Psoriasis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Psoriasis is a systemic, immune-mediated disease that is characterized by inflammation of the skin and joints. It commonly causes erythematous scaly patches on the skin. The scaly patches caused by psoriasis, called psoriatic plaques, are areas of inflammation and excessive skin production. Skin rapidly accumulates at these sites and takes on a silvery-white appearance. Plaques frequently occur on the skin of the elbows and knees, but can affect any area including the scalp and genitals. Psoriasis is hypothesized to be immune-mediated and is not contagious. Psoriasis is a chronic recurring condition which varies in severity from minor localized patches to complete body coverage. Fingernails and toenails are frequently affected, which is referred to as psoriatic nail dystrophy. Psoriasis can also cause inflammation of the joints, which is known as psoriatic arthritis. 10-15% of people with psoriasis have psoriatic arthritis. The International Psoriasis Council identifies four main forms of psoriasis: plaque-type psoriasis, guttate psoriasis, generalized pustular psoriasis (GPP), and erythrodermic psoriasis. The pathophysiology of psoriasis consists of interactions between cytokines, dendritic cells, and T lymphocytes (particularly Th1 and Th17). Psoriasis must be differentiated from other diseases that cause an erythematous, scaly rash such as cutaneous T cell lymphoma/mycosis fungoides, pityriasis rosea, pityriasis rubra pilaris, pityriasis lichenoides chronica, nummular dermatitis, secondary syphilis, Bowen’s disease, exanthematous pustulosis, hypertrophic lichen planus, Sneddon–Wilkinson disease, small plaque parapsoriasis, intertrigo, Langerhans cell histiocytosis, dyshidrotic dermatitis, tinea manuum/pedum/capitis, and seborrheic dermatitis. The prevalence of psoriasis is estimated to be between 500 and 4,600 cases annually per 100,000 people. The mainstay of therapy for psoriasis is topical agents applied directly onto the lesions. Topical agents include corticosteroids, vitamin D analogues, tar, anthralin, tazarotene, calcineurin inhibitors, and aloe vera extracts. Systemic therapy may also be used; this can include immunosupressants to counteract the progression of the disease.

Psoriasis was first described during ancient times and was referred to as “Tzaraat” in the Bible, though the term also included other skin conditions. Initially, psoriasis, leprosy, and other inflammatory skin conditions were thought to be the same, but with the advancement of medical science, psoriasis became known as a separate entity. The pathophysiology of psoriasis was described in 1960s and 1970s after histopathological study of the disease. The application of cat feces to red lesions on the skin, for example, was one of the earliest topical treatments employed in ancient Egypt. Onions, sea salt, urine, goose oil and semen, wasp droppings in sycamore milk, and soup made from vipers have all been reported as ancient treatments for psoriasis. Sulfur was fashionable as a treatment for psoriasis in the Victorian and Edwardian eras and has gained importance again in the modern era as a substitute for other treatments. Psoriasis is a life-long disease that often involves multiple relapses and remissions, though symptoms can be controlled with proper medication.

Psoriasis can be classified according to clinical appearance, morphology, and localization. The International Psoriasis Council identifies four main forms of psoriasis: plaque-type psoriasis, guttate psoriasis, generalized pustular psoriasis (GPP), and erythroderma. Psoriasis can also be classified according to disease severity into mild, moderate, and severe. Several further sub-phenotypes have been named according to distribution (localized vs. widespread), anatomical localization (flexural or inverse, scalp, palms/soles/nail), size (large vs. small) and thickness (thick vs. thin) of plaques, onset (early vs. late), and disease activity (active vs. stable).

Psoriasis is an immune-mediated disease with a genetic predisposition, although no specific immunogen has been implicated in the development of psoriasis. The pathophysiology consists of interactions between cytokines, dendritic cells, and T lymphocytes (particularly Th1 and Th17). Common triggers of psoriasis include injury to the skin, trauma, infection, and medications. T cells play a key role in the pathogenesis of psoriasis via the production of pro-inflammatory cytokines. Certain genes increase the likelihood of developing psoriasis; the first gene that was discovered to be linked to the development of psoriasis was HLA-Cw6, which is located at PSORS1 at chromosomal position 6p21.3. Microscopically, the skin displays parakeratosis, acanthosis, hyperkeratosis, Kogoj pustules, and Munro’s microabscesses. The red appearance of psoriatic lesions is due to dilated blood vessels in the skin.

Psoriasis is caused by complex interactions between genetics, the immune system, and environmental factors.

Psoriasis must be differentiated from other diseases that cause an erythematous, scaly rash, such as cutaneous T cell lymphoma/mycosis fungoides, pityriasis rosea, pityriasis rubra pilaris, pityriasis lichenoides chronica, nummular dermatitis, secondary syphilis, Bowen’s disease, exanthematous pustulosis, hypertrophic lichen planus, Sneddon–Wilkinson disease, small plaque parapsoriasis, intertrigo, Langerhans cell histiocytosis, dyshidrotic dermatitis, tinea manuum/pedum/capitis, and seborrheic dermatitis.

The prevalence of psoriasis is estimated to be between 500 and 4,600 cases annually per 100,000 people. Psoriasis usually affects individuals of the Caucasian race. Psoriasis tends to primarily affect Northern European and Southeast Asian countries.

Common risk factors in the development of psoriasis are genes which increase the susceptibility of developing psoriasis and environmental triggers. The presence of these risk factors may lead to auto-immunity and development of psoriasis.

The national psoriasis foundation recommends screening patients affected with psoriasis for psoriatic arthritis (PsA). The CASPAR criteria may be used to screen patients for psoriastic arthritis.

If left untreated, patients with psoriasis may progress to develop psoriatic arthritis, joint erosions, and conjunctivitis. Common complications of psoriasis include depression, psoriatic arthritis, chronic inflammatory bowel disease, non-alcoholic fatty liver disease, celiac disease, sensorineural hearing loss, osteopenia, and osteoarthritis. Psoriasis is a life-long disease that involves multiple relapses and remissions, though symptoms can be controlled with proper medication.

The hallmark of psoriasis is a papulosquamous, erythematous, scaly rash that can be commonly found on extensor surfaces of the body. Flexural surfaces may also be involved in cases of inverse psoriasis. Patients with psoriasis usually have a history of recent streptococcal throat infection, viral infection, immunization, use of antimalarial drugs, or trauma. The most common symptoms of psoriasis include pain, which has been described by patients as unpleasant, superficial, sensitive, itchy, hot, or burning (especially in erythrodermic psoriasis and in some cases of traumatized plaques or in the joints affected by psoriatic arthritis). Patients also present with pruritus (especially in eruptive, guttate psoriasis) and high fever in erythrodermic and pustular psoriasis. Other symptoms include dystrophic nails and long-term erythematous, scaly rash with recent presentation of arthralgia/arthralgia without any visible skin findings. Other extracutaneous symptoms include redness and tearing of eyes due to conjunctivitis or blepharitis. Avoidance of social interactions is common among patients, especially during the active phase of the disorder.

On physical examination, psoriasis is characterized by erythematous, scaling papules and plaques.

Laboratory findings consistent with the diagnosis of psoriasis include increased levels of Long Pentraxin 3 protein (PTX3) and complement levels.

There are no x-ray findings associated with psoriasis. However, x-rays can be used to diagnose psoriatic arthritis, which may lead to the erosion of bone tissue and characteristic “pencil-in-cup” deformities. Psoriatic arthritis may also lead to periostitis, dactylitis, or arthritis mutilans.

There are no ultrasound findings associated with cutaneous psoriasis, though ultrasound may be used as a bedside tool for the visualization of joints in cases of psoriatic arthritis.

There are no CT scan findings associated with psoriasis involving the skin, though a CT scan may be used to visualize the spine in cases psoriatic arthritis.

There are no MRI findings associated with cutaneous psoriasis, though an MRI may be used in cases of psoriatic arthritis (PsA) to catch the disease in its early phase.

There are no other imaging findings associated with psoriasis.

Skin biopsy may be helpful in the diagnosis of psoriasis. Common findings include perivascular and dermal inflammatory cell infiltration, vascular dilation, and the absence of the granular layer.

The mainstay of therapy for psoriasis consists of topical agents applied directly onto the lesions. Topical agents used to treat psoriasis include corticosteroids, vitamin D analogues, tar, anthralin, tazarotene, calcineurin inhibitors, and aloe vera extracts. Systemic therapy may also be used; this can include immunosupressants to counteract the progression of the disease. The first-line treatment for symptomatic psoriatic arthritis is NSAIDs.

Tonsillectomy may be used as a treatment for psoriasis.

There are no established measures for the primary prevention of psoriasis.

There are no established measures for the secondary prevention of psoriasis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Psoriasis was first described during ancient times. Psoriasis was referred to as “Tzaraat” in the Bible, although the term also included other skin conditions. Initially, psoriasis, leprosy, and other inflammatory skin conditions were thought to be the same, but with the advancement of medical science, psoriasis became known to be a separate entity. In the 1960s and 1970s, the understanding of the pathophysiology of psoriasis advanced substantially following histopathological study of the disease. During the 20th century, psoriasis was further differentiated into specific sub-types.

• Psoriasis is one of the longest-known illnesses afflicting humans and one of the most widely misunderstood.^[1]
• Psoriasis was first described during ancient times; it was referred to as “Tzaraat” in the Bible, although the term also included other skin conditions.
• In ancient times, psoriasis, leprosy, and other inflammatory skin conditions were thought to be the same entity.
• In the late 18th century, English dermatologists Robert Willan and Thomas Bateman differentiated psoriasis from other skin diseases, calling it Willan’s lepra. They assigned names to the condition based on the appearance of lesions.
• In the 19th century, psoriasis was described as a separate disease after clinical descriptions separated it from other conditions.
• In 1841, Viennese dermatologist Ferdinand von Hebra finally named the condition psoriasis, differentiating it from leprosy.
• The word psoriasis originates from the Greek word psora, which means to itch.^[2]
• In 1960s and 1970s, the understanding of the pathophysiology of psoriasis advanced substantially following histopathological study of the disease.
• During the 20th century, psoriasis was further differentiated into specific sub-types.

• Ancient Egyptians applied cat feces to red lesions on the skin, which was one of the earliest topical treatments employed in the management of psoriasis.
• Other known ancient treatments include the application of onions, sea salt, urine, goose oil and semen, wasp droppings in sycamore milk, and soup made from vipers topically on the skin.
• In the Victorian and Edwardian eras, sulfur was fashionable as a treatment for psoriasis. It has recently regained some credibility as a safe alternative to steroids and coal tar.
• During the 18th and 19th centuries, dermatologists used to apply Fowler’s solution, which contains a poisonous and carcinogenic arsenic compound, as a treatment for psoriasis.
• During the middle of the 20th century, Grenz Rays (also called ultrasoft x-rays or Bucky rays) was a popular treatment of psoriasis.
• During 1950-1960, undecylenic acid was investigated and used to treat psoriasis.^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Psoriasis can be classified according to clinical appearance, morphology, and localization. According to the International Psoriasis Council, psoriasis may be classified into four subtypes: plaque-type psoriasis, guttate psoriasis, generalized pustular psoriasis (GPP), and erythroderma. Several further subphenotypes have been named according to distribution (localized vs. widespread), anatomical localization (flexural or inverse, scalp, palms/soles/nail), size (large vs. small) and thickness (thick vs. thin) of plaques, onset (early vs. late), and disease activity (active vs. stable).

• The International Psoriasis Council classifies psoriasis into four main forms, according to clinical appearance, morphology and localization:^{[1][2][3][4][5][6]}
  • Plaque-type psoriasis
  • Guttate psoriasis
  • Generalized Pustular Psoriasis (GPP)
  • Erythroderma

Type of Psoriasis	Typical Lesion	Body Distribution	Associated Conditions
Plaque-type psoriasis	Oval or irregularly shaped Erythematous Sharply demarcated Raised plaques covered by silvery scales	Large plaques >3cm Small plaques <3cm Extensor surface of elbows and knees Scalp Lower back	Psoriatic arthritis Metabolic syndrome Inflammatory bowel disease Non-melanoma skin cancer Triggers include: Drugs including: Lithium Antimalarials Withdrawal of systemic steroids Beta blockers Non-steroidal anti-inflammatory drugs(NSAIDS) Angiotensin-converting enzyme (ACE) inhibitors Trazodone Terfenadine Gemfibrozil Antibiotics (tetracycline, penicillin) Imiquimod
Guttate psoriasis	Multiple Small Drop-shaped Scaly plaques	Trunk Upper extremities Thighs	2–4 weeks after a bacterial infection of the upper ways, notably streptococcal pharyngitis in children and adolescents
Generalized pustular psoriasis[7]	Four sub-types: Zumbusch Erythema, sheeted pustulation and scarlatiniform peeling Annular Gyrate and annular pustular lesions Localized Restricted areas of pustular psoriasis in and around ordinary psoriatic plaques Exanthematic Single short-lived episode following infection or drug exposure Episodic, widespread skin and systemic inflammation Sheeted, pinhead-sized, sterile, sub-corneal pustules	Generalized	High fever Fatigue Leukocytosis Triggers include: Pregnancy Infection Exposure to or withdrawal from drugs
Erythrodermic psoriasis (most severe)	Diffuse erythema	>70 % of the body surface area	Hypothermia Extremity edema Myalgias Fatigue High grade fever

Several further sub-phenotypes have been named according to:

• Distribution (localized vs. widespread)
• Anatomical localization (flexural or inverse, scalp, palms/soles/nail)
• Size (large vs. small)
• Thickness (thick vs. thin) of plaques
• Onset (early vs. late)
• Disease activity (active vs. stable)

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Psoriasis is usually graded as:

• Mild (affecting less than 3% of the body)
• Moderate (affecting 3-10% of the body)
• Severe (affecting >10% of the body)

The degree of severity is generally judged based on the following factors:

• The proportion of body surface area affected
• Disease activity (degree of plaque redness, thickness, and scaling)
• Response to previous therapies
• The impact of the disease on the patient’s quality of life

The Psoriasis Area Severity Index (PASI) is the most widely used measurement tool for psoriasis. PASI combines the assessment of the severity of lesions and the area affected into a single score ranging between 0 (no disease) to 72 (maximal disease).^[8] The PASI can be very difficult to use outside of trials, which has led to attempts to simplify the index for clinical use.^[9]

• Flexural psoriasis:
  • Smooth, inflamed patches of skin
  • Occurs in skin folds, particularly around the genitals (between the thigh and groin), axillae, under an overweight stomach (pannus), and under the breasts (inframammary fold)
  • Aggravated by friction and sweat and is vulnerable to fungal infections
• Nail psoriasis:
  • Changes in the appearance of finger and toe nails:
  • Discoloration under the nail plate, pitting of the nails, lines going across the nails, thickening of the skin under the nail, and the loosening (onycholysis) or crumbling of the nail
• Drug-induced psoriasis

• Napkin psoriasis
• Seborrheic-like psoriasis
• Pustular psoriasis

Psoriatic arthritis may be classified based on severity into the following types:^[10]

• Mild psoriatic arthritis
• Moderate psoriatic arthritis
• Severe psoriatic arthritis

Type of psoriatic arthritis	Response to therapy	Quality of life
Mild psoriatic arthritis	NSAIDs	Minimal
Moderate psoriatic arthritis	Requires disease modifying anti-rheumatic drugs (DMARD) or tumor necrosis factor blockers (TNF-blockers)	Daily life tasks affected including mental and physical tasks/ No response to NSAIDs
Severe psoriatic arthritis	Requires disease modifying anti-rheumatic drugs (DMARD) plus tumor necrosis factor blockers (TNF-blockers) or biologic agents	Unable to perform major daily tasks of living without pain or dysfunction; large impact on physical and mental functions

Psoriatic arthritis also, may be classified into different subtypes as below table:

Subtype	Disease pattern[11]	Percentage of patients affected	Radiological features[12]				Histopathological features[13][14][15]
			X-ray	Ultrasonography	Computed tomography|CT scan	MRI
Classical psoriatic arthritis	Involvement of the distal interphalangeal joints Involvement of nails	~5 %	Bony proliferation Bone erosion “Pencil-in-cup” deformity (distal head of a bone becomes pointed-like a sharpened pencil, and the neighboring surface becomes rounded due to erosion)	Synovitis Tenosynovitis Peritendinitis Retrocalcaneal or pre-Achilles bursitis	Useful in assessing spine disease Joint erosions Synovitis	Synovitis (usually secondary to extrasynovial involvement – helps to differentiate PsA from rheumatoid arthritis) Gadolinium contrast use can more reliably differentiate PsA from rheumatoid arthritis by relative enhancement and rate of enhancement on MRI Enthesitis Osteitis	Neovascularization Inflammatory infiltration with predominantly mononuclear cells (T lymphocytes, B lymphocytes and plasma cells, and macrophages) Synovial lining hyperplasia  High expression of E-selectin Synovial expression of S100A12
Destructive psoriatic arthritis (arthritis mutilans)	Severe joint destruction Involvement of any of the interphalangeal, metacarpophalangeal, or metatarsophalangeal joints Dactylitis Enthesitis Involvement of axial skeleton Involvement of nails Digital tapering (opera glass hands) Joint ankylosis	< 5 %
Symmetric polyarthritis	Involvement of joints on both sides of the body simultaneously Most similar to rheumatoid arthritis	~15 %
Asymmetric psoriatic arthritis	Involvement of < 3 joints Does not occur in the same joints on both sides of the body	~70 %
Ankylosing spondylitis-like psoriatic arthritis	Stiffness of the spine or neck, but can also affect the hands and feet, in a similar fashion to symmetric arthritis	~ 5 %

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Psoriasis is an immune-mediated disease with a genetic predisposition, though no specific immunogen has been implicated in the development of psoriasis. The pathophysiology of psoriasis consists of interactions between cytokines, dendritic cells, and T lymphocytes (particularly Th1 and Th17).^[1] Common triggers of psoriasis include injury to the skin, trauma, infection, and medications. T cells play a key role in the pathogenesis of psoriasis via the production of pro-inflammatory cytokines. Certain genes increase the likelihood of developing psoriasis; the first gene that was discovered to be linked to the development of psoriasis was HLA-Cw6, which is located at PSORS1 at chromosomal position 6p21.3. Microscopically, skin affected by psoriasis displays parakeratosis, acanthosis, hyperkeratosis, Kogoj pustules, and Munro’s microabscesses. The red appearance of psoriatic lesions is due to dilated blood vessels in the skin.

There are two main hypotheses about the development of psoriasis. The first hypothesis considers psoriasis as primarily a disorder of excessive growth and reproduction of skin cells, in which psoriasis is a manifestation of a fault of the epidermis and its keratinocytes. The second hypothesis views the disease as an immune-mediated disorder in which the excessive reproduction of skin cells is secondary to factors produced by the immune system. T cells (which normally help protect the body against infection) become active, migrate to the dermis, and trigger the release of cytokines (tumor necrosis factor-alpha [TNFα] in particular), which cause inflammation and the rapid production of skin cells. It is not known what initiates the activation of the T cells.

The immune-mediated nature of psoriasis has been demonstrated by multiple studies in which various treatments that target and inhibit the proliferation and activation of T cells have been used successfully.^[2][3][4]

• Psoriasis can be triggered by many factors, including:^[1]
  • Genetic susceptibility
  • Injury
  • Trauma (termed the “Koebner effect“)
  • Infection
  • Medications
  • Topical biological response modifier imiquimod (a TLR7 agonist)^[5]

• TNFα and nitric oxide synthase isoform (iNOS)-producing inflammatory dendritic cells infiltrate psoriatic skin. These dendritic cells have the ability to activate T-cells to differentiate into Th1 and Th17 cell lines.^[6][7][8][9]
• Macrophages and innate immune cells, as well as an increased number of endothelial cells (angiogenesis), have also been implicated in the pathogenesis of psoriasis.
• Inflammatory myeloid dendritic cells release IL-23 and IL-12 to activate IL-17-producing T cells, Th1 cells, and Th22 cells to produce numerous psoriatic cytokines, which include IL-17, IFN-γ, TNF, and IL-22. These cytokines mediate effects on keratinocytes to augment psoriatic inflammation.
• Injury to the skin causes cell death and the production of the Cathelicidin LL-37 (anti-microbial protein LL37) by keratinocytes. DNA/LL37 complexes bind to intracellular toll-like receptor 9 (TLR9) in dendritic cells (DCs), which causes activation and production of type I interferons IFN-α and -β.
• Myeloid DCs can be activated by the LL37/RNA complex, as well as by type 1 interferons, leading to T cell proliferation, activation, and the production of cytokines found in psoriasis.

• Activation and differentiation of T cell subsets are maintained by IL-12 and IL-23, which appear to be produced mainly from myeloid DC subsets in the skin. Psoriasis lesions contain T cells that produce IFN-γ, IL-17, and IL-22, produced by Th1, Th17, and Th22, respectively. There are also CD8+ T cell populations that make the same types of cytokines.
• In response to these cytokines, keratinocytes in the skin upregulate the production of mRNAs, which lead to the formation of many pro-inflammatory products.
• Chemokines produced by keratinocytes cause the migration of many leukocyte subsets (e.g., dendritic cells (DCs) and neutrophils).
• The innate immune system is also thought to play an important role in the development of psoriasis.

• Genes in the NF-κB pathway are associated with psoriasis.^[10][11]
• IκB is an inhibitor of the NF-κB pathway. After the initiation of NF-κB signaling by cytokines such as TNF-alpha, IκB is phosphorylated by IκB kinase (IKK) and subsequently targeted for proteosomal degradation. The degradation of IκB releases NF-κB for translocation to the nucleus, consequently leading to gene expression for pro-inflammatory products.^[12]

The pathogenesis of psoriatic arthritis (PsA) involves the following events:^[13]

• In joints there is a prominent lymphocytic infiltrate, limited to the dermal papillae in skin and to the underlying stroma.
• T lymphocytes, particularly CD4 cells, are the most common inflammatory cells in the skin and joints, with a CD4/CD8 ratio of 2:1.
• High levels of tumor necrosis factor alpha (TNF), IL-8, IL-6, IL-1, IL-10, and matrix metalloproteinases are present in the joint fluid of patients with early PsA.
• Collagenase mediated degradation of cartilage collagen begins in early phases of the disease and may be the result of the proteases produced as a result of above mentioned cytokines.

• The elevated levels of TNF leads to a high number of osteoclast precursor cells circulating in the blood.
• Osteoclast precursors migrate to the joint where they encounter increased expression of receptor activator of nuclear factor kappa B ligand ( NF-κB), which favors the differentiation and activation of osteoclasts.
• Osteoclasts eventually lead to the joint destruction seen in psoriatic arthritis.

• The first gene that was discovered to be linked to the development of psoriasis was HLA-Cw6, which is located at PSORS1 at chromosomal position 6p21.3.^[14]
• HLA-Cw6 codes for a major histocompatibility complex I (MHCI) allele.
• Presentation of intracellular proteins by MHCI leads to the activation of cytotoxic T cells (CD8+ T cells). This T-cell priming plays a key role in the pathogenesis of psoriasis.
• The ERAP1 loci has also been shown to be linked to the development of psoriasis and is found in individuals carrying the HLA-Cw6 mutation.^[15]
• MICA (MHC class I polypeptide-related sequence A) is also associated with psoriasis.^[16]
• The gene DDX58 (DEAD (Asp-Glu-Ala-Asp) box polypeptide 58), which encodes the protein RIG-I, and IFIH1, which encodes the protein MDA5, have also been implicated in the pathogenesis of psoriasis.^[17]
• Activation of RIG-I or MDA5 results in gene expression changes mainly mediated by NF-κB pathway.^[18]
• Two cytokines known to be significant mediators of psoriasis, TNFα and/or IFNγ, can increase expression of RIG-I and MDA5 expression in keratinocytes.^[19]
• Genes such as CARD14 and ZC3H12C are found to not only potentially alter immune cell or keratinocyte behavior, but also the biology of the vasculature. These mutations might, therefore, play a part in the cardiovascular comorbidities linked to psoriasis.^[20][21]
• Approximately one-third of people with psoriasis report a family history of the disease. Studies of monozygotic twins suggest a 70% chance of a twin developing psoriasis if the other twin has psoriasis. The concordance is 20% for dizygotic twins. These findings suggest both a genetic predisposition and an environmental component in the development of psoriasis.^[22]

Psoriasis is associated with the following conditions:^{[23][24][25][26][27][28][29][30][31][32][33][34]}

• Depression
• Psoriatic arthritis
• Chronic inflammatory bowel disease
• Non-alcoholic fatty liver disease
• Celiac disease
• Sensorineural hearing loss
• Osteopenia and osteoarthritis
• Diabetes
• Hypertension
• Conjunctivitis
• Uveitis
• Metabolic syndrome
• SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and osteitis)
• Alcohol abuse
• Smoking
• Migraine

• On gross inspection, psoriatic lesions have the following characteristics:
  • Red or salmon-colored plaques
  • Well-defined borders
  • Silvery-white dry scale
  • Usually located on the extensor surfaces like elbows, knees, and scalp, and in the lumbosacral area^[1]
• The surface area of the body affected by psoriasis can be measured roughly as a percentage of body area using the palm to represent 1% of the body. One-third of patients present with at least 10 percent body involvement, which is referred to as moderate-to-severe psoriasis.

• The epidermis is greatly thickened (acanthosis) as the keratinocytes migrate through the epidermis over 4–5 days.^[1]
• There is a loss of the normal granular layer of the skin and a thickening of the stratum corneum (hyperkeratosis).
• There is retention of nuclei in the upper layers and stratum corneum (parakeratosis).^[35]
• There is neutrophilic infiltration in the epidermis and stratum corneum (Kogoj pustules and Munro’s microabscesses).^[36]
• In the dermis, there are abundant mononuclear cells (mainly myeloid cells and T cells).
• The red-colored appearance of psoriatic lesions is due to dilated blood vessels.

• Psoriatic arthritis (PsA) affected synovial tissue is characterized by a T-cell infiltrate with an increase in vascularity.^[37]
• There is a reduction in macrophages compared with the synovial tissue found in rheumatoid arthritis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

There are no established causes of psoriasis. The development of psoriasis is secondary to a combination of genes and exposure to specific external factors or triggers, which increase an individual’s risk of developing psoriasis. These risk factors lead to complex interactions between the genetics, immune system, and the environment. To view the factors which may increase one’s susceptibility to the development psoriasis, click here.

• The development of psoriasis is secondary to a combination of genes and exposure to specific external factors or triggers, which increase an individual’s risk of developing psoriasis.
• The presence of these risk factors may cause an activation of the immune system, which can lead to disease.

To view the factors which may increase one’s susceptibility to the development of psoriasis, click here.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Psoriasis must be differentiated from other diseases that cause an erythematous, scaly rash such as cutaneous T cell lymphoma/mycosis fungoides, pityriasis rosea, pityriasis rubra pilaris, pityriasis lichenoides chronica, nummular dermatitis, secondary syphilis, Bowen’s disease, exanthematous pustulosis, hypertrophic lichen planus, Sneddon–Wilkinson disease, small plaque parapsoriasis, intertrigo, Langerhans cell histiocytosis, dyshidrotic dermatitis, tinea manuum/pedum/capitis, and seborrheic dermatitis.

• Psoriasis must be differentiated from other diseases that cause papulosquamous or erythematosquamous rash, especially when the psoriatic lesions are localized in such sites as the palms, soles, scalp, body folds, penis, and nails. The differential diagnosis of psoriasis includes:

Disease	Rash Characteristics	Signs and Symptoms	Associated Conditions	Images
Cutaneous T cell lymphoma/Mycosis fungoides[1]	Premycotic phase: A scaly, red rash in areas of the body that usually are not exposed to the sun. This rash does not cause symptoms and may last for months or years. Patch phase: Thin, erythematous, eczema-like rash. Plaque phase: Small raised bumps (papules) or hardened lesions on the skin, which may be erythematous. Tumor phase: Tumors form on the skin. Infection secondary to ulcers.	Epidermal atrophy or poikiloderma Generalized itching (pruritus) Pain in the affected area of the skin Insomnia Red (erythematous) patches scattered over the skin of the trunk and the extremities Tumor-like lobulated outgrowths form on the skin in the latter phase of the disease Weight loss Lymphadenopathy Malaise and fatigue Anemia May progress to Sezary syndrome (skin involvement plus hematogenous dissemination)	Sezary syndrome
Pityriasis rosea[2]	Pink or salmon in color, which may be scaly; referred to as “herald patch” Oval shape Long axis oriented along the cleavage lines Distributed on the trunk and proximal extremities Squamous marginal collarette and a “fir-tree” or “Christmas tree” distribution on posterior trunk Secondary to viral infections Resolves spontaneously after 6-8 weeks	Preceded by a prodrome of: Sore throat Gastrointestinal disturbance Fever Arthralgia	Infection by any of the following:[3] HHV-6 HHV-7 HHV-8
Pityriasis lichenoides chronica	Recurrent lesions are usually less evenly scattered than in cases of psoriasis Brownish red or orange-brown in color Lesions are capped by a single detachable, opaque, mica-like scale Often leave hypopigmented macules	High fever Malaise Myalgias Paraesthesia Pruritus	Infection by any of the following:[4] Epstein-Barr virus (EBV) Toxoplasma gondii Human immunodeficiency virus (HIV)
Nummular dermatitis[5]	Multiple coin-shaped eczematous lesions Commonly affecting the extremities (lower>upper) and trunk May ooze fluid and become dry and crusty	Often appears after a skin injury, such as a burn, abrasion (from friction), or insect bite Lesions commonly relapse after occasional remission or may persist for long periods Pruritus	Associated with: Dry skin Emotional stress Allergens (rubber chemicals, formaldehyde, neomycin, chrome, mercury, and nickel) Staphylococcus infection Seasonal variation Alcohol Drugs Atopy
Secondary syphilis[6]	Round, coppery, red colored lesions on palms and soles Papules with collarette of scales	Fever Generalized lymphadenopathy Sore throat Patchy hair loss Headache Weight loss Myalgia Fatigue	Associated with: Condylomata lata Corona verinata Positive VDRL test
Bowen’s disease[7]	Erythematous, small, scaly plaque, which enlarges erratically over time Scale is usually yellow or white and it is easily detachable without any bleeding Well-defined margins	Pruritus Pain Bleeding lesions	Associated with:[8] Erythroplasia of Queyrat (Bowen’s disease of the penis) Squamous cell carcinoma Solar radiation and ultraviolet (UV) exposure Radiotherapy Immunosuppression Arsenic exposure Human papilloma virus (HPV) type 16 Merkel cell polyomavirus Sjögren’s syndrome
Exanthematous pustulosis[9]	Numerous small, primarily non-follicular, sterile pustules, arising within large areas of edematous erythema	Fever Leukocytosis Intracorneal, subcorneal, and/or intraepidermal pustules with papillary dermal edema containing neutrophils and eosinophils	Associated with:[10] Antibiotics (penicillins, sulfonamides, tetracyclines) Carbamazepine Calcium channel blockers (Diltiazem) Hydroxychloroquine
Hypertrophic lichen planus[11]	Classically involves shin and ankles and is characterized by hyperkeratotic plaques and nodules covered by a scale Lesions may transform into hyperkeratotic thickened, elevated, purplish or reddish plaques and nodules	Chronic pruritus Scaling May be asymptomatic	Associated with Hepatitis C virus infection[12]
Sneddon–Wilkinson disease[13]	Flaccid pustules that are often generalized and have a tendency to involve the flexural areas Annular configuration	Pruritus May be asymptomatic	Associated with: Monoclonal gammopathy, usually an IgA paraproteinemia[14] Crohn’s disease[15] Osteomyelitis Adalimumab[16]
Small plaque parapsoriasis[17]	Erythematous plaques with fine scaly surface May present with elongated, finger-like patches Symmetrical distribution on the flanks Known as digitate dermatosis	Lesions may be asymptomatic May be mildly pruritic May fade or disappear after sun exposure during the summer season, but typically recur during the winter	May progress to mycosis fungoides[18]
Intertrigo[19]	Red and fleshy looking lesion in skin folds Itching Oozing May be sore	Pruritus Musty odor	Associated with: Infections (Fungal, bacterial, viral) Allergies Diabetes Obesity
Langerhans cell histiocytosis[20]	Scaling and crusting of scalp	Pathological fractures[21] Visceromegaly (hepatomegaly, spleenomegaly) Chronic cough Dyspnea[22] Lymphadenopathy	Associated with: Diabetes insipidus[23] Pancytopenia
Tinea manuum/pedum/capitis[24]	Scaling, flaking, and sometimes blistering of the affected areas Hair loss with a black dot on scalp in case of tinea capitis	Pruritus KOH preparation of the lesions confirms fungal infection	Associated with: Diabetes Immunosupression Intimate contact with infected person May lead to asthma exacerbation
Seborrheic dermatitis	Papulosquamous, scaly, flaky, itchy, and red rash found particularly at sebaceous gland-rich areas of the body	Pruritus	Associated with:[25] AIDS Stress[26] Fungal infection Fatigue Sleep deprivation Change of season Parkinson’s disease Biotin deficiency

Psoriatic arthritis must be differentiated from other diseases causing oligo/polyarthritis or arthritis of the axial skeleton, including:

Arthritis Type	Clinical Features							Body Distribution				Key Signs				Laboratory Abnormalities
	History of Psoriasis	Symmetric joint involvement	Asymmetric joint involvement	Enthesopathy	Dactylitis	Nail Dystrophy	Human immunodeficiency virus association	Upper extremity-hands	Lower extremity	Sacroiliac joints	Spine	Osteopenia	Joint Space	Ankylosis	Periostitis	Soft tissue swelling	ESR	Rheumatoid factor (RF)	HLA-B27
Psoriatic arthritis	+	+	++	+	+	+	+	+++ (DIP/PIP)	+++	++ (Unilateral)	++	–	++ (Widening)	++	+++ (Fluffy)	++	+	–	30-75%
Rheumatoid arthritis	–	++	+	–	–	–	–	+++ (MCP/wrist)	+++	+ (Unilateral)	++(Cervical)	+++	+++ (Narrowing)	+	+ (Linear)	+++	+++	+++	6-8%
Ankylosing spondylitis	–	+++	–	+	–	–	–	+	+	+++ (Bilateral)	+++	+++	++ (Narrowing)	+++	+++ (Fluffy)	+	+++	–	90%
Reactive arthritis (Reiter’s syndrome)	–	+++	–	+	+	–	–	++	+++	++ (Unilateral)	+	+	+ (Narrowing)	–	+++ (Fluffy)	++	++	–	75%

Key:+ : Infrequently present, ++ : Frequently present, +++ : Always present, – : Absent

References

1. ↑ “Mycosis Fungoides and the Sézary Syndrome Treatment (PDQ®)—Patient Version – National Cancer Institute”.
2. ↑ Mahajan K, Relhan V, Relhan AK, Garg VK (2016). “Pityriasis Rosea: An Update on Etiopathogenesis and Management of Difficult Aspects”. Indian J Dermatol. 61 (4): 375–84. doi:10.4103/0019-5154.185699. PMC 4966395. PMID 27512182.
3. ↑ Prantsidis A, Rigopoulos D, Papatheodorou G, Menounos P, Gregoriou S, Alexiou-Mousatou I, Katsambas A (2009). “Detection of human herpesvirus 8 in the skin of patients with pityriasis rosea”. Acta Derm. Venereol. 89 (6): 604–6. doi:10.2340/00015555-0703. PMID 19997691.
4. ↑ Smith KJ, Nelson A, Skelton H, Yeager J, Wagner KF (1997). “Pityriasis lichenoides et varioliformis acuta in HIV-1+ patients: a marker of early stage disease. The Military Medical Consortium for the Advancement of Retroviral Research (MMCARR)”. Int. J. Dermatol. 36 (2): 104–9. PMID 9109005.
5. ↑ Jiamton S, Tangjaturonrusamee C, Kulthanan K (2013). “Clinical features and aggravating factors in nummular eczema in Thais”. Asian Pac. J. Allergy Immunol. 31 (1): 36–42. PMID 23517392.
6. ↑ “STD Facts – Syphilis”.
7. ↑ Neagu TP, Ţigliş M, Botezatu D, Enache V, Cobilinschi CO, Vâlcea-Precup MS, GrinŢescu IM (2017). “Clinical, histological and therapeutic features of Bowen’s disease”. Rom J Morphol Embryol. 58 (1): 33–40. PMID 28523295.
8. ↑ Murao K, Yoshioka R, Kubo Y (2014). “Human papillomavirus infection in Bowen disease: negative p53 expression, not p16(INK4a) overexpression, is correlated with human papillomavirus-associated Bowen disease”. J. Dermatol. 41 (10): 878–84. doi:10.1111/1346-8138.12613. PMID 25201325.
9. ↑ Szatkowski J, Schwartz RA (2015). “Acute generalized exanthematous pustulosis (AGEP): A review and update”. J. Am. Acad. Dermatol. 73 (5): 843–8. doi:10.1016/j.jaad.2015.07.017. PMID 26354880.
10. ↑ Schmid S, Kuechler PC, Britschgi M, Steiner UC, Yawalkar N, Limat A, Baltensperger K, Braathen L, Pichler WJ (2002). “Acute generalized exanthematous pustulosis: role of cytotoxic T cells in pustule formation”. Am. J. Pathol. 161 (6): 2079–86. doi:10.1016/S0002-9440(10)64486-0. PMC 1850901. PMID 12466124.
11. ↑ Ankad BS, Beergouder SL (2016). “Hypertrophic lichen planus versus prurigo nodularis: a dermoscopic perspective”. Dermatol Pract Concept. 6 (2): 9–15. doi:10.5826/dpc.0602a03. PMC 4866621. PMID 27222766.
12. ↑ Shengyuan L, Songpo Y, Wen W, Wenjing T, Haitao Z, Binyou W (2009). “Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis”. Arch Dermatol. 145 (9): 1040–7. doi:10.1001/archdermatol.2009.200. PMID 19770446.
13. ↑ Lutz ME, Daoud MS, McEvoy MT, Gibson LE (1998). “Subcorneal pustular dermatosis: a clinical study of ten patients”. Cutis. 61 (4): 203–8. PMID 9564592.
14. ↑ Kasha EE, Epinette WW (1988). “Subcorneal pustular dermatosis (Sneddon-Wilkinson disease) in association with a monoclonal IgA gammopathy: a report and review of the literature”. J. Am. Acad. Dermatol. 19 (5 Pt 1): 854–8. PMID 3056995.
15. ↑ Delaporte E, Colombel JF, Nguyen-Mailfer C, Piette F, Cortot A, Bergoend H (1992). “Subcorneal pustular dermatosis in a patient with Crohn’s disease”. Acta Derm. Venereol. 72 (4): 301–2. PMID 1357895.
16. ↑ Sauder MB, Glassman SJ (2013). “Palmoplantar subcorneal pustular dermatosis following adalimumab therapy for rheumatoid arthritis”. Int. J. Dermatol. 52 (5): 624–8. doi:10.1111/j.1365-4632.2012.05707.x. PMID 23489057.
17. ↑ Lambert WC, Everett MA (1981). “The nosology of parapsoriasis”. J. Am. Acad. Dermatol. 5 (4): 373–95. PMID 7026622.
18. ↑ Väkevä L, Sarna S, Vaalasti A, Pukkala E, Kariniemi AL, Ranki A (2005). “A retrospective study of the probability of the evolution of parapsoriasis en plaques into mycosis fungoides”. Acta Derm. Venereol. 85 (4): 318–23. doi:10.1080/00015550510030087. PMID 16191852.
19. ↑ Janniger CK, Schwartz RA, Szepietowski JC, Reich A (2005). “Intertrigo and common secondary skin infections”. Am Fam Physician. 72 (5): 833–8. PMID 16156342.
20. ↑ Satter EK, High WA (2008). “Langerhans cell histiocytosis: a review of the current recommendations of the Histiocyte Society”. Pediatr Dermatol. 25 (3): 291–5. doi:10.1111/j.1525-1470.2008.00669.x. PMID 18577030.
21. ↑ Stull MA, Kransdorf MJ, Devaney KO (1992). “Langerhans cell histiocytosis of bone”. Radiographics. 12 (4): 801–23. doi:10.1148/radiographics.12.4.1636041. PMID 1636041.
22. ↑ Sholl LM, Hornick JL, Pinkus JL, Pinkus GS, Padera RF (2007). “Immunohistochemical analysis of langerin in langerhans cell histiocytosis and pulmonary inflammatory and infectious diseases”. Am. J. Surg. Pathol. 31 (6): 947–52. doi:10.1097/01.pas.0000249443.82971.bb. PMID 17527085.
23. ↑ Grois N, Pötschger U, Prosch H, Minkov M, Arico M, Braier J, Henter JI, Janka-Schaub G, Ladisch S, Ritter J, Steiner M, Unger E, Gadner H (2006). “Risk factors for diabetes insipidus in langerhans cell histiocytosis”. Pediatr Blood Cancer. 46 (2): 228–33. doi:10.1002/pbc.20425. PMID 16047354.
24. ↑ Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G (2004). “Dermatology for the practicing allergist: Tinea pedis and its complications”. Clin Mol Allergy. 2 (1): 5. doi:10.1186/1476-7961-2-5. PMC 419368. PMID 15050029.
25. ↑ Schwartz RA, Janusz CA, Janniger CK (2006). “Seborrheic dermatitis: an overview”. Am Fam Physician. 74 (1): 125–30. PMID 16848386.
26. ↑ Misery L, Touboul S, Vinçot C, Dutray S, Rolland-Jacob G, Consoli SG, Farcet Y, Feton-Danou N, Cardinaud F, Callot V, De La Chapelle C, Pomey-Rey D, Consoli SM (2007). “[Stress and seborrheic dermatitis]”. Ann Dermatol Venereol (in French). 134 (11): 833–7. PMID 18033062.CS1 maint: Unrecognized language (link)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

The prevalence of psoriasis is estimated to be between 500 and 4,600 cases annually per 100,000 people. Psoriasis usually affects individuals of the Caucasian race. Psoriasis tends to primarily affect Northern European and Southeast Asian countries.

• Worldwide, the prevalence of psoriasis ranges from a low of 500 cases per 100,000 persons to a high of 4,600 cases per 100,000 persons.^[1]
• The prevalence of psoriasis in the United States is 2,000 cases per 100,000 persons.^[2]
• Worldwide, the prevalence of psoriatic arthritis (PsA) ranges from a low of 100 cases per 100,000 persons to a high of 1,000 cases per 100,000 persons.^[2]
• Worldwide, 7,000 per 100,000 people with arthritis are affected by psoriasis.^[2]

• Worldwide, the incidence of psoriasis ranges from a low of 78.9 cases per 100,000 persons (United States) to 230 cases per 100,000 persons (Italy).^[3]

• Psoriasis has two peaks with regard to age. The mean age of the first peak is between 15 years to 25 years and the mean age of the second peak is between 55 and 60 years.^[4]

• Psoriasis tends to affect Caucasians more than other races, with a prevalence of 2,500 per 100,000 Caucasian persons in the United States, which is higher than other ethnic populations in the country.^[5]

• There is no gender predilection for psoriasis, although women are more severely affected than men once they have developed the disease.^[6]

• Psoriasis tends to primarily affect Northern European and Southeast Asian countries.^[7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

Common risk factors in the development of psoriasis are genes which increase the susceptibility of developing psoriasis and environmental triggers. The presence of these risk factors may lead to auto-immunity and development of psoriasis.

• The human genome has at least nine different loci implicated in the development of psoriasis (PSORS1-9).^[1]
• PSORS-1, a part of the major histocompatibility complex (MHC) on chromosome 6p2, is the major genetic determinant of psoriasis, and is responsible for up to 50% of genetic susceptibility to the disease.^[2]
• The second most well-characterized disease-susceptibility locus (PSORS2) is found within 17q24–q25.
• Missense mutations in CARD14 gene lead to activation of the NF-κB pathway.
• Another major gene involved in the development of psoriasis is a HLA class I allele, specifically HLA-Cw6.^[3]
• Psoriatic arthritis (PsA) has been shown to be associated with human leukocyte antigen (HLA) class 1.^[4]

• Both innate and adaptive immunity are involved in the development of psoriasis.
• The key cytokines of immune system involved in the development of psoriasis are tumor necrosis factor-alpha and interferon alpha.
• The LFA-1 integrin is also important in the immune pathogenesis of psoriasis and has been known to be a target for medications used for the management of psoriasis.
• Within the immune system, the development of psoriasis is based upon four key pathways/interactions:
  • Antigen presentation
  • NF-κB signaling
  • IL-23/IL-17 axis
  • Type I interferon (IFN) pathway

The environmental factors implicated in the development or aggravation of psoriasis are:^{[5][6][7][8][9][10][11]}

• Stress (physical and mental)
• Smoking
• Excessive alcohol consumption
• Infection (Streptococcal, HIV)
• Seasonal variation
• Medications (lithium, beta blockers, pegylated interferon alpha-2b, siltuximab)
• Obesity
• Skin injury
• Skin dryness

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

There are no established guidelines for the screening of cutaneous psoriasis. The national psoriasis foundation recommends screening patients already affected with psoriasis for psoriatic arthritis (PsA). The CASPAR criteria may be used to screen patients for psoriastic arthritis.

• Patients with psoriasis should be screened for the presence of PsA, since early detection and aggressive treatment appear to prevent joint damage.
• Patients with psoriasis should be monitored for the development of PsA.^[1]
• The simplest approach is to use the newly developed CASPAR (Classification criteria for psoriatic arthritis) criteria.
• The CASPAR criteria consists of established inflammatory articular disease with at least 3 points from the following features:^[2]
  • Current psoriasis
  • History of psoriasis (unless current psoriasis was present)
  • Family history of psoriasis (unless current psoriasis was present or there was a history of psoriasis)
  • Dactylitis
  • Juxtaarticular new bone formation
  • Rheumatoid factor negativity
  • Nail dystrophy

• Current psoriasis is given a score of 2 and all other features are given a score of 1.
• A score greater than equal to 3 warrants referral to a rheumatologist.

• Another questionnaire exists for psoriatic arthritis, called the Psoriasis Epidemiology Screening Tool (PEST).^[3]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]

If left untreated, patients with psoriasis may progress to develop psoriatic arthritis, joint erosions, and conjunctivitis. Common complications of psoriasis include depression, psoriatic arthritis, chronic inflammatory bowel disease, non-alcoholic fatty liver disease, celiac disease, sensorineural hearing loss, osteopenia, and osteoarthritis. Psoriasis is a life-long disease that involves multiple relapses and remissions, though symptoms can be controlled with proper medication.

The natural history of psoriasis differs according to the clinical sub-type. The symptoms of psoriasis usually develop in the second decade of life, beginning with such symptoms as skin lesions characterized by erythema and scales covering the lesions. The chronicity of psoriasis may cause significant distress for the affected patient, which can lead to a decrease in the patient’s quality of life.^[1]

• Plaque-type psoriasis is a chronic condition involving multiple relapses and remissions along the course of the disease.
• Extracutaneous involvement is common and the most commonly affected sites include joints and eyes.
• Typical presentation is that of plaques which persist on the same site for months to years, along with an asymmetric oligoarthritis with involvement of the distal (DIPs) and proximal (PIPs) interphalangeal joints of the hands and feet. Erosive joint disease usually develops years after joint involvement.

• Guttate psoriasis presents with spontaneous remissions occurring over the course of weeks to months. In adults, the lesions of guttate psoriasis may become chronic and progress to plaque-type psoriasis.
• It may be aggravated by extrinsic factors such as smoking, excessive alcohol use, pregnancy, HIV infection, and stress.

• Generalized pustular psoriasis is a severe form of psoriasis that can be triggered by:^[2]
  • Pregnancy
  • Rapid withdrawal of corticosteroids
  • Infections
  • Hypocalcemia

Psoriatic arthritis goes through the following stages of progression during its course, defined by the change in clinical damage:^[3]

• Stage 1:
  • Reflects no damaged joints
• Stage 2:
  • One to four damaged joints
• Stage 3:
  • Five to nine damaged joints
• Stage 4:
  • More than 10 joints

Individuals with psoriasis may develop the following complications:^[4]

• High-output cardiac failure in erythroderma^[5]
• Psoriatic arthritis
• Infections
• Cachexy
• Amyloidosis

• Anti-TNF medications given during the management of psoriasis may lead to:
  • Progressive multifocal leukoencephalopathy
  • Optic neuritis
  • Transverse myelitis
  • Multiple sclerosis
  • Infections

• Psoriasis is a lifelong condition.^[6] There is currently no cure but various treatments can help to control the symptoms.
• Many of the most effective agents used to treat severe psoriasis carry an increased risk of significant morbidity including skin cancers, lymphoma, and liver disease. However, the majority of people’s experience of psoriasis is that of minor localized patches, particularly on the elbows and knees, which can be treated with topical medication.
• Psoriasis does get worse over time but it is not possible to predict who will go on to develop extensive psoriasis or those in whom the disease may appear to vanish. Individuals will often experience flares and remissions throughout their lives.
• Controlling the signs and symptoms typically requires lifelong therapy.
• Psoriasis is linked to 2.5-fold increased risk for non-melanoma skin cancer in men and women, with no preponderance of any specific histologic subtype of cancer.^[7]

The Primary Care Dermatology Society and the British Association of Dermatologists suggests that the following groups of patients may require secondary care:^[8]

• Diagnostic uncertainty
• Request for further counseling or education, including demonstration of topical treatment
• Failure to respond to appropriately used topical therapy for three months
• Psoriasis at sites that are difficult to treat (scalp, face, palms, soles, genitals) if unresponsive to initial therapy
• Adverse reactions to topical therapies
• Need for systemic therapy and phototherapy
• Disability preventing work or excessive time off work
• Acute unstable psoriasis
• Erythrodermic or generalized pustular psoriasis (emergency referral indicated)

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