Template:Short description Template:Cs1 config Template:Good article Template:Use dmy dates Template:Infobox medical condition
Psoriasis is a long-lasting, noncontagious autoimmune disease characterized by patches of abnormal skin.<ref name=Lancet2015/><ref name=NIH2015/> These areas are red, pink, or purple, dry, itchy, and scaly.<ref name=Menter2008/><ref>Template:Cite book</ref> Psoriasis varies in severity from small localized patches to complete body coverage.<ref name="Menter2008">Template:Cite journal</ref> Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon.<ref name=Ely2010>Template:Cite journal</ref>
The five main types of psoriasis are plaque, guttate, inverse, pustular, and erythrodermic.<ref name=NIH2015/> Plaque psoriasis, also known as psoriasis vulgaris, makes up about 90% of cases.<ref name=Lancet2015/> It typically presents as red patches with white scales on top.<ref name=Lancet2015/> Areas of the body most commonly affected are the back of the forearms, shins, navel area, and scalp.<ref name=Lancet2015/> Guttate psoriasis has drop-shaped lesions.<ref name=NIH2015/> Pustular psoriasis presents as small, noninfectious, pus-filled blisters.<ref name=Jain2012/> Inverse psoriasis forms red patches in skin folds.<ref name=NIH2015/> Erythrodermic psoriasis occurs when the rash becomes very widespread and can develop from any of the other types.<ref name=Lancet2015/> Fingernails and toenails are affected in most people with psoriasis at some point in time.<ref name=Lancet2015/> This may include pits in the nails or changes in nail color.<ref name=Lancet2015>Template:Cite journal</ref>
Psoriasis is generally thought to be a genetic disease that is triggered by environmental factors.<ref name=Menter2008 /> If one twin has psoriasis, the other twin is three times more likely to be affected if the twins are identical than if they are nonidentical.<ref name=Lancet2015/> This suggests that genetic factors predispose to psoriasis.<ref name=Lancet2015/> Symptoms often worsen during winter and with certain medications, such as beta blockers or NSAIDs.<ref name=Lancet2015/> Infections and psychological stress can also play a role.<ref name=Menter2008/><ref name=NIH2015/> The underlying mechanism involves the immune system reacting to skin cells.<ref name=Lancet2015/> Diagnosis is typically based on the signs and symptoms.<ref name=Lancet2015/>
There is no known cure for psoriasis, but various treatments can help control the symptoms.<ref name=Lancet2015/> These treatments include steroid creams, vitamin D3 cream, ultraviolet light, immunosuppressive drugs, such as methotrexate, and biologic therapies targeting specific immunologic pathways.<ref name=NIH2015/> About 75% of skin involvement improves with creams alone.<ref name=Lancet2015/> The disease affects 2–4% of the population.<ref name=Parisi2013>Template:Cite journal</ref> Men and women are affected with equal frequency.<ref name=NIH2015/> The disease may begin at any age, but typically starts in adulthood.<ref name=NIH2015>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Psoriasis is associated with an increased risk of psoriatic arthritis, lymphomas, cardiovascular disease, Crohn's disease, and depression.<ref name=Lancet2015/> Psoriatic arthritis affects up to 30% of individuals with psoriasis.<ref name=Jain2012>Template:Cite book</ref>
The word "psoriasis" is from Greek {{#invoke:Lang|lang}} meaning Template:Gloss or Template:Gloss,<ref name="Ritchlin2007">Template:Cite book</ref> from [[wikt:psora|Template:Transliteration]] Template:Gloss, and [[wikt:-iasis#Suffix|Template:Transliteration]] Template:Gloss.
Signs and symptomsEdit
Plaque psoriasisEdit
Psoriasis vulgaris (also known as chronic stationary psoriasis or plaque-like psoriasis) is the most common form and affects 85–90% of people with psoriasis.<ref name="Palfreeman2013"/> Plaque psoriasis typically appears as raised areas of inflamed skin covered with silvery-white, scaly skin. These areas are called plaques and are most commonly found on the elbows, knees, scalp, and back.<ref name="Palfreeman2013"/><ref name=DAVIDSONS2010>Template:Cite book</ref>
- Psoriasis2010a.JPG
Plaques of psoriasis
- Psoriasis.jpg
A person's arm covered with plaque psoriasis
- Psoriasis of the palms.jpg
Psoriasis of the palms
- Riehl Zumbusch Tafel LII (1).jpg
Psoriasis of the scalp
Other formsEdit
Additional types of psoriasis comprise about 10% of cases. They include pustular, inverse, napkin, guttate, oral, and seborrheic-like forms.<ref name="Andrews">Template:Cite book</ref>
Pustular psoriasisEdit
Pustular psoriasis appears as raised bumps filled with noninfectious pus (pustules).<ref>Template:Cite journal</ref> The skin under and surrounding the pustules is red and tender.<ref name="Raychaudhuri2014" /> Pustular psoriasis can either be localized or more widespread throughout the body. Two types of localized pustular psoriasis include psoriasis pustulosa palmoplantaris and acrodermatitis continua of Hallopeau; both forms are localized to the hands and feet.<ref name="Rendon2019" />
Inverse psoriasisEdit
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.<ref name="Weigle2013" />
Napkin psoriasisEdit
Napkin psoriasis is a subtype of psoriasis common in infants under the age of two and is characterized by red papules with silver scales in the diaper area that may extend to the torso or limbs.<ref name="Gudjonsson2012" /><ref>Template:Cite journal</ref> Napkin psoriasis is often misdiagnosed as napkin dermatitis (diaper rash).<ref name="Gelmetti2009">Template:Cite journal</ref> It typically improves as children age and may later present in more common forms as plaque psoriasis or inverse psoriasis.<ref>Template:Cite journal</ref>
Guttate psoriasisEdit
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.<ref name=Saleh22>Template:Cite book</ref> Skin biopsy can also be performed which typically shows a psoriasiform reaction pattern characterized by epidermal hyperplasia with elongation of the rete ridges.<ref name=Saleh22/>
There is no firm evidence regarding the best management for guttate psoriasis; however, first-line therapy for mild guttate psoriasis typically includes topical corticosteroids.<ref name=Saleh22/><ref>Template:Cite journal</ref> Phototherapy can be used for moderate or severe guttate psoriasis. Biologic treatments have not been well studied in the treatment of guttate psoriasis.<ref name=Saleh22/>
Guttate psoriasis has a better prognosis than plaque psoriasis and typically resolves within 1–3 weeks; however, up to 40% of patients with guttate psoriasis eventually convert to plaque psoriasis.<ref name=Saleh22/><ref name="Weigle2013">Template:Cite journal</ref>
Erythrodermic psoriasisEdit
Psoriatic erythroderma (erythrodermic psoriasis) involves widespread inflammation and exfoliation of the skin over most of the body surface, often involving greater than 90% of the body surface area.<ref name="Rendon2019">Template:Cite journal</ref> It may be accompanied by severe dryness, itching, swelling, and pain. It can develop from any type of psoriasis.<ref name="Rendon2019" /> It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic glucocorticoids.<ref name="Zattra2012">Template:Cite journal</ref> 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.<ref name="DermNZ">{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>
MouthEdit
Psoriasis in the mouth is very rare, in contrast to lichen planus, another common papulosquamous disorder that commonly involves both the skin and mouth.<ref name="Yesudian2012">Template:Cite journal</ref> When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic,<ref name="Yesudian2012"/> but it may appear as white or grey-yellow plaques.<ref name="Yesudian2012"/> Fissured tongue is the most common finding in those with oral psoriasis and has been reported to occur in 6.5–20% of people with psoriasis affecting the skin. The microscopic appearance of oral mucosa affected by geographic tongue (migratory stomatitis) is very similar to the appearance of psoriasis.<ref>Template:Cite book</ref> A recent study found an association between the two conditions, and it suggests that geographic tongue might be a predictor for psoriasis.<ref>Template:Cite journal</ref>
Seborrheic-like psoriasisEdit
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.<ref name="Gudjonsson2012"/>
Psoriatic arthritisEdit
Psoriatic arthritis is a form of chronic inflammatory arthritis that has a highly variable clinical presentation and frequently occurs in association with skin and nail psoriasis.<ref name="Chimenti2013">Template:Cite journal</ref><ref name="Goldenstein2012"/> 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.<ref name="Chimenti2013"/> Psoriatic arthritis can also affect the hips, knees, spine (spondylitis), and sacroiliac joint (sacroiliitis).<ref name="Krawczyk2013">Template:Cite journal</ref> About 30% of individuals with psoriasis will develop psoriatic arthritis.<ref name="Palfreeman2013">Template:Cite journal</ref> Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.<ref name="Goldenstein2012">Template:Cite journal</ref>
Nail changesEdit
Psoriasis can affect the nails and produces a variety of changes in the appearance of fingers and toenails. Nail psoriasis occurs in 40–45% of people with psoriasis affecting the skin, and has a lifetime incidence of 80–90% in those with psoriatic arthritis.<ref name="Tan2012">Template:Cite journal</ref> 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.<ref name="Tan2012"/>
Medical signsEdit
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),<ref name="Gudjonsson2012">Template:Cite book</ref> and itching and pain localized to papules and plaques.<ref name="Weigle2013"/><ref name="Gudjonsson2012"/>
CausesEdit
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.<ref name="Prieto2013" /><ref name=":0" />
GeneticsEdit
Template:See also 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.<ref name=Krueger>Template:Cite journal</ref>
Psoriasis has a strong hereditary component, and many genes are associated with it, but how those genes work together is unclear. Most of the identified genes relate to the immune system, particularly the major histocompatibility complex (MHC) and T cells. Genetic studies are valuable due to their ability to identify molecular mechanisms and pathways for further study and potential medication targets.<ref name=Nestle>Template:Cite journal</ref>
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.<ref name=Nestle/> Genome-wide association scans have identified other genes that are altered to characteristic variants in psoriasis. Some of these genes express inflammatory signal proteins, which affect cells in the immune system that are also involved in psoriasis. Some of these genes are also involved in other autoimmune diseases.<ref name=Nestle/>
The major determinant is PSORS1, which probably accounts for 35–50% of psoriasis heritability.<ref>Template:Cite journal</ref> 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,<ref name="Prieto2013"/> which encodes an MHC class I protein; CCHCR1, variant WWC, which encodes a coiled coil protein overexpressed in psoriatic epidermis; and CDSN, variant allele 5, which encodes corneodesmosin, a protein expressed in the granular and cornified layers of the epidermis and upregulated in psoriasis.<ref name=Nestle/>
Two major immune system genes under investigation are interleukin-12 subunit beta (IL12B) on chromosome 5q, which expresses interleukin-12B; and IL23R on chromosome 1p, which expresses the interleukin-23 receptor and is involved in T cell differentiation. Interleukin-23 receptor and IL12B have both been strongly linked with psoriasis.<ref name="Prieto2013"/> T cells are involved in the inflammatory process that leads to psoriasis.<ref name=Nestle/> These genes are on the pathway that upregulates tumor necrosis factor-α and nuclear factor κB, two genes involved in inflammation.<ref name=Nestle/> The first gene directly linked to psoriasis was identified as the CARD14 gene located in the PSORS2 locus. A rare mutation in the gene encoding for the CARD14-regulated protein plus an environmental trigger was enough to cause plaque psoriasis (the most common form of psoriasis).<ref name = Jordan1>Template:Cite journal</ref><ref name = Jordan2>Template:Cite journal</ref>
LifestyleEdit
Conditions reported as worsening the disease include chronic infections, stress, and changes in season and climate.<ref name="Prieto2013"/> Other factors that might worsen the condition include hot water, scratching psoriasis skin lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity.<ref name=Prieto2013/><ref name=Clarke2011>Template:Cite journal</ref><ref name=Richard2013/><ref name=Shu2019>Template:Cite journal</ref> The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019.<ref name=Shu2019 />
HIVEdit
The rate of psoriasis in human immunodeficiency virus-positive (HIV) individuals is comparable to that of HIV-negative individuals, but psoriasis tends to be more severe in people infected with HIV.<ref name="Cedeno2011"/> A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with psoriasis than in those without the infection.<ref name="Cedeno2011"/> The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells,<ref name="Fife2007">Template:Cite journal</ref> whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T cells.<ref name="Wong2013">Template:Cite journal</ref><ref name="Martin2013">Template:Cite journal</ref> The diminished CD4+ T cell presence is thought to cause overactivation of CD8+ T cells, which are responsible for the exacerbation of psoriasis in HIV-positive people. Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy.<ref name=Rice>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> In those with long-term, well-controlled psoriasis, new HIV infection can trigger a severe flare-up of psoriasis and/or psoriatic arthritis.Template:Medical citation needed
MicrobesEdit
Psoriasis has been described as occurring after strep throat, and may be worsened by skin or gut colonization with Staphylococcus aureus, Malassezia spp., and Candida albicans.<ref name=":0">Template:Cite journal</ref> Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection (tonsillitis or pharyngitis).<ref name="Rendon2019" />
MedicationsEdit
Drug-induced psoriasis may occur with beta blockers,<ref name=Jain2012 /> lithium,<ref name=Jain2012 /> antimalarial medications,<ref name=Jain2012 /> nonsteroidal anti-inflammatory drugs,<ref name=Jain2012 /> terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor,<ref name=Jain2012 /> interleukins, interferons,<ref name=Jain2012 /> lipid-lowering medications,<ref name="Andrews"/>Template:Rp and paradoxically TNF inhibitors such as infliximab or adalimumab.<ref name="Guerra2013">Template:Cite journal</ref> Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect.<ref name=Weller2008>Template:Cite book</ref>
PathophysiologyEdit
Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin.<ref name="Ouyang2010">Template:Cite journal</ref> Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis.<ref name="Raychaudhuri2014"/> The sequence of pathological events in psoriasis is thought to start with an initiation phase in which an event (skin trauma, infection, or drugs) leads to activation of the immune system and then the maintenance phase consisting of chronic progression of the disease.<ref name="Nestle" /><ref name="Rendon2019" /> Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days.<ref name="Parrish2012"/> These changes are believed to stem from the premature maturation of keratinocytes induced by an inflammatory cascade in the dermis involving dendritic cells, macrophages, and T cells (three subtypes of immune cells).<ref name="Palfreeman2013"/><ref name="Cedeno2011">Template:Cite journal</ref> 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.<ref name=Nestle/><ref>Template:Cite journal</ref> These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate.<ref name=Nestle/> One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.<ref name=Nestle/> The inflammatory cytokines found in psoriatic nails and joints (in the case of psoriatic arthritis) are similar to those of psoriatic skin lesions, suggesting a common inflammatory mechanism.<ref name="Rendon2019" />
Gene mutations of proteins involved in the skin's ability to function as a barrier have been identified as markers of susceptibility for the development of psoriasis.<ref name="Roberson2010">Template:Cite journal</ref><ref name="Ramos2012">Template:Cite journal</ref>
Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis<ref name="Dombrowski2012">Template:Cite journal</ref> and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α.<ref name="Dombrowski2012"/> In response to these chemical messages from dendritic cells and T cells, keratinocytes also secrete cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor-α, which signal downstream inflammatory cells to arrive and stimulate additional inflammation.<ref name=Nestle/>
Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions<ref name="Ouyang2010"/> and induce the proliferation of T cells and type 1 helper T cells (Th1). Targeted immunotherapy, as well as psoralen and ultraviolet A (PUVA) therapy, can reduce the number of dendritic cells and favors a TH2 cell cytokine secretion pattern over a Th1/Th17 cell cytokine profile.<ref name=Nestle/><ref name="Wong2013"/> Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17.<ref name="Mudigonda2012">Template:Cite journal</ref> Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22.<ref name="Ouyang2010"/><ref name="Mudigonda2012"/> Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.<ref name="Mudigonda2012"/>
DiagnosisEdit
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.<ref name="Weigle2013"/> No special blood tests or diagnostic procedures are usually required to make the diagnosis.<ref name="Raychaudhuri2014"/>
The differential diagnosis of psoriasis includes dermatological conditions similar in appearance such as discoid eczema, seborrheic eczema, pityriasis rosea (may be confused with guttate psoriasis), nail fungus (may be confused with nail psoriasis) or cutaneous T cell lymphoma (50% of individuals with this cancer are initially misdiagnosed with psoriasis).<ref name=Weller2008 /> Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.<ref name=Weller2008/>
If the clinical diagnosis is uncertain, a skin biopsy or scraping may be performed to rule out other disorders and to confirm the diagnosis. Skin from a biopsy shows clubbed epidermal projections that interdigitate with dermis on microscopy. Epidermal thickening is another characteristic histologic finding of psoriasis lesions.<ref name="Raychaudhuri2014"/><ref name="Kunz2009">Template:Cite journal</ref> 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.<ref name="Raychaudhuri2014"/> Inflammatory infiltrates can typically be seen on microscopy when examining skin tissue or joint tissue affected by psoriasis. Epidermal skin tissue affected by psoriatic inflammation often has many CD8+ T cells, while a predominance of CD4+ T cells makes up the inflammatory infiltrates of the dermal layer of skin and joints.<ref name="Raychaudhuri2014"/>
ClassificationEdit
MorphologicalEdit
| Psoriasis Type | ICD-10 Code |
|---|---|
| Psoriasis Vulgaris | L40.0 |
| Generalized pustular psoriasis | L40.1 |
| Acrodermatitis continua | L40.2 |
| Pustulosis palmaris et plantaris | L40.3 |
| Guttate psoriasis | L40.4 |
| Psoriatic arthritis | L40.50 |
| Psoriatic spondylitis | L40.53 |
| Inverse psoriasis | L40.8 |
Psoriasis is classified as a papulosquamous disorder and is most commonly subdivided into different categories based on histological characteristics.<ref name=Menter2008 /><ref name=Jain2012/> Variants include plaque, pustular, guttate, and flexural psoriasis. Each form has a dedicated ICD-10 code.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> Psoriasis can also be classified into nonpustular and pustular types.<ref name="Fitz2">Template:Cite book</ref>
PathogeneticEdit
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.<ref name=Kupetsky2013 /> Type 1 accounts for about 75% of persons with psoriasis.<ref>Template:Cite journal</ref>
The classification of psoriasis as an autoimmune disease has sparked considerable debate. Researchers have proposed differing descriptions of psoriasis and psoriatic arthritis; some authors have classified them as autoimmune diseases<ref name="Raychaudhuri2014"/><ref name="Prieto2013"/><ref name="Weidemann2013">Template:Cite journal</ref> while others have classified them as distinct from autoimmune diseases and referred to them as immune-mediated inflammatory diseases.<ref name=Nestle/><ref name="Han2012">Template:Cite journal</ref><ref name="Quatresooz">Template:Cite journal</ref>
SeverityEdit
No consensus exists about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)≤10, a Psoriasis Area and Severity Index (PASI) score ≤10, and a Dermatology Life Quality Index (DLQI) score ≤10.<ref name="Mrowietz2011">Template:Cite journal</ref> Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.<ref name="Mrowietz2011"/>
The DLQI is a 10-question tool used to measure the impact of several dermatologic diseases on daily functioning. The DLQI score ranges from 0 (minimal impairment) to 30 (maximal impairment) and is calculated with each answer being assigned 0–3 points with higher scores indicating greater social or occupational impairment.<ref name="Mease2011">Template:Cite journal</ref>
The PASI is the most widely used measurement tool for psoriasis. It assesses the severity of lesions and the area affected and combines these two factors into a single score from 0 (no disease) to 72 (maximal disease).<ref>Template:Cite journal</ref> Nevertheless, the PASI can be too unwieldy to use outside of research settings, which has led to attempts to simplify the index for clinical use.<ref name="pmid15530297">Template:Cite journal</ref>
Co-morbiditiesEdit
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.<ref name=":1" /> Additionally, the co-morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition.<ref name=":1">Template:Cite journal</ref>
Cardiovascular complicationsEdit
There is 2.2 times increased risk of cardiovascular complications in people with psoriasis.<ref name=":2" /> Also, people with psoriasis are more susceptible to myocardial infarction (heart attack) and stroke.<ref name=":2" /> It has been speculated that there is systemic inflammation in psoriasis, which drives “psoriatic march” and can cause other inflammatory complications including cardiovascular complications.<ref name=":2">Template:Cite journal</ref> 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.<ref>Template:Cite journal</ref>
DepressionEdit
Depression or depressive symptoms are present in 28–55% of people with psoriasis.<ref name=":3" /> People with psoriasis are often stigmatized due to visible disfigurement of the skin. Social 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.<ref name=":3" /> There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases, including psoriasis.<ref name=":3">Template:Cite journal</ref>
Type 2 diabetesEdit
People with psoriasis are at increased risk of developing type 2 diabetes (~1.5 odds ratio).<ref name=":4" /> A genome-wide genetic study found that psoriasis and type 2 diabetes share four loci, namely, ACTR2, ERLIN1, TRMT112, and BECN1, which are connected via inflammatory NF-κB pathway.<ref name=":4">Template:Cite journal</ref>
ManagementEdit
While no cure is available for psoriasis,<ref name=Weller2008 /> many treatment options exist. Topical agents are typically used for mild disease, phototherapy for moderate disease, and systemic agents for severe disease.<ref name=Lancet07>Template:Cite journal</ref> There is no evidence to support the effectiveness of conventional topical and systemic drugs, biological therapy, or phototherapy for acute guttate psoriasis or an acute guttate flare of chronic psoriasis.<ref>Template:Cite journal</ref>
Topical agentsEdit
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.<ref name="Samarasekera2013">Template:Cite journal</ref> Very potent topical corticosteroids may be helpful in some cases, however, it is suggested to only use them for four weeks at a time and only if other less potent topical treatment options are not working.<ref>Template:Cite journal</ref>
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.<ref name="Mason2013">Template:Cite journal</ref>
For psoriasis of the scalp, a 2016 review found dual therapy (vitamin D analogs and topical corticosteroids) or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogs alone.<ref name=Schlager2016>Template:Cite journal</ref> Due to their similar safety profiles and minimal benefit of dual therapy over monotherapy, corticosteroid monotherapy appears to be an acceptable treatment for short-term treatment.<ref name=Schlager2016 />
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.<ref name="Asztalos2013">Template:Cite journal</ref> Certain emollients, though, have no impact on psoriasis plaque clearance or may even decrease the clearance achieved with phototherapy, e.g. the emollient salicylic acid is structurally similar to para-aminobenzoic acid, commonly found in sunscreen, and is known to interfere with phototherapy in psoriasis. Coconut oil, when used as an emollient in psoriasis, has been found to decrease plaque clearance with phototherapy.<ref name="Asztalos2013"/> Medicated creams and ointments applied directly to psoriatic plaques can help reduce inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques. Ointment and creams containing coal tar, dithranol, corticosteroids (i.e. desoximetasone), fluocinonide, vitamin 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.)<ref name="Clarke2011"/><ref>Template:Cite journal</ref>
Vitamin D analogs may be useful with steroids; steroids alone have a higher rate of side effects.<ref name="Mason2013" /> Vitamin D analogs may allow lower doses of steroids to be used.<ref>Template:Cite journal</ref>
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.<ref name="Halverstam2008">Template:Cite journal</ref> Decreases of PASI scores greater than 75% and remission for several months have commonly been observed.<ref name="Halverstam2008"/> Side effects may be mild such as itchiness, folliculitis, sunburn, poikiloderma, and a theoretical risk of nonmelanoma cancer or melanoma has been suggested.<ref name="Halverstam2008"/> Some studies indicate no increased risk of melanoma in the long term.<ref name="Katz2012"/> Data are inconclusive concerning nonmelanoma skin cancer risk, but support the idea that the therapy is associated with an increased risk of benign forms of sun-induced skin damage such as, but not limited to, actinic elastosis or liver spots.<ref name="Katz2012">Template:Cite journal</ref> Dead Sea balneotherapy is also effective for psoriatic arthritis.<ref name="Katz2012"/> 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.<ref>Template:Cite journal</ref> Glycerin is also an effective treatment for Psoriasis.<ref>Medical College of Georgia at Augusta University. "Glycerin is safe, effective in psoriasis model." ScienceDaily. [www.sciencedaily.com/releases/2021/10/211004104229.htm] (accessed 9 July 2023).</ref>
UV phototherapyEdit
Phototherapy in the form of sunlight has long been used for psoriasis.<ref name=Lancet07/> UVB wavelengths of 311–313 nanometers are most common. UV-B lamps have been developed for this treatment.<ref name=Lancet07/> The exposure time should be controlled to avoid overexposure and burning of the skin. The UVB lamps should have a timer that turns off the lamp when the time ends. The dose is increased in every treatment to let the skin get used to the light.<ref name=Lancet07/> Increased rates of cancer from treatment appear to be small.<ref name=Lancet07/> Narrowband UVB therapy has been demonstrated to have similar efficacy to psoralen and ultraviolet A phototherapy (PUVA).<ref name="Dogra2010"/> A 2013 meta-analysis found no difference in efficacy between NB-UVB and PUVA in the treatment of psoriasis, but NB-UVB is usually more convenient.<ref>Template:Cite journal</ref>
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.<ref name="radack">Template:Cite journal</ref>
UV light therapies all have risks; tanning beds are no exception, being listed by the World Health Organization as carcinogens.<ref>Template:Cite book</ref> Exposure to UV light is known to increase the risks of melanoma and squamous cell and basal cell carcinomas; younger people with psoriasis, particularly those under age 35, are at increased risk from melanoma from UV light treatment. A review of studies recommends that people who are susceptible to skin cancers exercise caution when using UV light therapy as a treatment.<ref name="radack" />
A major mechanism of NB-UVB is the induction of DNA damage in the form of pyrimidine 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.<ref name="Dogra2010">Template:Cite journal</ref> The activity of many types of immune cells found in the skin is also effectively suppressed by NB-UVB phototherapy treatments.<ref>Template:Cite journal</ref> The most common short-term side effect of this form of phototherapy is redness of the skin; less common side effects of NB-UVB phototherapy are itching and 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.<ref name="Dogra2010"/>
PUVA combines the oral or topical administration of psoralen with exposure to ultraviolet A (UVA) light. The mechanism of action of PUVA is unknown but probably involves activation of psoralen by UVA light, which inhibits the abnormally rapid production of 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).<ref name="Richard2013"/><ref name="Lapolla2011">Template:Cite journal</ref> 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.<ref name="Dunn2011">Template:Cite journal</ref>
Systemic agentsEdit
Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments.<ref name="Dogra2013">Template:Cite journal</ref> People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities.<ref name="Dogra2013"/> Pregnancy must be avoided for most of these treatments.Template:Medical citation needed The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.Template:Medical citation needed
Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids.<ref name="Rustin2012">Template:Cite journal</ref> 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.<ref name="Zattra2012"/> Oral corticosteroids should not be used as they can severely flare psoriasis upon their discontinuation.<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref>
Biologics are manufactured proteins that interrupt the immune process involved in psoriasis. Unlike generalized immunosuppressive medical therapies such as methotrexate, biologics target specific aspects of the immune system contributing to psoriasis.<ref name="Rustin2012"/> These medications are generally well-tolerated, and limited long-term outcome data have demonstrated biologics to be safe for long-term use in moderate to severe plaque psoriasis.<ref name="Rustin2012"/><ref name="Griffiths2012"/> However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.<ref name="Rustin2012"/>
Guidelines regard biologics as a third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.<ref name="Griffiths2012">Template:Cite journal</ref> 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.<ref name="Rustin2012"/>
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,<ref>Template:Cite journal</ref> have been developed against pro-inflammatory cytokines<ref>Template:Cite journal</ref> and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies.<ref name=Nestle/> IL-12 and IL-23 share a common domain, p40, which is the target of the FDA-approved ustekinumab.<ref name="Prieto2013">Template:Cite journal</ref> In 2017 the US FDA approved guselkumab for plaque psoriasis.<ref name=FDA-n-2017>Novel Drug Approvals for 2017 Template:Webarchive</ref> 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.<ref>Template:Cite journal</ref>
Two medications that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1.<ref name="Rustin2012"/> It also blocks the adhesion molecules on the endothelial cells that line blood vessels, which attract T cells. Efalizumab was voluntarily withdrawn from the European market in February 2009, and from the U.S. market in June 2009, by the manufacturer due to the medication's association with cases of progressive multifocal leukoencephalopathy.<ref name="Rustin2012"/> Alefacept also blocks the molecules that dendritic cells use to communicate with T cells and even causes natural killer cells to kill T cells as a way of controlling inflammation.<ref name=Nestle/> Apremilast may also be used.<ref name="Palfreeman2013"/>
Individuals with psoriasis may develop neutralizing antibodies against monoclonal antibodies. Neutralization occurs when an antidrug antibody prevents a monoclonal antibody such as infliximab from binding antigen in a laboratory test. Specifically, neutralization occurs when the anti-drug antibody binds to infliximab's antigen binding site instead of TNF-α. When infliximab no longer binds tumor necrosis factor alpha, it no longer decreases inflammation, and psoriasis may worsen. Neutralizing antibodies have not been reported against etanercept, a biologic medication that is a fusion protein composed of two TNF-α receptors. The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF-α receptor, and the development of immune tolerance.<ref>Template:Cite journal</ref>
There is strong evidence to indicate that infliximab, bimekizumab, ixekizumab, and risankizumab are the most effective biologics for treating moderate to severe cases of psoriasis.<ref name=":5">Template:Cite journal</ref> There is also some evidence to support use of secukinumab, brodalumab, guselkumab, certolizumab, and ustekinumab.<ref name="pmid26714681">Template:Cite journal</ref><ref name=":5" /> In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNF alpha biologics were found to be more effective than traditional systemic treatments.<ref name=":5" /> The immunologic pathways of psoriasis involve Th9, Th17, Th1 lymphocytes, and IL-22. The aforementioned biologic agents hinder different aspects of these pathways.Template:Citation needed
Another set of treatments for moderate to severe psoriasis are fumaric acid esters (FAE), which may be similar in effectiveness to methotrexate.<ref>Template:Cite journal</ref>
Apremilast (Otezla, Celgene) is an oral small-molecule inhibitor of the enzyme phosphodiesterase 4, which plays an important role in chronic inflammation associated with psoriasis.<ref>Template:Cite journal</ref>
It has been theorized that antistreptococcal medications may improve guttate and chronic plaque psoriasis; however, limited studies do not show that antibiotics are effective.<ref>Template:Cite journal</ref>
SurgeryEdit
Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.<ref name="Wu2014">Template:Cite journal</ref><ref>Template:Cite journal</ref>
DietEdit
Uncontrolled studies have suggested that individuals with psoriasis or psoriatic arthritis may benefit from a diet supplemented with fish oil rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).<ref name="Kaimal2010">Template:Cite journal</ref> A low-calorie diet appears to reduce the severity of psoriasis.<ref name=Shu2019/> Diet recommendations include consumption of cold water fish (preferably wild fish, not farmed) such as salmon, herring, and mackerel; extra virgin olive oil; legumes; vegetables; fruits; and whole grains; and avoid consumption of alcohol, red meat, and dairy products (due to their saturated fat). The effect of caffeine consumption (including from coffee, black tea, mate, and dark chocolate) remains to be determined.<ref name=BarreaNappi2016>Template:Cite journal</ref>
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.<ref name=AfifiDanesh2017>Template:Cite journal</ref>
There is a higher rate of celiac disease among people with psoriasis.<ref name=BarreaNappi2016 /><ref name=NiChiu2014>Template:Cite journal</ref> When adopting a gluten-free diet, disease severity generally decreases in people with celiac disease and those with anti-gliadin antibodies.<ref name="Kaimal2010"/><ref name=LefflerGreen2015>Template:Cite journal</ref><ref name=BhatiaMillsop2014>Template:Cite journal</ref>
PrognosisEdit
Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies.<ref name="Samarasekera2013"/> Depending on the severity and location of outbreaks, people may experience significant physical discomfort and some disability, affecting the person's quality of life.<ref name="Prieto2013" /> Itching and pain can interfere with basic functions, such as self-care and sleep.<ref name="Parrish2012" /> Participation in sporting activities, certain occupations, and caring for family members can become difficult activities for those with plaques located on their hands and feet.<ref name="Parrish2012" /> Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for dandruff.<ref name="Dessinioti2013">Template:Cite journal</ref>
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.<ref name=Menter2008 /> People with psoriasis often feel prejudiced against due to the commonly held incorrect belief that psoriasis is contagious.<ref name="Parrish2012">Template:Cite journal</ref> Psychological distress can lead to significant depression and social isolation; a high rate of thoughts about suicide has been associated with psoriasis.<ref name="Gelmetti2009"/> Many tools exist to measure the quality of life of people with psoriasis and other dermatological disorders. Clinical research has indicated individuals often experience a diminished quality of life.<ref name=Bhosle>Template:Cite journal</ref> Children with psoriasis may encounter bullying.<ref>Template:Cite journal</ref>
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.<ref name=Habif2010>Template:Cite book</ref>
Cardiovascular diseaseEdit
Psoriasis has been associated with obesity<ref name=Menter2008 /> 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.<ref name=Sh2014>Template:Cite journal</ref> Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis.<ref name=Sh2014/> Younger people with psoriasis may also be at increased risk for developing diabetes.<ref name=Habif2010 /> Individuals with psoriasis or psoriatic arthritis have a slightly higher risk of heart disease and heart attacks when compared to the general population. Cardiovascular disease risk appeared to be correlated with the severity of psoriasis and its duration. There is no strong evidence to suggest that psoriasis is associated with an increased risk of death from cardiovascular events. Methotrexate may provide a degree of protection for the heart.<ref name="Richard2013">Template:Cite journal</ref><ref name=Habif2010 />
The odds of having hypertension are 1.58 times Template:Nowrap 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 Template:Nowrap greater when compared to odds of the general population. The link between psoriasis and hypertension is not currentlyTemplate:When 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 Template:Nowrap higher in people with mild psoriasis and 1.63 times Template:Nowrap higher in people with severe psoriasis.<ref name="Tablazon2013"/> There may be a slightly increased risk of stroke associated with psoriasis, especially in severe cases.<ref name="Richard2013"/><ref>Template:Cite news</ref> 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.<ref name="Ghazizadeh2011">Template:Cite journal</ref> 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.<ref name="Ghazizadeh2011"/> Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome.<ref name="Raychaudhuri2014">Template:Cite journal</ref><ref name="Tablazon2013">Template:Cite journal</ref>
Other diseasesEdit
The rates of Crohn's disease and ulcerative colitis are increased when compared with the general population, by a factor of 3.8 and 7.5 respectively.<ref name=Menter2008 /> People with psoriasis also have a higher risk of celiac disease.<ref name=BarreaNappi2016 /><ref name=BhatiaMillsop2014 /> Few studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned.<ref name=Menter2008 /> Psoriasis has been associated with a 16% increase in overall relative risk for non-skin cancer, thought to be attributed to systemic therapy, particularly methotrexate.<ref name="Richard2013"/> People treated with long-term systemic therapy for psoriasis have a 52% increased risk 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.<ref name="Richard2013"/> 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%.<ref name="Richard2013"/> There is no increased risk of melanoma associated with psoriasis.<ref name="Richard2013"/> People with psoriasis have a higher risk of developing cancer.<ref>Template:Cite journal
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EpidemiologyEdit
Psoriasis is estimated to affect 2–4% of the population of the western world.<ref name="Parisi2013" /> The rate of psoriasis varies according to age, region and ethnicity; a combination of environmental and genetic factors is thought to be responsible for these differences.<ref name=Parisi2013/> Psoriasis is about five times more common in people of European descent than in people of Asian descent,<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> more common in countries farther from the equator,<ref name="Guerra2013" /> relatively uncommon in African Americans, and extremely uncommon in Native Americans.<ref name="Weller2008" /> Psoriasis has been estimated to affect about 6.7Template:Spacesmillion Americans.<ref name="NIH2015" />
Psoriasis can occur at any age, although it is more frequent in adults and commonly appears for the first time between the ages of 15 and 25 years.<ref name="NIH2015" /> Approximately one-third of people with psoriasis report being diagnosed before age 20.<ref>Template:Cite journal</ref> Psoriasis affects both sexes equally.<ref name="Kupetsky2013">Template:Cite journal</ref>
People with inflammatory bowel disease such as Crohn's disease or ulcerative colitis are at an increased risk of developing psoriasis.<ref name="Guerra2013" />
HistoryEdit
Scholars believe psoriasis to have been included among the various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible.<ref>E. V. Hulse, "The Nature of Biblical 'Leprosy' and the Use of Alternative Medical Terms in Modern Translations of the Bible," Palestine Exploration Quarterly 107.2 (1975): 87-105.</ref> The person was deemed "impure" (see tumah and taharah) during their affected phase and is ultimately treated by the kohen.<ref name="Gruber2004">Template:Cite journal</ref> However, it is more likely that this confusion arose from the use of the same Greek term for both conditions. The Greeks used the term Template:Transliteration ({{#invoke:Lang|lang}}) for scaly skin conditions. They used the term Template:Transliteration ({{#invoke:Lang|lang}}) to describe itchy skin conditions.<ref name="Gruber2004"/> 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: {{#invoke:Lang|lang}} and {{#invoke:Lang|lang}}.<ref>Template:Cite journal</ref>
Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus.<ref name="Benedek2013"/> The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813.<ref name="Benedek2013">Template:Cite journal</ref> 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.<ref name="Gruber2004"/> Mercury was also used for psoriasis treatment during this time.<ref name="Gruber2004"/> Sulfur, iodine, and phenol were also commonly used treatments for psoriasis during this era when it was incorrectly believed that psoriasis was an infectious disease.<ref name="Gruber2004"/> Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s.<ref name="Gruber2004"/><ref name="Benedek2013 Part 2"/> During the same time, psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis.<ref name="Benedek2013 Part 2">Template:Cite journal</ref>
Society and cultureEdit
The International Federation of Psoriasis Associations (IFPA) is the global umbrella organization for national and regional psoriasis associations and also gathers the leading experts in psoriasis and psoriatic arthritis research for scientific conferences every three years.<ref>International Federation of Psoriasis Associations Template:Webarchive. Ifpa-pso.org. Retrieved on 8 June 2013.</ref> 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<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</ref> and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries.
CostEdit
The annual cost of treating psoriasis in the United States is estimated as high as $32.5Template:Spacesbillion, including $12.2Template:Spacesbillion 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.<ref>Template:Cite journal</ref>
ResearchEdit
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.<ref name="Dubois2013"/>
Many novel medications being researched during the 2010s target the Th17/IL-23 axis,<ref name="Dubois2013"/> particularly IL-23p19 inhibitors, as IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections.<ref name=Patel2012>Template:Cite journal</ref> 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.<ref name=Patel2012 /> Another avenue of research has focused on the use of vascular endothelial growth factor inhibitors to treat psoriasis.<ref name="Weidemann2013"/> Oral agents being investigated during the 2010s as alternatives to medications administered by injection include Janus kinase 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.<ref name="Dubois2013">Template:Cite journal</ref><ref name=Patel2012/> These agents have potentially severe side-effects due to their immunosuppressive mechanisms.<ref name=Patel2012/>
ReferencesEdit
Further readingEdit
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External linksEdit
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