin are 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. Oral corticosteroids should not be used as they can severely flare psoriasis upon their discontinuation.{{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}}

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. 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. However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.

Guidelines regard biologics as a third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.{{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 }} The safety of biologics during pregnancy has not been assessed. European guidelines recommend avoiding biologics if a pregnancy is planned; anti-TNF therapies such as infliximab are not recommended for use in chronic carriers of the hepatitis B virus or individuals infected with HIV.

Several monoclonal antibodies target cytokines, the molecules that cells use to send inflammatory signals to each other. TNF-α is one of the main executor inflammatory cytokines. Four 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,{{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 }} have been developed against pro-inflammatory cytokines{{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 }} and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies. IL-12 and IL-23 share a common domain, p40, which is the target of the FDA-approved ustekinumab.{{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 | issue = 613086 | pages = 613086 | date = August 2013 | pmid = 24069534 | pmc = 3771250 | doi = 10.1155/2013/613086 | doi-access = free | title-link = doi }} In 2017 the US FDA approved guselkumab for plaque psoriasis.[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 }} There have been few studies of the efficacy of anti-TNF medications for psoriasis in children. One randomized control study suggested that 12 weeks of etanercept treatment reduced the extent of psoriasis in children with no lasting adverse effects.{{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 | pages = CD010017 | date = November 2015 | volume = 2019 | pmid = 26598969 | pmc = 6493213 | doi = 10.1002/14651858.CD010017.pub2 }}

Two medications that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1. 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. Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes natural killer cells to kill T cells as a way of controlling inflammation. Apremilast may also be used.

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.{{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 }}

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.{{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 | pages = CD011535 | date = July 2023 | pmid = 37436070 | pmc = 10337265 | doi = 10.1002/14651858.CD011535.pub6 }} There is also some evidence to support use of secukinumab, brodalumab, guselkumab, certolizumab, and ustekinumab.{{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 }} In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNF alpha biologics were found to be more effective than traditional systemic treatments. The immunologic pathways of psoriasis involve Th9, Th17, Th1 lymphocytes, and 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.{{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 | pages = CD010497 | date = August 2015 | pmid = 26258748 | pmc = 6464505 | doi = 10.1002/14651858.CD010497.pub2 }}

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.{{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 |url=https://pubmed.ncbi.nlm.nih.gov/26089047/ |access-date=17 September 2024|doi-access=free }}

It has been theorized that antistreptococcal medications may improve guttate and chronic plaque psoriasis; however, limited studies do not show that antibiotics are effective.{{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 | pages = CD011571 | date = March 2019 | issue = 3 | pmid = 30835819 | pmc = 6400423 | doi = 10.1002/14651858.cd011571.pub2 }}

Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.{{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 }}{{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 }}

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).{{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 }} A low-calorie diet appears to reduce the severity of psoriasis. Diet recommendations include consumption of cold water fish (preferably wild fish, not 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.{{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 | pages = 743 | date = July 2016 | pmid = 27455297 | pmc = 4962284 | doi = 10.3390/ijerph13070743 | doi-access = free | title-link = doi }}

Many patients report improvements after consuming less tobacco, caffeine, sugar, nightshades (tomatoes, eggplant, peppers, paprika and white potatoes) and taking probiotics and oral Vitamin D.{{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 }}

There is a higher rate of celiac disease among people with psoriasis.{{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 }} When adopting a gluten-free diet, disease severity generally decreases in people with celiac disease and those with anti-gliadin antibodies.{{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 }}{{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 }}

Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies. Depending on the severity and location of outbreaks, people may experience significant physical discomfort and some disability, affecting the person's quality of life. Itching and pain can interfere with basic functions, such as self-care and sleep. 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. Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for dandruff.{{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 }}

File:Women_with_vitiligo_Psoriasis2.jpg 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 concerns. Psoriasis has been associated with low self-esteem and depression is more common among those with the condition. People with psoriasis often feel prejudiced against due to the commonly held incorrect belief that psoriasis is contagious.{{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 }} Psychological distress can lead to significant depression and social isolation; a high rate of thoughts about suicide has been associated with psoriasis. Many tools exist to measure the quality of life of people with psoriasis and other dermatological disorders. Clinical research has indicated individuals often experience a diminished quality of life.{{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 | pages = 35 | date = June 2006 | pmid = 16756666 | pmc = 1501000 | doi = 10.1186/1477-7525-4-35 | doi-access = free }} Children with psoriasis may encounter bullying.{{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 }}

Several conditions are associated with psoriasis including obesity, cardiovascular, and metabolic disturbances. These occur more frequently in older people. Nearly half of individuals with psoriasis over the age of 65 have at least three comorbidities (concurrent conditions), and two-thirds have at least two comorbidities.{{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}}

Psoriasis has been associated with obesity and several other cardiovascular and metabolic disturbances. The number of new cases per year of diabetes is 27% higher in people affected by psoriasis than in those without the condition.{{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 }} Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis. Younger people with psoriasis may also be at increased risk for developing diabetes. Individuals with psoriasis or psoriatic arthritis have a slightly higher risk of heart disease and 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.{{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 }}

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 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. There may be a slightly increased risk of stroke associated with psoriasis, especially in severe cases.{{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}} Treating high levels of cholesterol with statins 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.{{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 }} These 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 LFA-1. Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome.{{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 }}{{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 }}

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. People with psoriasis also have a higher risk of celiac disease. Few studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned. 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. People treated with long-term systemic therapy for psoriasis have a 52% increased risk cancers of the lung and bronchus, a 205% increase in the risk of developing cancers of the upper gastrointestinal tract, a 31% increase in the risk of developing 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. The risk for development of non-melanoma skin cancers is also increased. Psoriasis increases the risk of developing squamous cell carcinoma of the skin by 431% and increases the risk of basal cell carcinoma by 100%. There is no increased risk of melanoma associated with psoriasis. People with psoriasis have a higher risk of developing cancer.{{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 }}

Psoriasis is estimated to affect 2–4% of the population of the western world. 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. Psoriasis is about five times more common in people of European descent than in people of Asian descent,{{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 }} more common in countries farther from the equator, relatively uncommon in African Americans, and extremely uncommon in Native Americans. Psoriasis has been estimated to affect about 6.7{{Spaces}}million Americans.

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. Approximately one-third of people with psoriasis report being diagnosed before age 20.{{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 }} Psoriasis affects both sexes equally.{{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 }}

People with inflammatory bowel disease such as Crohn's disease or ulcerative colitis are at an increased risk of developing psoriasis.

Scholars believe psoriasis to have been included among the various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible.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. The person was deemed "impure" (see tumah and taharah) during their affected phase and is ultimately treated by the kohen.{{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 }} 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. It became known as Willan's lepra in the late 18th century when English dermatologists 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}}.{{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 }}

Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus. The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813.{{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 }} Admiral 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 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. Mercury was also used for psoriasis treatment during this time. 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. Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s. During the same time, psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis.{{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 }}

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.[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. The Psoriasis International Network, a program of the Fondation René Touraine, gathers dermatologists, rheumatologists, 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{{cite web |author= |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}} and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries.

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 psychiatric disorders are factored in. Expenses linked to co-morbidities are estimated at an additional $23,000 per person per year.{{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 }}

The role of insulin resistance in the pathogenesis of psoriasis is under investigation. Preliminary research has suggested that antioxidants such as polyphenols may have beneficial effects on the inflammation characteristic of psoriasis.

Many novel medications being researched during the 2010s target the Th17/IL-23 axis, particularly IL-23p19 inhibitors, as IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections.{{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 | pages = 16 | date = December 2012 | pmid = 23205338 | pmc = 3510410 | doi = 10.1007/s13555-012-0016-4 }} Other cytokines such as IL-17 and IL-22 also have been targets for inhibition as they play important roles in the pathogenesis of psoriasis. Another avenue of research has focused on the use of vascular endothelial growth factor inhibitors to treat psoriasis. Oral agents being investigated during the 2010s as alternatives to medications administered by injection include Janus kinase inhibitors, protein kinase C inhibitors, mitogen-activated protein kinase inhibitors, and phosphodiesterase 4 inhibitors, all of which have proven effective in various phase 2 and 3 clinical trials.{{cite journal | vauthors = Dubois Declercq S, Pouliot R | title = Promising new treatments for psoriasis | journal = TheScientificWorldJournal | volume = 2013 | issue = 980419 | pages = 980419 | date = July 2013 | pmid = 23935446 | pmc = 3713318 | doi = 10.1155/2013/980419 | doi-access = free | title-link = doi }} These agents have potentially severe side-effects due to their immunosuppressive mechanisms.

{{Reflist}}

{{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 |url-status=dead }}
• {{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/ | url-status=dead | archive-date=29 February 2016 | hdl=10665/204417 }}

{{refend}}

{{Commons category}}

• {{cite web | title=Psoriatic arthritis | website=Genetics Home Reference | url=https://ghr.nlm.nih.gov/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}}

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Category:Autoimmune diseases

Category:Cutaneous conditions

Category:Psoriasis

Category:Wikipedia emergency medicine articles ready to translate

Category:Wikipedia medicine articles ready to translate