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Psoriasis
Foundation Year 2 Doctor, West Midlands Deanery
GP Registrar, West Midlands VTS Training Scheme
GP Registrar, West Midlands VTS Training Scheme
General Practitioner and Associate Clinical Professor, Warwick Medical School and Honorary Editor, RCGP Publications
Email: k.chiu{at}doctors.org.uk
| Abstract |
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Psoriasis (derived from the Greek word psora meaning to itch) is a common immune-mediated papulosquamous skin disease. First recognized as an independent condition by English dermatologist Robert Willan in 1798, the term is now used to include a variety of clinical appearances with different morphology, distribution, severity and course. Although common, the pathogenesis of psoriasis is not well understood and involves a multitude of genetic and environmental factors. Management of psoriasis includes controlling the extent and severity of disease and its complications, improving the patient's quality of life while minimizing potentially toxic side effects of treatments. This review aims to provide an overview of this complex condition, from its presentation, diagnosis, management in primary care and the referral criteria to secondary care.
| Incidence and prevalence |
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The prevalence of psoriasis shows variation according to ethnic group. It is highest in Caucasian population and lower in Asian and South American Indian populations. There is also a latitudinal difference, lower closer to the equator. It is equally common in males and females and its onset may be at any age. There appears to be a bimodal age distribution, with the first peak at mean age of 15–20 years and the second peak at 55–60 years. It is uncommon below the age of 10.
| The GP curriculum and psoriasis GP curriculum statement 15.10 states that GPs must be able to manage primary contact with patients who have a skin problem. In particular, GP should:
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In the UK, the age- and sex-adjusted incidence of psoriasis is between 6 and 14 per 10 000 individuals, while the prevalence is estimated to be around 1.5%.
| Genetic factors |
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The genetic basis of psoriasis remains unknown but current evidence suggests that it may be a multifactorial genetic disorder. Only a small minority of cases behave in the Mendelian manner. The risks of psoriasis in children of affected parents are estimated to be 41% if both parents are affected, 14% if only one is affected, 6% if one sibling is affected and 2% if there is no first-degree family history.
There is an association of psoriasis with HLA allele HLA-Cw6. Possession of this allele is associated with an earlier age of onset and a positive family history of psoriasis (classification type I psoriasis of Henseler and Christopher). Type II psoriasis lacks the HLA association and its onset occurs much later, after 40 years. Several susceptibility loci have been identified, referred to as PSORS1-6, but the association between genes and susceptibility is not fully understood.
| Environmental factors |
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Multiple environmental factors have been implicated in psoriasis. Streptococcal throat infection appears to trigger guttate psoriasis and it can also exacerbate chronic plaque psoriasis. Stress is a well known factor for psoriasis onset or flare-up. Development of psoriasis after stresses can range from 2 days up to a month. Trauma to skin, such as cuts or scratching, may induce a Koebner response (appearance of lesions along a site of injury) in psoriasis. Obese patients are more likely to present with severe psoriasis and polyunsaturated fatty acids, gluten and alcohol have shown to be related to more severe psoriasis. Smoking is associated with the onset of psoriasis and consumption of more than 20 cigarettes daily has been associated with more than two-fold increased risk of severe psoriasis. Medications such as antimalarials, beta blockers, lithium, Nonsteroidal anti-inflammatory drugs (NSAIDs), ACEinhibitors, gemfibrozil (lipid lowering drug), interferons
and g and imiquimod (immune response modifier) are also associated with exacerbation of the condition. Ultraviolet radiation improves psoriasis and unsurprisingly is used as a therapeutic agent. | Histology |
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Histological hallmarks of Psoriasis include:
- Epidermal hyperplasia with thick keratin layers. Increased epidermal turnover also leads to inability of the epidermal cells to adequately differentiate into normal keratin scales.
- Dilated and prominent blood vessels in the dermis—keratin scales can be peeled back to show the dilated vessels beneath (Auspitz sign). The presence of dilated vessels is also partly responsible for the reddening and erythema seen clinically.
- An inflammatory infiltrate of leucocytes, predominantly into the dermis
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| Clinical presentation |
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The International Psoriasis Council has classified psoriasis according to its phenotype: plaque, guttate, pustular and erythroderma.
Chronic plaque psoriasis (psoriasis vulgaris) is the most common form of psoriasis, accounting for around 90% of presentations. Patients with this form of psoriasis present with plaques—pink or red in colour with a scaling surface and often with well-demarcated borders. It commonly affects the flexures (elbows and knees). Affected areas are not usually itchy. Plaques can range in size from millimetres to much larger skin areas. Other involved areas include the scalp, nails and genitals, and they may be the only presentation of the disease on the skin.
There are several sub-classifications of plaque psoriasis:
- Flexural/intertriginous psoriasis are well-defined thin plaques with minimal scales. It has the classical shiny appearance and is found in intertriginous areas (submammary, groins, axillae, genitalia and natal cleft).
- Seborrhoeic psoriasis has similar morphology and anatomical distribution to seborrhoeic dermatitis (nasolabial folds, medial cheeks, nose, ears, eyebrows, hair line, scalp, presternal and interscapular regions) and the two are sometimes difficult to distinguish
- The scalp is the most commonly involved anatomical site for psoriasis. Its morphology can either be similar to flexural/intertriginious or seborrhoeic psoriasis.
- Palmar/plantar psoriasis presents as confluent redness and scaling, discrete plaques extending to the wrist and margins of the soles and heels
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Guttate psoriasis (derived from the latin word gutta meaning drop) describes small papules that erupt typically over a period of 1 month, persist for another and resolve by the third month. It usually has a centripetal distribution, but can also involve the limbs. This form of psoriasis is found commonly in young people, with a preceding streptococcal infection in two-thirds of the cases.
Pustular psoriasis can either be localized or generalized. Characteristic features of localized pustular psoriasis include nail dystrophy and paronychial redness and scaling. It may also manifest as chronic deep lesions of the palms and soles. Generalized pustular psoriasis is sheets of small, monomorphic pustules. It is classically associated with withdrawal of systemic glucocorticosteroid and patients are constitutionally upset.
When confluent psoriasis involves more than 90% of the skin surface, it is known as erythroderma. Erythrodermic psoriasis can be life threatening. Among these patients, characteristic scaling is usually absent. There is significant heat loss, dehydration and metabolic disturbance caused by increased cutaneous blood flow.
Palmoplantar pustulosis, sometimes known as pustular psoriasis, presents as sterile, yellow pustules on a background of erythema and scaling, affecting only the palms and soles. It is associated with psoriatic nail involvement. However, its association with psoriasis is debatable as the genetics and demographics are different from other forms of psoriasis. Many believe it to be a separate disease entity.
| Psoriasis—a systemic disease? |
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Psoriasis is now considered a systemic inflammatory condition analogous to other inflammatory immune disorders. Population studies from Sweden have found that psoriasis is associated with a spectrum of disease (Lindegård 1986). More recently, have found that psoriasis confers an independent risk for myocardial infarction, an important and previously unrecognized cause of morbidity and mortality.
| Psoriatic nail disease |
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Nail changes in psoriasis usually presents as thickening and pits on the surface of the nail. The nail may also detach from its nail bed (onycholysis). In general, fingernails are affected more than toenails. Thickening of the nail is the result of subungual hyperkeratosis (collection of keratinous material under the nail), whereas the pits are thought to be caused by defective nail formation.
| Psoriatic joint disease |
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Usually, patients have psoriatic skin changes prior to manifesting any joint disease but this is not always the case. Psoriatic arthritis often presents with joint pain, stiffness, erythema and swelling. The most commonly affected joints are the distal interphalangeal joints. There is a two-fold increase in the incidence of psoriasis in patients with seronegative arthritis. NSAIDs are the mainstay of early treatment. In severe cases, disease-modifying medications such as Methotrexate may be required.
| Treatment |
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Treatment for psoriasis aims to control the extent and severity of disease and improve quality of life while minimizing potentially toxic side effects. When deciding on treatment, patient age, sex, occupation and co-morbidities should be considered as well as disease severity and anatomical location. Patients should be reminded of the option of no treatment in mild disease and be educated about exacerbating factors and triggers (Box 1). Compliance to treatment remains a problem in managing the disease (Fig. 1).
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Box 1. Exacerbating factors in psoriasis:
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Treatment modalities comprise topical therapies, phototherapy and systemic agents. Most patients with mild to moderate psoriasis can be managed in primary care. Referral to secondary care is needed when these treatments fail.
| Topical agents |
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Topical agents used in the treatment of psoriasis are emollients, keratolytics, topical steroids, vitamin D3 analogues, dithranol and topical retinoids. Application of these should ideally be administered by the primary health care team, dermatology outreach teams or at nurse led outpatient treatment centres.
Emollients may be water or lipid based and are used to soften the hyperkeratotic surface of plaques. Emollients soothe, smooth and hydrate the skin. Several examples are available, with choice of agent often being influenced by patient preference. The most effective emollients, such as 50/50 (liquid and white soft paraffin), may be limited by their greasiness and adverse cosmetic effects which can lead to poor compliance. Effects of emollients are short lived and should be applied several times a day. Specialist preparations for bathing are also available to maintain hydration.
Topical corticosteroids are widely used in the treatment of psoriasis. They are an effective, rapid acting and a cosmetically acceptable form of treatment. Potency ranges from mild to strong allowing strength to be adjusted according to severity of disease (Box 2). Occlusive therapy, in which a thin polythene film is used to provide a high concentration of topical agent to an area of severe disease, can greatly enhance effectiveness. It must only be used for restricted periods and on limited areas. Local side effects, the development of tolerance and a relapse of disease on treatment withdrawal limit their use.
Box 2. Potency of topical corticosteroids (least potent to most potent)
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Coal tar is one of the oldest treatments for psoriasis and is used for its anti-inflammatory properties. It is available in a variety of forms and strengths, including creams, ointments and shampoos. Although there have previously been concerns regarding its safety (it is a known carcinogen in higher, non-therapeutic concentrations), it is an effective treatment for inducing remission. Coal tar is commonly administered in hospital or day care settings, and it is available over the counter to patients off prescription. Treatment is limited by the unpleasant smell and messy application. Synergistic use with ultraviolet-B (UVB) radiation is a very effective method of treating mild psoriasis.
Keratolytic agents such as salicylic acid can be used on palms, soles and the scalp to aid in the removal of surface scaly plaques. They enhance the penetration of other agents, but may cause toxicity in high concentrations.
Dithranol is used as short contact therapy whereby application is limited to 15–30 minutes of skin contact and then washed away. Dithranol is extremely irritant and for this reason should only be applied to affected skin areas. The lowest concentration of 0.1% should be used initially; this can be increased if tolerated to therapeutic concentrations. Dithranol stains clothing and can therefore be less cosmetically acceptable. Greater efficacy is seen when used in conjunction with UVB phototherapy, high-potency corticosteroids or calcipotriol.
Topical vitamin D analogues such as calcipotriol and calcitriol act by inhibiting epidermal cell proliferation and enhancing cell differentiation. Although a well-established first-line treatment for psoriasis, the relatively slower response rate together with a better long-term safety profile makes them a useful maintenance therapy. They may be used as monotherapy or as combination therapy to reduce the dose and duration of other antipsoriatic agents such as photochemotherapy.
Tazarotene is a topical retinoid (vitamin A derivative) used in the treatment of mild to moderate plaque psoriasis. It is applied once daily for up to 12 weeks duration. Care must be taken to avoid application to normal areas of skin due to its irritant effect. Excessive exposure to UV light should also be avoided. Due to its potentially teratogenic potential, this treatment should not be given to pregnant patients. It is not recommended for breastfeeding mothers, as there is currently no evidence whether tezarotene can pass through breast milk and its potential effect on babies and children is unknown. It is not recommended to patients under the age of 18.
| Phototherapy |
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Phototherapy is used in secondary care for patients with widespread guttate or chronic psoriasis or those with refractory disease. Two forms are recognized, treatment with UVB light or photochemotherapy with psoralen-ultraviolet-A (PUVA). Both may be combined with other therapies to provide greater efficacy and minimize the total cumulative dose, thereby reducing the risk of chronic adverse effects.
Broadband or narrowband UVB therapy is typically administered two to three times per week. It is contraindicated in patients with malignancy and systemic lupus erythematosus but can be used in pregnant women and children.
PUVA therapy involves the administration of topical or oral psoralens and long wave UVA. Although unlicensed in the UK, it continues to be used as treatment for resistant psoriasis. PUVA therapy carries both local side effects, such as skin burning and pain and chronic adverse effects such as premature skin ageing, pigmentation and carcinogenicity.
Box 3. Guidelines for referral to secondary care. Primary Care Dermatology Society and British Association of Dermatologists
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Box 4. Content of the referral letter: (adapted form British Association of Dermatologists Guidelines)
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| Systemic therapies |
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Systemic disease-modifying agents such as methotrexate, ciclosporin and acitretin are used for severe unresponsive psoriasis under the supervision of dermatologists in the hospital setting. Indications include repeated hospital admissions, extensive chronic plaque psoriasis in the elderly or infirm and severe psoriatic arthropathy. Acitretin, an oral retinoid, is highly teratogenic and must be used with caution in women of child-bearing age. Methotrexate inhibits DNA synthesis and may be administered orally, intramuscularly or intravenously once a week. Ciclosporin is an immunosuppressant drug effective against all clinical subtypes of psoriasis. It is usually used as short-course therapy for 4–12 weeks but can also be prescribed for maintenance or long-term continuous therapy. Although effective treatments for severe and disabling disease, all patients receiving systemic disease-modifying drugs need close monitoring and supervision during treatment due to potentially toxic side effects.
| Biological agents |
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Research into the role of genetics and immunology in the pathogenesis of psoriasis has led to the development of biological agents to target specific pathways of the disease process. Recombinant molecules such as cytokines and monoclonal antibodies are under development as future treatment modalities. The theory of T-cell mediation in the development of psoriasis has led to investigation of agents that target T-cell activation. Alefacept is the first T-cell inhibitor to be approved for the treatment of psoriasis in the USA in 2003. TNF-
inhibitors such as infliximab are predominantly used in the treatment of psoriatic arthropathy, although their use in psoriasis may become more widespread in the future. Continual research into the aetiology of psoriasis may lead to the potential use of gene therapy in the treatment of the disease.
| Psychological issues and psoriasis |
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It is worth noting that, like other chronic conditions, psoriasis has a major impact on the patient's quality of life. The appearance of the psoriasis is well documented to cause stigmatization, anxiety, depression and suicidal ideation. Interestingly, these negative feelings have no relation to either the physical severity or anatomical location of psoriasis. When dealing with psoriasis, psychological intervention may have a role. Many frameworks, some generic to all chronic diseases and others specific to psoriasis, have been used to assess the quality of life in patients. Currently, there is no universally accepted model and a strategy of how to tackle these issues is yet to be established. Nevertheless, when dealing with patients with psoriasis, a holistic biopsychosocial model of medicine should be used.
| Referral criteria |
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Many patients with psoriasis should be able to self-manage the condition with appropriate education, guidance and support from the primary health care team and dermatology outreach teams. Box 3 outlines guidelines for referral to secondary care and the relevant information that should be included in the referral is listed in Box 4. Ideally, primary and secondary care services should work in collaboration to offer cost-effective and efficient service provision.
Key points
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| References |
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British Association of Dermatologists. Psoriasis Guideline. (2006) www.bad.org.uk.
Bundu-Kamara S. Therapeutic management of psoriasis. Hospital Pharmacist (2002) 9:191–199.
Gelfand JM, Weinstein R, Porter SB, Neimann AL, Berlin JA, Margolis DJ. Prevalence and treatment of psoriasis in the United Kingdom: a population-based study. Archives of Dermatology (2005) 141((12)):1537–41.
Griffiths CE, Barker JN. Pathogenesis and clinical features of psoriasis. Lancet (2007) 370((9583)):263–71.[CrossRef][Web of Science][Medline]
Griffiths CE, Christophers E, Barker JN, et al. A classification of psoriasis vulgaris according to phenotype. British Journal of Dermatology (2007) 156((2)):258–62.[CrossRef][Web of Science][Medline]
Gudjonsson JE, Elder JT. Psoriasis: epidemiology. Clinics in Dermatology (2007) 25((6)):535–46.[CrossRef][Web of Science][Medline]
Kirby B, Fortune DG, Bhushan M, Chalmers RJ, Griffiths CE. The Salford Psoriasis Index: an holistic measure of psoriasis severity. British Journal of Dermatology (2000) 142((4)):728–32.[CrossRef][Web of Science][Medline]
Langley RG, Krueger GG, Griffiths CE. Psoriasis: epidemiology, clinical features, and quality of life. Annals of the Rheumatic Diseases (2005) 64((Suppl 2)):ii18–23;. discussion ii24–5.
Lindegård B. Diseases associated with psoriasis in a general population of 159,200 middle-aged, urban, native Swedes. Dermatologica (1986) 172((6)):298–304.[Web of Science][Medline]
Menter A, Griffiths EM. Current and future management of psoriasis. Lancet (2007) 370:272–84.[CrossRef][Web of Science][Medline]
Smith CH, Barker JNWN. Psoriasis and its management. British Medical Journal (2006) 333:380–384.
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