Chronic Plaque Psoriasis

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Synonyms: psoriasis vulgaris (chronic stationary type)

Psoriasis is a common, chronic, relapsing, inflammatory skin disorder with a strong genetic basis. Psoriasis is a T cell-mediated autoimmune disorder, resulting from the interaction between multiple genetic and environmental factors. T cells are induced to produce cytokines, which stimulate keratinocyte proliferation and the production of dermal antigenic adhesion molecules in the local blood vessels, further stimulating the T-cell cytokine response.

  • The prevalence of psoriasis is estimated to be about 1.3-2.2% in the UK, with the highest prevalence being in white people.
  • Men and women are equally affected.
  • It can occur at any age but the majority of cases first present before the age of 35 years. It is uncommon in children.
  • Plaque psoriasis accounts for 90% of all people with psoriasis.
  • Joint disease is associated with psoriasis in a significant proportion of patients (reported in one study to be 13.8%).

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Risk factors

  • There is a multifactorial pattern of inheritance. About 30% of patients with psoriasis have a family history. Twin studies support the role of genetic factors with a three-fold increase in concordance in monozygotic twins compared with fraternal twins.[2] Linkage studies suggest multiple susceptibility loci.
  • Environmental factors: a number of factors may trigger or exacerbate plaque psoriasis, including:
    • Sunlight: there is usually a decrease in severity during periods of increased sun exposure (ie it often improves in the summer and is worse in the winter) but a small minority has an aggravation of symptoms during strong sunlight and sunburn can also lead to an exacerbation of plaque psoriasis.
    • Infection:
      • Streptococcal infection is strongly associated with the development of guttate psoriasis, but this may also apply to chronic plaque psoriasis.
      • HIV infection and AIDS - although other comorbid skin conditions may mimic psoriasis.[3]
    • Psychological stress is widely believed to play a role but evidence for a causal relationship is lacking.
    • Postpartum hormonal changes.
    • Drugs including:
    • Smoking and alcohol.
    • Trauma - psoriasis may be spread to uninvolved skin by various types of trauma.

Associated diseases

Psoriasis is associated with:[5]

  • Psoriatic arthritis - a seronegative inflammatory arthritis, which between 7-40% of people with psoriasis will develop.
  • Inflammatory bowel disease.
  • Metabolic syndrome (abdominal obesity, hypertension, insulin resistance, dyslipidaemia).
  • A number of studies have suggested that people with psoriasis may have an increased risk of cardiovascular disease, lymphoma and non-melanoma skin cancer.[1] 

An assessment of any patient with psoriasis should include disease severity, the impact of disease on physical, psychological and social well-being, whether they have psoriatic arthritis, and the presence of any comorbidities.[1] 

Chronic plaque psoriasis is typified by itchy, well-demarcated circular-to-oval bright red/pink elevated lesions (plaques) with overlying white or silvery scale, distributed symmetrically over extensor body surfaces and the scalp.

  • Fissuring within plaques can occur when lesions are present over joint lines or on the palms and soles.
  • Gentle scraping accentuates the scale (vigorous scraping causes pinpoint bleeding - Auspitz' sign).
  • The psoriatic lesions are a very distinctive rich, full, red colour. When present on the legs, lesions sometimes carry a blue or violaceous tint.
    PSORIASIS PLAQUES
  • Psoriatic plaques occasionally appear to be immediately encircled by a paler peripheral zone.
  • New lesions often appear at sites of injury or trauma to the skin (Köbner's reaction), typically 1-2 weeks after the skin has been injured.
  • Plaque psoriasis presents slightly differently in children. Plaques are not as thick, and the lesions are less scaly. Psoriasis may often appear in the nappy region in infancy and in flexural areas in children. The disease more commonly affects the face in children than it does with adults.
  • Nail changes are often seen, with pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign (yellow-red discolouration of the nail bed looking like a drop of oil beneath the nail). See also the separate article on Psoriatic Nail Disease.
    PSORIASIS OF HAND

Acute episodes of plaque psoriasis may evolve into more severe disease - eg, pustular or erythrodermic psoriasis.

Assessment of severity[1] 

The extent and duration of the disease is very variable. Lesions vary in size from one to several centimetres. The number of lesions may range from few to many at any given time. Smaller plaques may coalesce into larger lesions, especially on the legs and sacral regions.

When assessing the disease severity, the following should be recorded:

  • The results of a static Physician's Global Assessment (six-point scale assessing overall disease severity at the point of assessment as clear, nearly clear, mild, moderate, severe or very severe).
  • The patient's assessment of current disease severity - eg, using the static Patient's Global Assessment.
  • The body surface area affected.
  • Any involvement of nails, high-impact and difficult-to-treat sites (eg, the face, scalp, palms, soles, flexures and genitals).
  • Any systemic upset, such as fever and malaise, which are common in unstable forms of psoriasis such as erythroderma or generalised pustular psoriasis.

Psoriasis may be classified as mild, where it affects <5% of the body's surface area, moderate where it affects 5-10%, and severe at >10% involvement.[6] 

Tools such as the Psoriasis Area and Severity Index (PASI) may be used to express disease severity, based on severity of lesions and extent of skin involvement.[7] [8] 

Diagnosis is usually made on clinical findings. Skin biopsy is very rarely required to confirm diagnosis.

Management options for the treatment of psoriasis include:[1] 

  • First-line therapy which includes traditional topical therapies - eg, corticosteroids, vitamin D analogues, dithranol and tar preparations.
  • Second-line therapy which includes phototherapy, broad-band or narrow-band ultraviolet B light, with or without supervised application of complex topical therapies such as dithranol in Lassar's paste or crude coal tar and photochemotherapy, psoralens in combination with UVA irradiation (PUVA), and non-biological systemic agents such as ciclosporin, methotrexate and acitretin.
  • Third-line therapy which refers to systemic biological therapies that use molecules designed to block specific molecular steps important in the development of psoriasis, such as the TNF antagonists adalimumab, etanercept and infliximab, and ustekinumab, anti-IL12-23 monoclonal antibody.

There is no strong evidence that any of the interventions have a disease-modifying effect or impact beyond improvement of the psoriasis itself.

General

  • Give a full explanation of psoriasis, including reassurance that it is neither infectious nor malignant, with appropriate written patient information.
  • Discuss treatment options (including no active treatment), likely benefit from treatment, and side-effects; agree a management plan.
  • Ask directly about the social and psychological effects of psoriasis and signpost sources of support, such as patient support groups.[9] Psoriasis' impact is not directly related to the overall area affected or disease activity, but more to the site distribution and the attitudes of the patient. Tools such as the Dermatology Life Quality Index may be helpful.[10]
  • Consider an individual's cardiovascular risk where the psoriasis is severe (affecting >10% of the body's surface area; if there has been previous inpatient treatment or the patient has had UV light treatment or other systemic therapy) and monitor and manage this appropriately.[5] Whilst only severe psoriasis has been shown to confer a substantially increased cardiovascular risk, offer all healthy lifestyle advice concerning smoking, alcohol, body weight and exercise.
  • Screen for the development of psoriatic arthropathy and advise to seek medical help for unexplained joint pain or swelling. The psoriasis epidemiology screening tool (PEST) is suggested.[11]

Topical therapy[12]

The sequence of choice of topical agents will vary according to the extent and pattern of psoriasis, and patient preference. Try to keep the number of treatments per day to a minimum to improve concordance.

Practical support and advice about the use and application of topical treatments should be provided. A potent corticosteroid applied once daily, plus vitamin D or a vitamin D analogue applied once daily (applied separately, one in the morning and the other in the evening) for up to four weeks should be offered as initial treatment for adults with trunk or limb psoriasis.[1] 

  • Regular emollients reduce scale and itch. Use liberally and frequently (apply 3-4 times a day in the direction of hair growth) to soften and reduce scaling and irritation. Use a combination of bath oil, soap substitute and emollient. Do not underestimate quantities for prescriptions: adults with generalised disease will need 500 g emollient/week. Ideally, patients should have a daily soak in the bath (with bath oil), then pat their skin dry, and then apply a thick layer of emollient.
  • Topical steroids:
    • Short-term/intermittent use of a potent topical steroid (eg, beclometasone 0.1%) or a combination product with calcipotriol (eg, Dovobet®).
    • A Cochrane review found that potent to very potent corticosteroids perform as well as vitamin D analogues, with a lower incidence of local adverse events but combining corticosteroid with vitamin D analogue was the most effective.[13]
    • Potent steroids should be used for up to two weeks (with no more than 50 g used per week) whilst Dovobet® is licensed for up to four weeks' use.
    • Topical use of potent corticosteroids on widespread psoriasis can lead to systemic as well as to local side-effects, and the development of complications such as erythroderma or generalised pustular psoriasis.
    • Current guidelines therefore suggest that potent steroids can be used in the short term to gain control of chronic plaque psoriasis in a primary care setting, but that long-term use should be avoided.[12]
  • Vitamin D analogues, usually calcipotriol (eg, Dovonex®), are used for longer-term treatment. Where this causes local irritation, switch to alternatives such as calcitriol or tacalcitol. Improvement generally occurs within two weeks, but improvement frequently reaches plateau at eight weeks. Do not exceed the maximum recommended dosage, due to risk of hypercalcaemia and parathyroid hormone suppression.

If a vitamin D analogue is not tolerated or is ineffective, options include:

  • Coal tar (solution, cream or lotion) - preparations with between 1% and 5% are as effective as stronger ones; stronger tar preparations tend to be messy. A large cohort study did not show any increase in cancer (both skin and non-skin malignancies) associated with the past user of topical tar treatments.[14]
  • Tazarotene gel - a vitamin A analogue that is clean and odourless. Irritation is common (occurs in about 20%) but it is minimised by applying tazarotene sparingly to the plaques and avoiding normal skin. It should not be used by pregnant women or women planning a pregnancy, due to potential teratogenicity.
  • Short contact dithranol - for 30-minute exposures in patients with few but relatively large plaques, building from 1-10% (as tolerated).[15] Patients need to be shown how to apply creams carefully to minimise side-effects (skin irritation and temporary skin staining). Products can cause permanent staining of fabrics and bath.

Scalp psoriasis[12]
For patients with thick scaling of the scalp, initial treatment with overnight application of salicylic acid, tar preparations, or oil preparations (eg, olive oil, coconut oil) to remove thick scale is recommended.

Facial and flexural psoriasis[12]

  • Moderate-potency topical corticosteroids (eg, clobetasone butyrate) are recommended for short-term use in facial and flexural psoriasis.
  • If moderate-potency topical corticosteroids are ineffective in facial and flexural psoriasis, then vitamin D analogues or tacrolimus ointment are recommended for intermittent use.

Widespread plaque psoriasis
For very widespread plaque psoriasis, the same treatments may be appropriate but dithranol is often impracticable and more potent corticosteroids hazardous if used on a long-term basis.

Secondary care referral

Referral to a dermatology specialist is indicated if:[1] 

  • There is diagnostic uncertainty.
  • Psoriasis is severe or extensive - eg, more than 10% of the body surface area is affected.
  • Psoriasis cannot be controlled with topical therapy.
  • Any associated nail disease has a major functional or cosmetic impact.
  • Psoriasis is having a major impact on a person's physical, psychological or social well-being.

Secondary care management[12]

  • Phototherapy is a second-line treatment and is used for extensive and widespread disease, or where there is resistance to topical treatment:[9]
    • Narrow-band ultraviolet B (UVB) therapy offers superior efficacy with less risk of burning:
      • The National Institute for Health and Clinical Excellence (NICE) recommends that narrow-band UVB phototherapy should be offered to people with plaque psoriasis that cannot be controlled with topical treatments alone. Treatment with narrow-band UVB phototherapy can be given three or two times a week. A response may be achieved more quickly with treatment three times a week.[1] 
      • The major drawback of this therapy is the time commitment required for treatments and the accessibility of the UVB equipment. Home phototherapy is cost-effective and safe but not widely available.[16][17]
      • Advise patients against the use of sunbeds as a UV source for self-treatment.
    • Photochemotherapy uses a photosensitising drug (eg, PUVA) to treat patients with more extensive or resistant disease. Therapy is usually administered 2-3 times per week, with maintenance treatments every 2-4 weeks until remission.
      • Adverse effects of PUVA therapy include nausea, pruritus, and a burning sensation.
      • Long-term complications include increased risks of skin damage and skin cancer.
      • PUVA has been combined with oral retinoid derivatives to decrease the cumulative dose of UVA radiation to the skin.
  • Systemic agents are reserved for severe or refractory psoriasis.
    • Systemic non-biological therapy should be offered to people if psoriasis cannot be controlled with topical therapy and it has a significant impact on physical, psychological or social well-being, and one or more of the following apply:[1] 
      • psoriasis is extensive (eg, more than 10% of body surface area affected or a PASI score of more than 10); or
      • psoriasis is localised and associated with significant functional impairment and/or high levels of distress (eg, severe nail disease or involvement at high-impact sites such as the face, flexures, genitalia, scalp, palms and soles); or
      • phototherapy has been ineffective, cannot be used or has resulted in rapid relapse (defined as greater than 50% of baseline disease severity within three months).
    • Methotrexate is the first choice of systemic agent for people with psoriasis who fulfil the criteria for systemic therapy except that ciclosporin should be offered as the first choice of systemic agent for people who need rapid or short-term disease control (eg, a psoriasis flare), have palmoplantar pustulosis, or are considering conception (both men and women) and systemic therapy cannot be avoided.[1]
    • Methotrexate is useful for extensive chronic plaque psoriasis in patients who are inadequately controlled by topical therapy alone,[9] or where there is concomitant psoriatic arthropathy. Methotrexate can cause a clinically significant rise in transaminases and long-term therapy may be associated with liver fibrosis.[1] 
    • Ciclosporin is used for short-term intermittent use, usually with a course of treatment for 4-12 weeks, to induce remission, which could be repeated later following relapse.[9]
    • Acitretin is an oral retinoid. It is indicated for severe extensive psoriasis resistant to other forms of therapy. It is only moderately effective in many cases and it is therefore usually combined with other treatments.[9]
    • Fumaric acid esters may be considered as an alternative maintenance therapy in patients who are not suitable for the above agents.
    • Second-tier agents include hydroxycarbamide, mycophenolate, sulfasalazine, azathioprine and leflunomide.
  • Biological therapies - etanercept, efalizumab, adalimumab, infliximab and ustekinumab - are recommended as a treatment option for adults with plaque psoriasis when the following criteria are both met:[18][19][20][21]
    • The disease is severe.
    • The psoriasis has not responded to standard systemic therapies including ciclosporin, methotrexate and PUVA, or the person is intolerant of, or has a contra-indication to, these treatments.
  • Treatment should be discontinued if there is an inadequate response. Efalizumab should only be used if the psoriasis has failed to respond to etanercept.
  • Changing to an alternative biological drug should be considered in adults if:[1] 
    • the psoriasis does not respond adequately to a first biological drug, ie 10 weeks after starting treatment for infliximab, 12 weeks for etanercept, and 16 weeks for adalimumab and ustekinumab (primary failure); or
    • the psoriasis initially responds adequately but subsequently loses this response, (secondary failure); or
    • the first biological drug cannot be tolerated or becomes contra-indicated.

Chronic plaque psoriasis is often associated with significant psychosocial difficulties. The quality of life may be severely affected by pruritus, dry and peeling skin, fissuring, and the adverse effects of therapy.[1] 

Self-consciousness and embarrassment about appearance may lead to significant anxiety and depression.

Aggressive use of topical steroids may induce progression to pustular and erythrodermic forms of psoriasis.

  • The course of plaque psoriasis is unpredictable. It is often intractable to treatment, with relapses occurring in most patients.
  • Both early onset and a family history of disease are considered poor prognostic indicators.
  • Pustular flares of disease may be provoked by systemic corticosteroid therapy. Such flares can be fatal. Disease-related mortality is otherwise very rare in psoriasis.
  • Adverse effects of systemic treatments (eg, hepatic fibrosis from methotrexate) and phototherapy (eg, PUVA-induced skin cancers with metastases) are the primary disease-related causes of death.
  • Avoiding specific exacerbating factors may help to prevent or minimise flare-ups but the cause of disease exacerbation is often unknown.
  • Efforts should be made to prevent or detect and treat the non-cutaneous complications of psoriasis, such as cardiovascular disease and depression.

Further reading & references

  1. Psoriasis, NICE Clinical Guideline (Oct 2012)
  2. Rahman P, Elder JT; Genetic epidemiology of psoriasis and psoriatic arthritis. Ann Rheum Dis. 2005 Mar;64 Suppl 2:ii37-9; discussion ii40-1.
  3. Morar N, Willis-Owen SA, Maurer T, et al; HIV-associated psoriasis: pathogenesis, clinical features, and management. Lancet Infect Dis. 2010 Jul;10(7):470-8.
  4. Patel U, Mark NM, Machler BC, et al; Imiquimod 5% cream induced psoriasis: a case report, summary of the literature Br J Dermatol. 2011 Mar;164(3):670-2. doi: 10.1111/j.1365-2133.2010.10124.x. Epub
  5. Boehncke WH, Boehncke S, Schon MP; Managing comorbid disease in patients with psoriasis. BMJ. 2010 Jan 15;340:b5666. doi: 10.1136/bmj.b5666.
  6. Menter A, Griffiths CE; Current and future management of psoriasis. Lancet. 2007 Jul 21;370(9583):272-84.
  7. PASI score; DermNet NZ
  8. Psoriasis area severity index calculator
  9. Psoriasis - General Management, British Association of Dermatologists (2008)
  10. Dermatology life quality index
  11. Helliwell PS, Psoriatic arthropathy and its presentation in primary care, Hands On (Arthritis Research Council), series 6, 2009
  12. Diagnosis and management of psoriasis and psoriatic arthritis in adults; Scottish Intercollegiate Guidelines Network - SIGN (October 2010)
  13. Mason AR, Mason J, Cork M, et al; Topical treatments for chronic plaque psoriasis. Cochrane Database Syst Rev. 2009 Apr 15;(2):CD005028.
  14. Roelofzen JH, Aben KK, Oldenhof UT, et al; No increased risk of cancer after coal tar treatment in patients with psoriasis J Invest Dermatol. 2010 Apr;130(4):953-61. Epub 2009 Dec 17.
  15. Clinical guidelines: Topical Dithranol, British Association of Dermatologists (BAD)
  16. Koek MB, Buskens E, van Weelden H, et al; Home versus outpatient ultraviolet B phototherapy for mild to severe psoriasis: BMJ. 2009 May 7;338:b1542. doi: 10.1136/bmj.b1542.
  17. Koek MB, Sigurdsson V, van Weelden H, et al; Cost effectiveness of home ultraviolet B phototherapy for psoriasis: economic BMJ. 2010 Apr 20;340:c1490. doi: 10.1136/bmj.c1490.
  18. Etanercept and efalizumab for the treatment of adults with psoriasis, NICE Technology Appraisal (2006)
  19. Psoriasis - infliximab; NICE Technology Appraisal (January 2008)
  20. Adalimumab for the treatment of psoriasis; NICE Technology Appraisal Guidance (June 2008)
  21. Ustekinumab for the treatment of adults with moderate to severe psoriasis, NICE Technology Appraisal Guidance (September 2009)

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Huw Thomas
Current Version:
Peer Reviewer:
Dr John Cox
Last Checked:
20/11/2012
Document ID:
2679 (v25)
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