Psoriasis

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Psoriasis
Back and arms of a person with severe psoriasis
Pronunciation	/səˈraɪəsɪs,ps-,sɒ-,sɔː-,soʊ-/ [1] [2]
Specialty	Dermatology (primarily); immunology, rheumatology and other specialties (e.g., cardiology and vascular medicine, nephrology, hepatology/gastroenterology, endocrinology, hematology) (indirectly/by association)
Symptoms	Red (purple on darker skin), itchy, scaly patches of skin[3]
Complications	Psoriatic arthritis [4]
Usual onset	Adulthood[5]
Duration	Long-term[4]
Causes	Genetic disease triggered by environmental factors[3]
Diagnostic method	Based on symptoms[4]
Treatment	Steroid creams, vitamin D3 cream, ultraviolet light, immunosuppressive drugs such as methotrexate and biologics [5]
Frequency	79.7 million[6] / 2–4%[7]

Psoriasis is a long-lasting, noncontagious autoimmune disease characterized by patches of abnormal skin.^{[4] [5]} These areas are red, pink, or purple, dry, itchy, and scaly.^{[3] [8]} Psoriasis varies in severity from small localized patches to complete body coverage.^[3] Injury to the skin can trigger psoriatic skin changes at that spot, which is known as the Koebner phenomenon.^[9]

The five main types of psoriasis are plaque, guttate, inverse, pustular, and erythrodermic.^[5] Plaque psoriasis, also known as psoriasis vulgaris, makes up about 90% of cases.^[4] It typically presents as red patches with white scales on top.^[4] Areas of the body most commonly affected are the back of the forearms, shins, navel area, and scalp.^[4] Guttate psoriasis has drop-shaped lesions.^[5] Pustular psoriasis presents as small, noninfectious, pus-filled blisters.^[10] Inverse psoriasis forms red patches in skin folds.^[5] Erythrodermic psoriasis occurs when the rash becomes very widespread and can develop from any of the other types.^[4] Fingernails and toenails are affected in most people with psoriasis at some point in time.^[4] This may include pits in the nails or changes in nail color.^[4]

Psoriasis is generally thought to be a genetic disease that is triggered by environmental factors.^[3] 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.^[4] This suggests that genetic factors predispose to psoriasis.^[4] Symptoms often worsen during winter and with certain medications, such as beta blockers or NSAIDs.^[4] Infections and psychological stress can also play a role.^{[3] [5]} The underlying mechanism involves the immune system reacting to skin cells.^[4] Diagnosis is typically based on the signs and symptoms.^[4]

There is no known cure for psoriasis, but various treatments can help control the symptoms.^[4] These treatments include steroid creams, vitamin D₃ cream, ultraviolet light, immunosuppressive drugs, such as methotrexate, and biologic therapies targeting specific immunologic pathways.^[5] About 75% of skin involvement improves with creams alone.^[4] The disease affects 2–4% of the population.^[7] Men and women are affected with equal frequency.^[5] The disease may begin at any age, but typically starts in adulthood.^[5] Psoriasis is associated with an increased risk of psoriatic arthritis, lymphomas, cardiovascular disease, Crohn's disease, and depression.^[4] Psoriatic arthritis affects up to 30% of individuals with psoriasis.^[10]

The word "psoriasis" is from Greek ψωρίασις meaning 'itching condition' or 'being itchy',^[11] from psora 'itch', and -iasis 'action, condition'.

Psoriasis causes patches of skin to become raised, red, and scaly. These areas can itch, burn, or feel sore, and they may crack or bleed. Some people have only a few small patches, while others have more widespread symptoms that can affect daily activities and sleep.

Psoriasis causes areas of skin to grow and shed faster than usual, forming thick, scaly patches that can itch or hurt. These patches most often appear on the elbows, knees, scalp, and lower back, but any skin surface can be affected. Symptoms may come and go, with periods of flare and remission.

Psoriatic erythroderma involves redness, scaling, and shedding over most of the body (often more than 90% of the skin). The skin can be extremely dry, itchy, swollen, and painful. This form can be life-threatening because severe inflammation interferes with temperature control and the skin's barrier function. It may result from sudden withdrawal of systemic glucocorticoids or a flare of unstable plaque psoriasis.^{[12] [13] [14]}

Guttate psoriasis presents with many small, drop-like pink or red spots with fine scale. These appear mainly on the trunk, limbs, and scalp, and usually spare the palms and soles. It often develops 1–3 weeks after a streptococcal infection and is most common in children and young adults.^[15] Most cases improve within weeks, although up to 40% later develop plaque psoriasis.^{[15] [16]}

Inverse psoriasis causes smooth, red, irritated patches in skin folds, such as the armpits, groin, under the breasts, and between the buttocks. Heat, friction, and infection can make symptoms worse.^[16]

Psoriasis vulgaris (plaque psoriasis) is the most common form, affecting about 85–90% of people with psoriasis.^{[17] [18]} It appears as raised, red patches covered with a silvery-white scale. Common sites include the elbows, knees, scalp, and back.^[17]

• Multiple plaques on the elbow
  Multiple plaques on the elbow
• Plaque psoriasis on the arm
  Plaque psoriasis on the arm
• Plaque psoriasis on the palms
  Plaque psoriasis on the palms
• Plaque psoriasis on the scalp
  Plaque psoriasis on the scalp

Pustular psoriasis causes raised bumps filled with non-infectious pus (pustules). The surrounding skin is red and tender. It may be limited to the hands and feet (psoriasis pustulosa palmoplantaris, acrodermatitis continua of Hallopeau) or affect larger areas of the body.^{[19] [20] [12]}

Seborrheic-like psoriasis shares features of psoriasis and seborrheic dermatitis. It usually causes red plaques with greasy scale on the scalp, forehead, sides of the nose, around the mouth, over the sternum, and in skin folds.^[21]

Oral psoriasis is rare. When it occurs, it may appear as white or grey-yellow plaques or be symptom-free. Fissured tongue is the most common oral finding. Geographic tongue has a similar microscopic appearance and may be associated with psoriasis.^[22]

Nail psoriasis can cause tiny pits in the nail surface, white spots, dark streaks from bleeding, yellow-red "oil-drop" discoloration, thickening under the nail, separation (onycholysis), or crumbling. Nail changes occur in about 40–45% of people with skin psoriasis and in most people with psoriatic arthritis.^[23]

Napkin psoriasis affects infants under two, causing red areas with silvery scale in the diaper region, sometimes spreading to the torso or limbs. It is often mistaken for diaper rash. Symptoms usually improve with age, although some children later develop plaque psoriasis or inverse psoriasis.^{[21] [24] [25]}

Localized pustular psoriasis and plaque psoriasis may affect the palms and soles, causing cracking, soreness, and difficulty with daily tasks.^[12]

Psoriatic arthritis is an inflammatory arthritis linked to psoriasis. It often causes painful, swollen joints in the fingers and toes, producing "sausage-like" swelling (dactylitis). Larger joints and the spine may also be involved. About 30% of people with psoriasis develop psoriatic arthritis, usually after the skin disease appears.^{[26] [27] [28] [17]}

Clinicians may look for:

• Auspitz's sign – pinpoint bleeding when scale is gently lifted
• Koebner phenomenon – new lesions where skin has been injured^[21]
• Itch, soreness, or pain in plaques and papules.^{[16] [21]}

The cause of psoriasis is not fully understood. It is considered a chronic, immune-mediated condition in which genetic susceptibility interacts with environmental and immunological triggers. Factors associated with the onset or worsening of psoriasis include inherited variation in immune-related genes, seasonal and climate changes, skin injury, infections, an immunocompromised state, obesity, and the use of certain medications.^{[29] [30] [31] [32]}

Around one-third of people with psoriasis report a family history of the disease, and multiple genetic loci associated with the condition have been identified. Twin studies consistently show higher concordance for psoriasis in monozygotic twins than in dizygotic twins, with estimates generally ranging from 35–70% for monozygotic pairs and 12–30% for dizygotic pairs, depending on the population studied.^{[33] [31]}

Psoriasis has a strong hereditary component, and many genes are associated with it, although how these genes act together is not fully clear. Most identified genes relate to the immune system, particularly the major histocompatibility complex (MHC) and T cells. Genetic research helps to identify molecular mechanisms and pathways that may be targeted by medications.^{[30] [34]}

Classic genome-wide linkage analysis has identified at least nine loci (PSORS1 through PSORS9) associated with psoriasis.^[30] Genome-wide association scans have identified additional susceptibility loci, several encoding inflammatory signal proteins that regulate immune cells involved in psoriasis. Some of these genes are also implicated in other autoimmune diseases.^{[30] [34]}

The major determinant is PSORS1, which probably accounts for 35–50% of psoriasis heritability.^[35] This locus contains genes that influence immune function or encode skin proteins overexpressed in psoriasis. Three genes within PSORS1 have shown strong association with psoriasis vulgaris: HLA-C variant HLA-Cw6,^[29] encoding an MHC class I protein; CCHCR1 , variant WWC, encoding a coiled coil protein overexpressed in psoriatic epidermis; and CDSN , variant allele 5, encoding corneodesmosin.^[30]

Two immune-related genes strongly linked with psoriasis are interleukin-12 subunit beta (IL12B) on chromosome 5q and IL23R on chromosome 1p, which encodes the interleukin-23 receptor. These variants contribute to pathways leading to tumour necrosis factor α and nuclear factor κB activation.^{[29] [34] [30]}

The first gene directly linked to psoriasis by sequencing was CARD14 , located in the PSORS2 locus. Rare mutations in the gene, together with environmental triggers, were sufficient to cause plaque psoriasis in affected families.^{[36] [37]}

Estimates of psoriasis prevalence in people living with human immunodeficiency virus (HIV) vary among studies; some report rates similar to the general population, while others suggest slightly higher or lower rates. The condition is, however, consistently described as more severe in individuals with HIV.^{[38] [39]} A higher rate of psoriatic arthritis has also been reported in HIV-positive individuals.^[38]

The immune response in HIV infection is often characterized by cellular signals from the T_h2 subset of CD4+ T cells,^[40] whereas psoriasis vulgaris is associated with signals typical of T_h1 and T_h17 pathways.^{[41] [42]} Reduced CD4+ T cell numbers in advanced HIV may lead to relative overactivation of CD8+ T cells, potentially contributing to psoriasis flares.^{[40] [39]} Psoriasis in those with HIV/AIDS can be severe and is often challenging to manage with conventional therapies.^[43]

Conditions reported as worsening psoriasis include chronic infections, psychological stress, and seasonal or climate-related changes.^{[29] [32]} Other factors associated with flares include exposure to very hot water, scratching existing lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity.^{[29] [44] [45] [46]} Weight reduction in people with obesity may modestly improve psoriasis severity, although high-quality trials examining smoking cessation or reduced alcohol intake as specific psoriasis treatments remain limited.^{[46] [32]}

Drug-induced or drug-triggered psoriasis has been reported with several medication classes, including beta blockers,^[10] lithium,^[10] antimalarial medications,^[10] nonsteroidal anti-inflammatory drugs (NSAIDs),^[10] terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor,^[10] certain interleukins and interferons,^[10] and some lipid-lowering medications.^{[47] : 197} TNF inhibitors such as infliximab and adalimumab can paradoxically induce psoriasiform eruptions.^[48] Withdrawal of corticosteroids—especially abrupt cessation of potent topical steroids—can worsen psoriasis through a rebound effect.^[49]

Psoriasis may occur or flare after infections, particularly of the upper respiratory tract. It has been associated with strep throat and may be worsened by colonisation with microorganisms such as Staphylococcus aureus , Malassezia species, and Candida albicans , although the clinical significance of these associations remains uncertain.^[50] Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection such as tonsillitis or pharyngitis.^[12]

Altered skin and gut microbiota have been observed in people with psoriasis and psoriatic arthritis and may contribute to immune dysregulation in genetically susceptible individuals, although causal relationships remain under investigation.^{[51] [32]}

Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin.^[52] Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis.^[20] 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.^{[30] [12]} Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days.^[53] 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).^{[17] [38]} 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.^{[30] [54]} These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate.^[30] One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.^[30] 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.^[12]

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.^{[55] [56]}

Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis^[57] and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α.^[57] 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.^[30]

Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions^[52] 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.^{[30] [41]} Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17.^[58] Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22.^{[52] [58]} Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.^[58]

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.^[16] No special blood tests or diagnostic procedures are usually required to make the diagnosis.^[20]

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).^[49] Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.^[49]

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.^{[20] [60]} 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.^[20] 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.^[20]

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.^{[3] [10]} Variants include plaque, pustular, guttate, and flexural psoriasis. Each form has a dedicated ICD-10 code.^[61] Psoriasis can also be classified into nonpustular and pustular types.^[62]

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.^[63] Type 1 accounts for about 75% of persons with psoriasis.^[64]

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^{[20] [29] [65]} while others have classified them as distinct from autoimmune diseases and referred to them as immune-mediated inflammatory diseases.^{[30] [66] [67]}

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.^[68] Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.^[68]

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.^[69]

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).^[70] 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.^[71]

Psoriasis is not just a skin disease. The symptoms of psoriasis can sometimes go beyond the skin and can hurt the quality of life of the affected individuals.^[72] Additionally, the co-morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition.^[72]

There is a 2.2 times increased risk of cardiovascular complications in people with psoriasis.^[73] Also, people with psoriasis are more susceptible to myocardial infarction (heart attack) and stroke.^[73] It has been speculated that there is systemic inflammation in psoriasis, which drives "psoriatic march" and can cause other inflammatory complications including cardiovascular complications.^[73] 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.^[74]

Depression or depressive symptoms are present in 28–55% of people with psoriasis.^[75] 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 the observed increased incidence of depression in people with psoriasis.^[75] There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases, including psoriasis.^[75]

People with psoriasis are at increased risk of developing type 2 diabetes (~1.5 odds ratio).^[76] A genome-wide genetic study found that psoriasis and type 2 diabetes share four loci, namely, ACTR2, ERLIN1, TRMT112, and BECN1, which are connected via the inflammatory NF-κB pathway.^[76]

Psoriasis treatment aims to manage symptoms, clear plaques, and prevent flare-ups. Approaches range from creams and light therapy to oral and injectable medicines, depending on severity.^[49]

There is no cure for psoriasis, but many effective treatments can control it. Typically, topical therapies are used for mild disease, phototherapy for moderate cases, and oral or injectable medicines (systemic treatments) for severe or resistant forms.^[77] For guttate psoriasis, evidence for these standard options is limited.^[78]

Creams, ointments, and lotions are the first step for most people with psoriasis. They reduce redness and itching, slow rapid skin-cell growth, and help soften thick scales.

Topical corticosteroids are the most effective short-term option for calming inflammation and itch. Stronger products should only be used for limited periods to avoid thinning the skin.^{[79] [80]} Synthetic forms of vitamin D such as calcipotriol and calcitriol help slow overactive cell growth and often work best when combined with steroid creams.^{[81] [82]}

Two newer prescription creams—tapinarof (an aryl-hydrocarbon-receptor modulator) and roflumilast (a phosphodiesterase-4 inhibitor)—were approved in 2022. Both reduce inflammation and can be used on sensitive skin areas such as the face or body folds.^{[83] [84]}

Regular use of moisturizers—such as petroleum jelly, mineral oil, or thick creams—reduces dryness and helps other medicines work better. Bathing in salt water (for example, the Dead Sea) combined with gradual sunlight exposure can improve plaques for several months, with only mild side effects such as itch or sunburn.^{[85] [86]}

Controlled exposure to ultraviolet (UV) light slows the overgrowth of skin cells and reduces inflammation. Narrow-band UVB (311–313 nm) is the standard medical form, and supervised use carries a low cancer risk.^[77]

Home phototherapy units can be as effective as clinic treatment, though mild redness is more common.^[87] A focused 308-nm excimer laser can target small, stubborn plaques. PUVA (a light-sensitizing medicine plus UVA light) is also effective but may cause nausea, itching, or fatigue, and long-term use can increase the risk of squamous cell carcinoma.^{[88] [89]}

Systemic treatments are used when psoriasis is widespread or unresponsive to creams and light therapy. They act throughout the body and require periodic blood tests to check for side effects.^[90]

Common choices include methotrexate, ciclosporin, dimethyl fumarate, and retinoids. These medicines suppress overactive immune responses or slow rapid cell growth.^[91] Corticosteroid tablets are avoided because stopping them suddenly can cause severe flare-ups.^[92]

Apremilast is a tablet that blocks the PDE-4 enzyme linked to inflammation.^[93] Deucravacitinib, approved in 2022, targets TYK2, an enzyme in the same immune pathway, and is taken once daily.^[94] Fumaric acid esters have similar overall effectiveness to methotrexate.^[95]

Biologic drugs are engineered proteins that block specific immune signals driving psoriasis. They are given by injection or infusion and generally well tolerated.^[96] They are used when topical, light, and oral treatments have not worked.^[96]

Main biologic classes

• **TNF-α inhibitors** – adalimumab, etanercept, infliximab
• **IL-17 inhibitors** – secukinumab, ixekizumab, bimekizumab
• **IL-12/23 inhibitor** – ustekinumab
• **IL-23 inhibitors** – guselkumab, risankizumab, tildrakizumab

Biologics that target IL-17 or IL-23 often produce the highest rates of skin clearance in clinical studies.^[97] In 2022, spesolimab became the first approved treatment for flares of generalized pustular psoriasis.^[98]

People using systemic treatments are screened for infections such as tuberculosis or hepatitis before starting therapy. Non-live vaccines can usually be given without interrupting treatment; live vaccines are scheduled around the medicine's clearance time.^[99] Among biologics, certolizumab pegol has the best data for use during pregnancy because very little crosses the placenta.^[100] Biosimilar and interchangeable versions of biologics—especially adalimumab—offer lower-cost but equally effective alternatives.^[101]

In selected cases, removing the tonsils has improved chronic plaque or guttate psoriasis and palmoplantar pustulosis, possibly by reducing immune triggers.^{[102] [103]}

Diet can influence psoriasis severity. Low-calorie and Mediterranean-style eating patterns—featuring fish, olive oil, vegetables, fruit, and whole grains—are linked with fewer flare-ups.^{[104] [105]} People with celiac disease or antibodies to gluten often improve on a gluten-free diet.^[106] Omega-3 fatty acids from fish oil may help reduce inflammation in skin and joints.^[104] Limiting alcohol, red meat, and sugary foods may support other treatments, though research is ongoing.^[107]

Modern care often follows a "treat-to-target" strategy—aiming for clear or almost clear skin, usually defined as 90 % improvement or less than 1 % of body surface area affected within three months. If this goal is not reached, therapy is adjusted or changed.^[108]

• See also: List of biologic therapies for psoriasis*

Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies.^[79] Depending on the severity and location of outbreaks, people may experience significant physical discomfort and some disability, affecting the person's quality of life.^[29] Itching and pain can interfere with basic functions, such as self-care and sleep.^[53] 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.^[53] Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for dandruff.^[109]

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.^[3] People with psoriasis often feel prejudiced against due to the commonly held incorrect belief that psoriasis is contagious.^[53] Psychological distress can lead to significant depression and social isolation; a high rate of thoughts about suicide has been associated with psoriasis.^[25] Many tools exist to measure the quality of life of people with psoriasis and other dermatological disorders. Clinical research has indicated that individuals often experience a diminished quality of life.^[110] Children with psoriasis may encounter bullying.^[111]

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.^[112]

Psoriasis has been associated with obesity ^[3] 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.^[113] Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis.^[113] Younger people with psoriasis may also be at increased risk for developing diabetes.^[112] 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.^{[45] [112]}

The odds of having hypertension are 1.58 times ( 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 ( i.e., 107%) greater when compared to the odds of the general population. The link between psoriasis and hypertension is not currently^{[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 ( i.e. 31%) higher in people with mild psoriasis and 1.63 times ( i.e. 63%) higher in people with severe psoriasis.^[114] There may be a slightly increased risk of stroke associated with psoriasis, especially in severe cases.^{[45] [115]} 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.^[116] 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.^[116] Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome.^{[20] [114]}

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.^[3] People with psoriasis also have a higher risk of celiac disease.^{[105] [106]} Few studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned.^[3] 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.^[45] 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.^[45] The risk for the 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%.^[45] There is no increased risk of melanoma associated with psoriasis.^[45] People with psoriasis have a higher risk of developing cancer.^[117]

Psoriasis is estimated to affect 2–4% of the population of the Western world.^[7] 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.^[7] Psoriasis is about five times more common in people of European descent than in people of Asian descent,^[118] more common in countries farther from the equator,^[48] relatively uncommon in African Americans, and extremely uncommon in Native Americans.^[49] Psoriasis has been estimated to affect about 6.7 million Americans.^[5]

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.^[5] Approximately one-third of people with psoriasis report being diagnosed before age 20.^[119] Psoriasis affects both sexes equally.^[63]

People with inflammatory bowel disease, such as Crohn's disease or ulcerative colitis, are at an increased risk of developing psoriasis.^[48]

Scholars believe psoriasis to have been included among the various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible.^[120] The person was deemed "impure" (see tumah and taharah) during their affected phase and is ultimately treated by the kohen.^[121] 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 lepra (λέπρα) for scaly skin conditions. They used the term psora (ψώρα) to describe itchy skin conditions.^[121] 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: leprosa graecorum and psora leprosa.^[122]

Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus.^[123] The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813.^[123] 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.^[121] Mercury was also used for psoriasis treatment during this time.^[121] 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.^[121] Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s.^{[121] [124]} During the same time, psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis.^[124]

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.^[125] 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^[126] and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries. October 29 is World Psoriasis Day^[127] .

The annual cost of treating psoriasis in the United States is estimated as high as 32ドル.5 billion, including 12ドル.2 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ドル per person per year.^[128]

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.^[129]

Many novel medications being researched during the 2010s target the Th17/IL-23 axis,^[129] particularly IL-23p19 inhibitors, as IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections.^[130] 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.^[130] Another avenue of research has focused on the use of vascular endothelial growth factor inhibitors to treat psoriasis.^[65] 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.^{[129] [130]} These agents have potentially severe side-effects due to their immunosuppressive mechanisms.^[130]

• "Psoriatic arthritis". Genetics Home Reference.
• "Psoriasis". MedlinePlus. U.S. National Library of Medicine.

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