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Wikipedia

Psoriasis

January 09, 2024

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.[8][3] 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]

Psoriasis
Back and arms of a person with psoriasis
Pronunciation
SpecialtyDermatology (primarily);
immunology, rheumatology and other specialties (e.g., cardiology and vascular medicine, nephrology, hepatology/gastroenterology, endocrinology, haematology) (indirectly/by association)
SymptomsRed (purple on darker skin), itchy, scaly patches of skin[3]
ComplicationsPsoriatic arthritis[4]
Usual onsetAdulthood[5]
DurationLong-term[4]
CausesGenetic disease triggered by environmental factors[3]
Diagnostic methodBased on symptoms[4]
TreatmentSteroid creams, vitamin D3 cream, ultraviolet light, immunosuppressive drugs such as methotrexate and biologics[5]
Frequency79.7 million[6] / 2–4%[7]

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".

Signs and symptoms edit

Plaque psoriasis edit

 
Psoriatic plaque, showing a silvery center surrounded by a reddened border

Psoriasis vulgaris (also known as chronic stationary psoriasis or plaque-like psoriasis) is the most common form and affects 85–90% of people with psoriasis.[12] 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.[12][13]

  •  
    Plaques of psoriasis
  •  
    A person's arm covered with plaque psoriasis
  •  
    Psoriasis of the palms

Other forms edit

Additional types of psoriasis comprise about 10% of cases. They include pustular, inverse, napkin, guttate, oral, and seborrheic-like forms.[14]

Pustular psoriasis edit

 
Severe generalized pustular psoriasis

Pustular psoriasis appears as raised bumps filled with noninfectious pus (pustules).[15] The skin under and surrounding the pustules is red and tender.[16] 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.[17]

Inverse psoriasis edit

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.[18]

Napkin psoriasis edit

Napkin psoriasis is a subtype of psoriasis common in infants characterized by red papules with silver scale in the diaper area that may extend to the torso or limbs.[19] Napkin psoriasis is often misdiagnosed as napkin dermatitis (diaper rash).[20]

Guttate psoriasis edit

 
Example of guttate psoriasis

Guttate psoriasis is an inflammatory condition characterized by numerous small, scaly, red or pink, droplet-like lesions (papules). These numerous papules appear over large areas of the body, primarily the trunk, limbs, and scalp, but typically spares 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.[21] Skin biopsy can also be performed which typically shows a psoriasiform reaction pattern characterized by epidermal hyperplasia and rate ridge prolongation.[21]

There is no firm evidence regarding best management for guttate psoriasis; however, first line therapy for mild guttate psoriasis typically includes topical corticosteroids.[21][22] Phototherapy can be used for moderate or severe guttate psoriasis. Biologic treatments have not been well studied in the treatment of guttate psoriasis.[21]

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.[21][18]

Erythrodermic psoriasis edit

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.[17] It may be accompanied by severe dryness, itching, swelling, and pain. It can develop from any type of psoriasis.[17] It is often the result of an exacerbation of unstable plaque psoriasis, particularly following the abrupt withdrawal of systemic glucocorticoids.[23] 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.[24]

Mouth edit

Psoriasis in the mouth is very rare, in contrast to lichen planus, another common papulosquamous disorder that commonly involves both the skin and mouth.[25] When psoriasis involves the oral mucosa (the lining of the mouth), it may be asymptomatic,[25] but it may appear as white or grey-yellow plaques.[25] 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.[26] However, modern studies have failed to demonstrate any link between the two conditions.[27]

Seborrheic-like psoriasis edit

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.[19]

Psoriatic arthritis edit

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.[28][29] 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.[28] Psoriatic arthritis can also affect the hips, knees, spine (spondylitis), and sacroiliac joint (sacroiliitis).[30] About 30% of individuals with psoriasis will develop psoriatic arthritis.[12] Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75% of cases.[29]

Nail changes edit

 
Psoriasis of a fingernail, with visible pitting
 
Effect of psoriasis on the toenails

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.[31] 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.[31]

Medical signs edit

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 scale is removed), Koebner phenomenon (psoriatic skin lesions induced by trauma to the skin),[19] and itching and pain localized to papules and plaques.[18][19]

Causes edit

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.[32][33]

Genetics edit

See also: List of human leukocyte antigen alleles associated with cutaneous conditions

Around one-third of people with psoriasis report a family history of the disease, and researchers have identified genetic loci associated with the condition. Identical twin studies suggest a 70% chance of a twin developing psoriasis if the other twin has the disorder. The risk is around 20% for fraternal twins. These findings suggest both a genetic susceptibility and an environmental response in developing psoriasis.[34]

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.[35]

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.[35] 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.[35]

The major determinant is PSORS1, which probably accounts for 35–50% of psoriasis heritability.[36] 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,[32] 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.[35]

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.[32] T cells are involved in the inflammatory process that leads to psoriasis.[35] These genes are on the pathway that upregulate tumor necrosis factor-α and nuclear factor κB, two genes involved in inflammation.[35] 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).[37][38]

Lifestyle edit

Conditions reported as worsening the disease include chronic infections, stress, and changes in season and climate.[32] Others factors that might worsen the condition include hot water, scratching psoriasis skin lesions, skin dryness, excessive alcohol consumption, cigarette smoking, and obesity.[32][39][40][41] The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019.[41]

HIV edit

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.[42] A much higher rate of psoriatic arthritis occurs in HIV-positive individuals with psoriasis than in those without the infection.[42] The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells,[43] 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.[44][45] The diminished CD4+-T cell presence is thought to cause an 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.[46] In those with long-term, well-controlled psoriasis, new HIV infection can trigger a severe flare-up of psoriasis and/or psoriatic arthritis.[medical citation needed]

Microbes edit

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.[33] Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection (tonsillitis or pharyngitis).[17]

Medications edit

Drug-induced psoriasis may occur with beta blockers,[10] lithium,[10] antimalarial medications,[10] nonsteroidal anti-inflammatory drugs,[10] terbinafine, calcium channel blockers, captopril, glyburide, granulocyte colony-stimulating factor,[10] interleukins, interferons,[10] lipid-lowering medications,[14]: 197  and paradoxically TNF inhibitors such as infliximab or adalimumab.[47] Withdrawal of corticosteroids (topical steroid cream) can aggravate psoriasis due to the rebound effect.[48]

Pathophysiology edit

Psoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin.[49] Abnormal production of skin cells (especially during wound repair) and an overabundance of skin cells result from the sequence of pathological events in psoriasis.[16] 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.[35][17] Skin cells are replaced every 3–5 days in psoriasis rather than the usual 28–30 days.[50] 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 white blood cells).[12][42] 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.[35][51] These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate.[35] One hypothesis is that psoriasis involves a defect in regulatory T cells, and in the regulatory cytokine interleukin-10.[35] 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.[17]

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.[52][53]

Deoxyribonucleic acid (DNA) released from dying cells acts as an inflammatory stimulus in psoriasis[54] and stimulates the receptors on certain dendritic cells, which in turn produce the cytokine interferon-α.[54] 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.[35]

Dendritic cells bridge the innate immune system and adaptive immune system. They are increased in psoriatic lesions[49] 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 T22 cell cytokine secretion pattern over a Th1/Th17 cell cytokine profile.[35][44] Psoriatic T cells move from the dermis into the epidermis and secrete interferon-γ and interleukin-17.[55] Interleukin-23 is known to induce the production of interleukin-17 and interleukin-22.[49][55] Interleukin-22 works in combination with interleukin-17 to induce keratinocytes to secrete neutrophil-attracting cytokines.[55]

Diagnosis edit

 
Micrograph of psoriasis vulgaris. Confluent parakeratosis, psoriasiform epidermal hyperplasia [(A), EH], hypogranulosis, and influx of numerous neutrophils in the corneal layer [(A), arrow]. (B) Transepidermal migration of neutrophils from the dermis to the corneal layer (arrows).[56]

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.[18] No special blood tests or diagnostic procedures are usually required to make the diagnosis.[16][57]

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).[48] Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis.[48]

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.[16][58] 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.[16] 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 the joints.[16]

Classification edit

Morphological edit

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.[59] Psoriasis can also be classified into nonpustular and pustular types.[60]

Pathogenetic edit

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.[61] Type 1 accounts for about 75% of persons with psoriasis.[62]

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[16][32][63] while others have classified them as distinct from autoimmune diseases and referred to them as immune-mediated inflammatory diseases.[35][64][65]

Severity edit

 
Distribution of severity

No consensus exists about how to classify the severity of psoriasis. Mild psoriasis has been defined as a percentage of body surface area (BSA)≤10, a Psoriasis Area and Severity Index (PASI) score ≤10, and a Dermatology Life Quality Index (DLQI) score ≤10.[66] Moderate to severe psoriasis was defined by the same group as BSA >10 or PASI score >10 and a DLQI score >10.[66]

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.[67]

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).[68] 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.[69]

Co-morbidities edit

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.[70] Additionally, the co-morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition.[70]

Cardiovascular complications edit

There is 2.2 times increased risk of cardiovascular complications in people with psoriasis.[71] Also, people with psoriasis are more susceptible to myocardial infarction (heart attack) and stroke.[71] It has been speculated that there is systemic inflammation in psoriasis, which drives “psoriatic march” and can cause other inflammatory complications including cardiovascular complications.[71] 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 11% reduction in aortic vascular inflammation when there is 75% reduction in PASI score.[72]

Depression edit

Depression or depressive symptoms are present in 28–55% of people with psoriasis.[73] 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.[73] There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases, including psoriasis.[73]

Type 2 diabetes edit

People with psoriasis are at increased risk of developing type 2 diabetes (~1.5 odds ratio).[74] A genome-wide based genetic study found that psoriasis and type 2 diabetes share four loci, namely, ACTR2, ERLIN1, TRMT112, and BECN1, which are connected via inflammatory NFkB pathway.[74]

Management edit

 
Schematic of psoriasis treatment ladder

While no cure is available for psoriasis,[48] many treatment options exist. Topical agents are typically used for mild disease, phototherapy for moderate disease, and systemic agents for severe disease.[75] 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.[76]

Topical agents edit

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.[77] 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.[78]

Vitamin D analogues such as paricalcitol are superior to placebo. Combination therapy with vitamin D and a corticosteroid are superior to either treatment alone and vitamin D is superior to coal tar for chronic plaque psoriasis.[79]

For psoriasis of the scalp, a 2016 review found dual therapy (vitamin D analogues and topical corticosteroids) or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogues alone.[80] 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.[80]

Moisturizers and emollients such as mineral oil, petroleum jelly, calcipotriol, and decubal (an oil-in-water emollient) were found to increase the clearance of psoriatic plaques. Some emollients have been shown to be even more effective at clearing psoriatic plaques when combined with phototherapy.[81] 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.[81] 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.)[39][82]

Vitamin D analogues may be useful with steroids; steroids alone have a higher rate of side effects.[79] Vitamin D analogues may allow less steroids to be used.[83]

Another topical therapy used to treat psoriasis is a form of balneotherapy, which involves daily baths in the Dead Sea. This is usually done for four weeks with the benefit 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.[84] Decreases of PASI scores greater than 75% and remission for several months have commonly been observed.[84] Side effects may be mild such as itchiness, folliculitis, sunburn, poikiloderma, and a theoretical risk of nonmelanoma cancer or melanoma has been suggested.[84] Some studies indicate no increased risk of melanoma in the long term.[85] Data are inconclusive with respect to 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.[85] Dead Sea balneotherapy is also effective for psoriatic arthritis.[85] 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.[86] Glycerin is also an effective treatment for Psoriasis.[87]

UV phototherapy edit

Phototherapy in the form of sunlight has long been used for psoriasis.[75] UVB wavelengths of 311–313 nanometers are most common. These lamps have been developed for this treatment.[75] 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.[75] Increased rates of cancer from treatment appear to be small.[75] Narrowband UVB therapy has been demonstrated to have similar efficacy to psoralen and ultraviolet A phototherapy (PUVA).[88] 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.[89]

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.[90]

UV light therapies all have risks; tanning beds are no exception, being listed by the World Health Organization as carcinogens.[91] 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.[90]

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.[88] The activity of many types of immune cells found in the skin is also effectively suppressed by NB-UVB phototherapy treatments.[92] 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.[88]

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).[40][93] 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.[94]

Systemic agents edit

 
Pictures of a person with psoriasis (and psoriatic arthritis) at baseline and eight weeks after initiation of infliximab therapy

Psoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments.[95] People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities.[95] Pregnancy must be avoided for most of these treatments.[medical citation needed] The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued.[medical citation needed]

Non-biologic systemic treatments frequently used for psoriasis include methotrexate, ciclosporin, hydroxycarbamide, fumarates such as dimethyl fumarate, and retinoids.[96] 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.[23] Oral corticosteroids should not be used as they can severely flare psoriasis upon their discontinuation.[97]

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.[96] 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.[96][98] However, due to their immunosuppressive actions, biologics have been associated with a small increase in the risk for infection.[96]

Guidelines regard biologics as third-line treatment for plaque psoriasis following inadequate response to topical treatment, phototherapy, and non-biologic systemic treatments.[98] 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.[96]

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,[99] have been developed against pro-inflammatory cytokines[100] and inhibit the inflammatory pathway at a different point than the anti-TNF-α antibodies.[35] IL-12 and IL-23 share a common domain, p40, which is the target of the FDA-approved ustekinumab.[32] In 2017 the US FDA approved guselkumab for plaque psoriasis.[101] 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.[102]

Two medications that target T cells are efalizumab and alefacept. Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA-1.[96] 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.[96] 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.[35] Apremilast may also be used.[12]

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.[103]

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.[104] There is also some evidence to support use of secukinumab, brodalumab, guselkumab, certolizumab, and ustekinumab.[105][104] In general, anti-IL17, anti-IL12/23, anti-IL23, and anti-TNF alpha biologics were found to be more effective than traditional systemic treatments.[104] The immunologic pathways of psoriasis involve Th9, Th17, Th1 lymphocytes, and IL-22. The aforementioned biologic agents hinder different aspects of these pathways.[citation needed]

Another set of treatments for moderate to severe psoriasis are fumaric acid esters (FAE), which may be similar in effectiveness to methotrexate.[106]

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.[medical citation needed]

It has been theorized that antistreptococcal medications may improve guttate and chronic plaque psoriasis; however, the limited studies do not show that antibiotics are effective.[107]

Surgery edit

Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis, guttate psoriasis, and palmoplantar pustulosis.[108][109]

Diet edit

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).[110] A low-calorie diet appears to reduce the severity of psoriasis.[41] 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 consumption of caffeine (including coffee, black tea, mate, and dark chocolate) remains to be determined.[111]

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.[112]

There is a higher rate of celiac disease among people with psoriasis.[111][113] When adopting a gluten-free diet, disease severity generally decreases in people with celiac disease and those with anti-gliadin antibodies.[110][114][115]

Prognosis edit

Most people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies.[77] Depending on the severity and location of outbreaks, people may experience significant physical discomfort and some disability, affecting the person's quality of life.[32] Itching and pain can interfere with basic functions, such as self-care and sleep.[50] 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.[50] Plaques on the scalp can be particularly embarrassing, as flaky plaque in the hair can be mistaken for dandruff.[116]

 
Filipina with psoriasis

Individuals with psoriasis may feel self-conscious about their appearance and have a poor self-image that stems from fear of public rejection and psychosexual 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.[50] Psychological distress can lead to significant depression and social isolation; a high rate of thoughts about suicide has been associated with psoriasis.[20] 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.[117] Children with psoriasis may encounter bullying.[118]

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.[119]

Cardiovascular disease edit

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.[120] Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis.[120] Younger people with psoriasis may also be at increased risk for developing diabetes.[119][121] 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.[40][119]

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 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.[121][122] 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.[123] There may be a slightly increased risk of stroke associated with psoriasis, especially in severe cases.[40][124] 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.[125] 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.[125] Compared to individuals without psoriasis, those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome.[16][123]

Other diseases edit

The rates of Crohn 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.[111][115] Few studies have evaluated the association of multiple sclerosis with psoriasis, and the relationship has been questioned.[3][126] 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.[40] 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.[40] 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%.[40] There is no increased risk of melanoma associated with psoriasis.[40] People with psoriasis have a higher risk of developing cancer.[127]

Epidemiology edit

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,[128] more common in countries farther from the equator,[47] relatively uncommon in African Americans, and extremely uncommon in Native Americans.[48] 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.[129] Psoriasis affects both sexes equally.[61]

People with inflammatory bowel disease such as Crohn disease or ulcerative colitis are at an increased risk of developing psoriasis.[47]

History edit

Scholars believe psoriasis to have been included among the various skin conditions called tzaraath (translated as leprosy) in the Hebrew Bible. The person was deemed "impure" (see tumah and taharah) during their affected phase and is ultimately treated by the kohen.[130] 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.[130] 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.[131]

Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus.[132] The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813.[132] 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.[130] Mercury was also used for psoriasis treatment during this time period.[130] 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.[130] Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s.[130][133] During the same time period, psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis.[133]

Society and culture edit

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.[134] 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, and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries.

Cost edit

The annual cost for treating psoriasis in the United States is estimated as high as $32.5 billion, including $12.2 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 per person per year.[135]

Research edit

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.[136]

Many novel medications being researched during the 2010s target the Th17/IL-23 axis,[136] particularly IL-23p19 inhibitors, as IL-23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections.[137] 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.[137] Another avenue of research has focused on the use of vascular endothelial growth factor inhibitors to treat psoriasis.[63] 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.[136][137] These agents have potentially severe side-effects due to their immunosuppressive mechanisms.[137]

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Further reading edit

External links edit

 
Wikimedia Commons has media related to Psoriasis.
  • "Psoriatic arthritis". Genetics Home Reference.
  • "Psoriasis". MedlinePlus. U.S. National Library of Medicine.

January 09, 2024
psoriasis, long, lasting, noncontagious, autoimmune, disease, characterized, patches, abnormal, skin, these, areas, pink, purple, itchy, scaly, varies, severity, from, small, localized, patches, complete, body, coverage, injury, skin, trigger, psoriatic, skin,. 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 8 3 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 PsoriasisBack and arms of a person with psoriasisPronunciation s e ˈ r aɪ e s ɪ s p s s ɒ s ɔː s oʊ 1 2 SpecialtyDermatology primarily immunology rheumatology and other specialties e g cardiology and vascular medicine nephrology hepatology gastroenterology endocrinology haematology indirectly by association SymptomsRed purple on darker skin itchy scaly patches of skin 3 ComplicationsPsoriatic arthritis 4 Usual onsetAdulthood 5 DurationLong term 4 CausesGenetic disease triggered by environmental factors 3 Diagnostic methodBased on symptoms 4 TreatmentSteroid creams vitamin D3 cream ultraviolet light immunosuppressive drugs such as methotrexate and biologics 5 Frequency79 7 million 6 2 4 7 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 pswriasis meaning itching condition or being itchy 11 from psora itch and iasis action condition Contents 1 Signs and symptoms 1 1 Plaque psoriasis 1 2 Other forms 1 2 1 Pustular psoriasis 1 2 2 Inverse psoriasis 1 2 3 Napkin psoriasis 1 2 4 Guttate psoriasis 1 2 5 Erythrodermic psoriasis 1 2 6 Mouth 1 2 7 Seborrheic like psoriasis 1 3 Psoriatic arthritis 1 4 Nail changes 1 5 Medical signs 2 Causes 2 1 Genetics 2 2 Lifestyle 2 3 HIV 2 4 Microbes 2 5 Medications 3 Pathophysiology 4 Diagnosis 4 1 Classification 4 1 1 Morphological 4 1 2 Pathogenetic 4 1 3 Severity 5 Co morbidities 5 1 Cardiovascular complications 5 2 Depression 5 3 Type 2 diabetes 6 Management 6 1 Topical agents 6 2 UV phototherapy 6 3 Systemic agents 6 4 Surgery 6 5 Diet 7 Prognosis 7 1 Cardiovascular disease 7 2 Other diseases 8 Epidemiology 9 History 10 Society and culture 10 1 Cost 11 Research 12 References 13 Further reading 14 External linksSigns and symptoms editPlaque psoriasis edit nbsp Psoriatic plaque showing a silvery center surrounded by a reddened borderPsoriasis vulgaris also known as chronic stationary psoriasis or plaque like psoriasis is the most common form and affects 85 90 of people with psoriasis 12 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 12 13 nbsp Plaques of psoriasis nbsp A person s arm covered with plaque psoriasis nbsp Psoriasis of the palmsOther forms edit Additional types of psoriasis comprise about 10 of cases They include pustular inverse napkin guttate oral and seborrheic like forms 14 Pustular psoriasis edit nbsp Severe generalized pustular psoriasisPustular psoriasis appears as raised bumps filled with noninfectious pus pustules 15 The skin under and surrounding the pustules is red and tender 16 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 17 Inverse psoriasis edit 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 18 Napkin psoriasis edit Napkin psoriasis is a subtype of psoriasis common in infants characterized by red papules with silver scale in the diaper area that may extend to the torso or limbs 19 Napkin psoriasis is often misdiagnosed as napkin dermatitis diaper rash 20 Guttate psoriasis edit nbsp Example of guttate psoriasisGuttate 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 spares 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 21 Skin biopsy can also be performed which typically shows a psoriasiform reaction pattern characterized by epidermal hyperplasia and rate ridge prolongation 21 There is no firm evidence regarding best management for guttate psoriasis however first line therapy for mild guttate psoriasis typically includes topical corticosteroids 21 22 Phototherapy can be used for moderate or severe guttate psoriasis Biologic treatments have not been well studied in the treatment of guttate psoriasis 21 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 21 18 Erythrodermic psoriasis edit 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 17 It may be accompanied by severe dryness itching swelling and pain It can develop from any type of psoriasis 17 It is often the result of an exacerbation of unstable plaque psoriasis particularly following the abrupt withdrawal of systemic glucocorticoids 23 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 24 Mouth edit Psoriasis in the mouth is very rare in contrast to lichen planus another common papulosquamous disorder that commonly involves both the skin and mouth 25 When psoriasis involves the oral mucosa the lining of the mouth it may be asymptomatic 25 but it may appear as white or grey yellow plaques 25 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 26 However modern studies have failed to demonstrate any link between the two conditions 27 Seborrheic like psoriasis edit 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 19 Psoriatic arthritis edit 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 28 29 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 28 Psoriatic arthritis can also affect the hips knees spine spondylitis and sacroiliac joint sacroiliitis 30 About 30 of individuals with psoriasis will develop psoriatic arthritis 12 Skin manifestations of psoriasis tend to occur before arthritic manifestations in about 75 of cases 29 Nail changes edit nbsp Psoriasis of a fingernail with visible pitting nbsp Effect of psoriasis on the toenailsPsoriasis 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 31 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 31 Medical signs edit 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 scale is removed Koebner phenomenon psoriatic skin lesions induced by trauma to the skin 19 and itching and pain localized to papules and plaques 18 19 Causes editThe 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 32 33 Genetics edit See also List of human leukocyte antigen alleles associated with cutaneous conditions Around one third of people with psoriasis report a family history of the disease and researchers have identified genetic loci associated with the condition Identical twin studies suggest a 70 chance of a twin developing psoriasis if the other twin has the disorder The risk is around 20 for fraternal twins These findings suggest both a genetic susceptibility and an environmental response in developing psoriasis 34 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 35 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 35 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 35 The major determinant is PSORS1 which probably accounts for 35 50 of psoriasis heritability 36 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 32 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 35 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 32 T cells are involved in the inflammatory process that leads to psoriasis 35 These genes are on the pathway that upregulate tumor necrosis factor a and nuclear factor kB two genes involved in inflammation 35 The first gene directly linked to psoriasis was identified as the CARD14gene 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 37 38 Lifestyle edit Conditions reported as worsening the disease include chronic infections stress and changes in season and climate 32 Others factors that might worsen the condition include hot water scratching psoriasis skin lesions skin dryness excessive alcohol consumption cigarette smoking and obesity 32 39 40 41 The effects of stopping cigarette smoking or alcohol misuse have yet to be studied as of 2019 41 HIV edit 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 42 A much higher rate of psoriatic arthritis occurs in HIV positive individuals with psoriasis than in those without the infection 42 The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4 helper T cells 43 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 44 45 The diminished CD4 T cell presence is thought to cause an 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 46 In those with long term well controlled psoriasis new HIV infection can trigger a severe flare up of psoriasis and or psoriatic arthritis medical citation needed Microbes edit 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 33 Guttate psoriasis often affects children and adolescents and can be triggered by a recent group A streptococcal infection tonsillitis or pharyngitis 17 Medications edit Drug induced psoriasis may occur with beta blockers 10 lithium 10 antimalarial medications 10 nonsteroidal anti inflammatory drugs 10 terbinafine calcium channel blockers captopril glyburide granulocyte colony stimulating factor 10 interleukins interferons 10 lipid lowering medications 14 197 and paradoxically TNF inhibitors such as infliximab or adalimumab 47 Withdrawal of corticosteroids topical steroid cream can aggravate psoriasis due to the rebound effect 48 Pathophysiology editPsoriasis is characterized by an abnormally excessive and rapid growth of the epidermal layer of the skin 49 Abnormal production of skin cells especially during wound repair and an overabundance of skin cells result from the sequence of pathological events in psoriasis 16 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 35 17 Skin cells are replaced every 3 5 days in psoriasis rather than the usual 28 30 days 50 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 white blood cells 12 42 These immune cells move from the dermis to the epidermis and secrete inflammatory chemical signals cytokines such as interleukin 36g tumor necrosis factor a interleukin 1b interleukin 6 and interleukin 22 35 51 These secreted inflammatory signals are believed to stimulate keratinocytes to proliferate 35 One hypothesis is that psoriasis involves a defect in regulatory T cells and in the regulatory cytokine interleukin 10 35 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 17 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 52 53 Deoxyribonucleic acid DNA released from dying cells acts as an inflammatory stimulus in psoriasis 54 and stimulates the receptors on certain dendritic cells which in turn produce the cytokine interferon a 54 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 a which signal downstream inflammatory cells to arrive and stimulate additional inflammation 35 Dendritic cells bridge the innate immune system and adaptive immune system They are increased in psoriatic lesions 49 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 T22 cell cytokine secretion pattern over a Th1 Th17 cell cytokine profile 35 44 Psoriatic T cells move from the dermis into the epidermis and secrete interferon g and interleukin 17 55 Interleukin 23 is known to induce the production of interleukin 17 and interleukin 22 49 55 Interleukin 22 works in combination with interleukin 17 to induce keratinocytes to secrete neutrophil attracting cytokines 55 Diagnosis edit nbsp Micrograph of psoriasis vulgaris Confluent parakeratosis psoriasiform epidermal hyperplasia A EH hypogranulosis and influx of numerous neutrophils in the corneal layer A arrow B Transepidermal migration of neutrophils from the dermis to the corneal layer arrows 56 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 18 No special blood tests or diagnostic procedures are usually required to make the diagnosis 16 57 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 48 Dermatologic manifestations of systemic illnesses such as the rash of secondary syphilis may also be confused with psoriasis 48 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 16 58 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 16 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 the joints 16 Classification edit Morphological edit Psoriasis Type ICD 10 CodePsoriasis Vulgaris L40 0Generalized pustular psoriasis L40 1Acrodermatitis continua L40 2Pustulosis palmaris et plantaris L40 3Guttate psoriasis L40 4Psoriatic arthritis L40 50Psoriatic spondylitis L40 53Inverse psoriasis L40 8Psoriasis 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 59 Psoriasis can also be classified into nonpustular and pustular types 60 Pathogenetic edit 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 61 Type 1 accounts for about 75 of persons with psoriasis 62 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 16 32 63 while others have classified them as distinct from autoimmune diseases and referred to them as immune mediated inflammatory diseases 35 64 65 Severity edit nbsp Distribution of severityNo 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 66 Moderate to severe psoriasis was defined by the same group as BSA gt 10 or PASI score gt 10 and a DLQI score gt 10 66 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 67 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 68 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 69 Co morbidities editPsoriasis 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 70 Additionally the co morbidities increase the treatment and financial burden of psoriasis and should be considered when managing this condition 70 Cardiovascular complications edit There is 2 2 times increased risk of cardiovascular complications in people with psoriasis 71 Also people with psoriasis are more susceptible to myocardial infarction heart attack and stroke 71 It has been speculated that there is systemic inflammation in psoriasis which drives psoriatic march and can cause other inflammatory complications including cardiovascular complications 71 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 11 reduction in aortic vascular inflammation when there is 75 reduction in PASI score 72 Depression edit Depression or depressive symptoms are present in 28 55 of people with psoriasis 73 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 73 There is some evidence that increased inflammatory signals in the body could also contribute to depression in people with chronic inflammatory diseases including psoriasis 73 Type 2 diabetes edit People with psoriasis are at increased risk of developing type 2 diabetes 1 5 odds ratio 74 A genome wide based genetic study found that psoriasis and type 2 diabetes share four loci namely ACTR2 ERLIN1 TRMT112 and BECN1 which are connected via inflammatory NFkB pathway 74 Management edit nbsp Schematic of psoriasis treatment ladderWhile no cure is available for psoriasis 48 many treatment options exist Topical agents are typically used for mild disease phototherapy for moderate disease and systemic agents for severe disease 75 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 76 Topical agents edit 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 77 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 78 Vitamin D analogues such as paricalcitol are superior to placebo Combination therapy with vitamin D and a corticosteroid are superior to either treatment alone and vitamin D is superior to coal tar for chronic plaque psoriasis 79 For psoriasis of the scalp a 2016 review found dual therapy vitamin D analogues and topical corticosteroids or corticosteroid monotherapy to be more effective and safer than topical vitamin D analogues alone 80 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 80 Moisturizers and emollients such as mineral oil petroleum jelly calcipotriol and decubal an oil in water emollient were found to increase the clearance of psoriatic plaques Some emollients have been shown to be even more effective at clearing psoriatic plaques when combined with phototherapy 81 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 81 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 39 82 Vitamin D analogues may be useful with steroids steroids alone have a higher rate of side effects 79 Vitamin D analogues may allow less steroids to be used 83 Another topical therapy used to treat psoriasis is a form of balneotherapy which involves daily baths in the Dead Sea This is usually done for four weeks with the benefit 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 84 Decreases of PASI scores greater than 75 and remission for several months have commonly been observed 84 Side effects may be mild such as itchiness folliculitis sunburn poikiloderma and a theoretical risk of nonmelanoma cancer or melanoma has been suggested 84 Some studies indicate no increased risk of melanoma in the long term 85 Data are inconclusive with respect to 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 85 Dead Sea balneotherapy is also effective for psoriatic arthritis 85 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 86 Glycerin is also an effective treatment for Psoriasis 87 UV phototherapy edit Phototherapy in the form of sunlight has long been used for psoriasis 75 UVB wavelengths of 311 313 nanometers are most common These lamps have been developed for this treatment 75 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 75 Increased rates of cancer from treatment appear to be small 75 Narrowband UVB therapy has been demonstrated to have similar efficacy to psoralen and ultraviolet A phototherapy PUVA 88 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 89 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 90 UV light therapies all have risks tanning beds are no exception being listed by the World Health Organization as carcinogens 91 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 90 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 88 The activity of many types of immune cells found in the skin is also effectively suppressed by NB UVB phototherapy treatments 92 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 88 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 40 93 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 94 Systemic agents edit nbsp Pictures of a person with psoriasis and psoriatic arthritis at baseline and eight weeks after initiation of infliximab therapyPsoriasis resistant to topical treatment and phototherapy may be treated with systemic therapies including medications by mouth or injectable treatments 95 People undergoing systemic treatment must have regular blood and liver function tests to check for medication toxicities 95 Pregnancy must be avoided for most of these treatments medical citation needed The majority of people experience a recurrence of psoriasis after systemic treatment is discontinued medical citation needed Non biologic systemic treatments frequently used for psoriasis include methotrexate ciclosporin hydroxycarbamide fumarates such as dimethyl fumarate and retinoids 96 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 23 Oral corticosteroids should not be used as they can severely flare psoriasis upon their discontinuation 97 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 96 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 96 98 However due to their immunosuppressive actions biologics have been associated with a small increase in the risk for infection 96 Guidelines regard biologics as third line treatment for plaque psoriasis following inadequate response to topical treatment phototherapy and non biologic systemic treatments 98 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 96 Several monoclonal antibodies target cytokines the molecules that cells use to send inflammatory signals to each other TNF a is one of the main executor inflammatory cytokines Four monoclonal antibodies MAbs infliximab adalimumab golimumab and certolizumab pegol and one recombinant TNF a decoy receptor etanercept have been developed to inhibit TNF a signaling Additional monoclonal antibodies such as ixekizumab 99 have been developed against pro inflammatory cytokines 100 and inhibit the inflammatory pathway at a different point than the anti TNF a antibodies 35 IL 12 and IL 23 share a common domain p40 which is the target of the FDA approved ustekinumab 32 In 2017 the US FDA approved guselkumab for plaque psoriasis 101 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 102 Two medications that target T cells are efalizumab and alefacept Efalizumab is a monoclonal antibody that specifically targets the CD11a subunit of LFA 1 96 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 96 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 35 Apremilast may also be used 12 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 a 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 a receptors The lack of neutralizing antibodies against etanercept is probably secondary to the innate presence of the TNF a receptor and the development of immune tolerance 103 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 104 There is also some evidence to support use of secukinumab brodalumab guselkumab certolizumab and ustekinumab 105 104 In general anti IL17 anti IL12 23 anti IL23 and anti TNF alpha biologics were found to be more effective than traditional systemic treatments 104 The immunologic pathways of psoriasis involve Th9 Th17 Th1 lymphocytes and IL 22 The aforementioned biologic agents hinder different aspects of these pathways citation needed Another set of treatments for moderate to severe psoriasis are fumaric acid esters FAE which may be similar in effectiveness to methotrexate 106 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 medical citation needed It has been theorized that antistreptococcal medications may improve guttate and chronic plaque psoriasis however the limited studies do not show that antibiotics are effective 107 Surgery edit Limited evidence suggests removal of the tonsils may benefit people with chronic plaque psoriasis guttate psoriasis and palmoplantar pustulosis 108 109 Diet edit 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 110 A low calorie diet appears to reduce the severity of psoriasis 41 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 consumption of caffeine including coffee black tea mate and dark chocolate remains to be determined 111 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 112 There is a higher rate of celiac disease among people with psoriasis 111 113 When adopting a gluten free diet disease severity generally decreases in people with celiac disease and those with anti gliadin antibodies 110 114 115 Prognosis editMost people with psoriasis experience nothing more than mild skin lesions that can be treated effectively with topical therapies 77 Depending on the severity and location of outbreaks people may experience significant physical discomfort and some disability affecting the person s quality of life 32 Itching and pain can interfere with basic functions such as self care and sleep 50 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 50 Plaques on the scalp can be particularly embarrassing as flaky plaque in the hair can be mistaken for dandruff 116 nbsp Filipina with psoriasisIndividuals 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 50 Psychological distress can lead to significant depression and social isolation a high rate of thoughts about suicide has been associated with psoriasis 20 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 117 Children with psoriasis may encounter bullying 118 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 119 Cardiovascular disease edit 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 120 Severe psoriasis may be even more strongly associated with the development of diabetes than mild psoriasis 120 Younger people with psoriasis may also be at increased risk for developing diabetes 119 121 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 40 119 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 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 121 122 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 123 There may be a slightly increased risk of stroke associated with psoriasis especially in severe cases 40 124 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 125 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 TNFa as well as decreased activity of the immune protein LFA 1 125 Compared to individuals without psoriasis those affected by psoriasis are more likely to satisfy the criteria for metabolic syndrome 16 123 Other diseases edit The rates of Crohn 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 111 115 Few studies have evaluated the association of multiple sclerosis with psoriasis and the relationship has been questioned 3 126 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 40 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 40 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 40 There is no increased risk of melanoma associated with psoriasis 40 People with psoriasis have a higher risk of developing cancer 127 Epidemiology editPsoriasis 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 128 more common in countries farther from the equator 47 relatively uncommon in African Americans and extremely uncommon in Native Americans 48 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 20 129 Psoriasis affects both sexes equally 61 People with inflammatory bowel disease such as Crohn disease or ulcerative colitis are at an increased risk of developing psoriasis 47 History editScholars believe psoriasis to have been included among the various skin conditions called tzaraath translated as leprosy in the Hebrew Bible The person was deemed impure see tumah and taharah during their affected phase and is ultimately treated by the kohen 130 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 lepra for scaly skin conditions They used the term psora pswra to describe itchy skin conditions 130 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 131 Psoriasis is thought to have first been described in Ancient Rome by Cornelius Celsus 132 The British dermatologist Thomas Bateman described a possible link between psoriasis and arthritic symptoms in 1813 132 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 130 Mercury was also used for psoriasis treatment during this time period 130 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 130 Coal tars were widely used with ultraviolet light irradiation as a topical treatment approach in the early 1900s 130 133 During the same time period psoriatic arthritis cases were treated with intravenously administered gold preparations in the same manner as rheumatoid arthritis 133 Society and culture editThe 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 134 The Psoriasis International Network a program of the Fondation Rene 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 and Psoriasis Australia offer advocacy and education about psoriasis in their respective countries Cost edit The annual cost for treating psoriasis in the United States is estimated as high as 32 5 billion including 12 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 per person per year 135 Research editThe 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 136 Many novel medications being researched during the 2010s target the Th17 IL 23 axis 136 particularly IL 23p19 inhibitors as IL 23p19 is present in increased concentrations in psoriasis skin lesions while contributing less to protection against opportunistic infections 137 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 137 Another avenue of research has focused on the use of vascular endothelial growth factor inhibitors to treat 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the risk of diabetes mellitus a systematic review and meta analysis JAMA Dermatology 149 1 84 91 doi 10 1001 2013 jamadermatol 406 PMID 23407990 Armstrong AW Harskamp CT Armstrong EJ March 2013 The association between psoriasis and hypertension a systematic review and meta analysis of observational studies Journal of Hypertension 31 3 433 42 discussion 442 3 doi 10 1097 HJH 0b013e32835bcce1 PMID 23249828 S2CID 23724435 a b Tablazon IL Al Dabagh A Davis SA Feldman SR February 2013 Risk of cardiovascular disorders in psoriasis patients current and future American Journal of Clinical Dermatology 14 1 1 7 doi 10 1007 s40257 012 0005 5 PMID 23329076 S2CID 207482092 Psoriasis Linked to Stroke Risk BBC August 2011 Archived from the original on 28 August 2011 a b Ghazizadeh R Tosa M Ghazizadeh M May 2011 Clinical improvement in psoriasis with treatment of associated hyperlipidemia The American Journal of the Medical Sciences 341 5 394 8 doi 10 1097 MAJ 0b013e3181ff8eeb PMID 21233693 S2CID 12519829 Hsu LN Armstrong AW November 2012 Psoriasis and autoimmune disorders a review of the literature Journal of the American Academy of Dermatology 67 5 1076 9 doi 10 1016 j jaad 2012 01 029 PMID 23062896 Trafford AM Parisi R Kontopantelis E Griffiths CE Ashcroft DM October 2019 Association of Psoriasis With the Risk of Developing or Dying of Cancer A Systematic Review and Meta analysis JAMA Dermatology 155 12 1390 1403 doi 10 1001 jamadermatol 2019 3056 PMC 6802036 PMID 31617868 Lay summary in Bakalar N 16 October 2019 Psoriasis Tied to Increased Cancer Risk The New York Times Psoriasis affects more than 8 million people in the U S National Psoriasis Foundation Retrieved 12 July 2021 Benoit S Hamm H 2007 Childhood psoriasis Clinics in Dermatology 25 6 555 62 doi 10 1016 j clindermatol 2007 08 009 PMID 18021892 a b c d e f Gruber F Kastelan M Brajac I 2004 Psoriasis treatment yesterday today and tomorrow Acta Dermatovenerologica Croatica 12 1 30 4 PMID 15072746 Meenan FO March 1955 A note on the history of psoriasis Irish Journal of Medical Science 30 351 141 2 doi 10 1007 bf02949688 PMID 14353580 S2CID 27467338 a b Benedek TG June 2013 Psoriasis and psoriatic arthropathy historical aspects part I Journal of Clinical Rheumatology 19 4 193 8 doi 10 1097 RHU 0b013e318293eaeb PMID 23669809 S2CID 5813486 a b Benedek TG August 2013 Psoriasis and psoriatic arthropathy historical aspects part II Journal of Clinical Rheumatology 19 5 267 71 doi 10 1097 RHU 0b013e31829d4ad4 PMID 23872545 S2CID 199596315 International Federation of Psoriasis Associations Archived 21 November 2008 at the Wayback Machine Ifpa pso org Retrieved on 8 June 2013 Evans C June 2016 Managed care aspects of psoriasis and psoriatic arthritis The American Journal of Managed Care 22 8 Suppl s238 43 PMID 27356195 Archived from the original on 2 February 2017 a b c Dubois Declercq S Pouliot R July 2013 Promising new treatments for psoriasis TheScientificWorldJournal 2013 980419 980419 doi 10 1155 2013 980419 PMC 3713318 PMID 23935446 a b c d Patel M Day A Warren RB Menter A December 2012 Emerging therapies for the treatment of psoriasis Dermatology and Therapy 2 1 16 doi 10 1007 s13555 012 0016 4 PMC 3510410 PMID 23205338 Further reading editBaker BS 2008 From Arsenic to Biologicals A 200 Year History of Psoriasis Beckenham UK Garner ISBN 978 0 9551603 2 5 Guidelines for the assessment and management of psoriasis U S National Guideline Clearinghouse Archived from the original on 27 September 2013 Retrieved 26 July 2013 World Health Organization 2016 Global report on psoriasis World Health Organization WHO hdl 10665 204417 ISBN 9789241565189 Archived from the original on 29 February 2016 External links edit nbsp Wikimedia Commons has media related to Psoriasis Psoriatic arthritis Genetics Home Reference Psoriasis MedlinePlus U S National Library of Medicine Portal nbsp Medicine Retrieved from https en wikipedia org w index php title Psoriasis amp oldid 1187772218, wikipedia, wiki, 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