Plaque Psoriasis

Psoriasis is a common, chronic, relapsing, inflammatory skin disorder with a strong genetic basis. Plaque psoriasis is the most common type of psoriasis.

• Psoriasis can affect persons of any race; however, epidemiologic studies have shown a higher prevalence in western European and Scandinavian populations. In these groups, 1.5-3% of the population is affected by the disease.¹
• Psoriasis is thought to be rare in West Africans.

Risk factors

• Both genetic and environmental factors have been implicated in the pathophysiology of psoriasis.
• Genetic factors: HLA-B13, B17, and Cw6 are all associated with plaque psoriasis. Studies of twin siblings have supported the role of genetic factors but also suggested that environmental factors also play a role in the aetiology of plaque psoriasis.
• Environmental factors: a number of factors may exacerbate plaque psoriasis, including:
• Trauma
• Sunlight: there is usually a decrease in severity during periods of increased sun exposure but a small minority have an aggravation of symptoms during strong sunlight. Sunburn can also lead to an exacerbation of plaque psoriasis.
• Infection, e.g. streptococcal, HIV infection
• Psychological stress
• Drugs: e.g. lithium, beta-blockers and non-steroidal anti-inflammatory drugs, and withdrawal of systemic steroids.
• Smoking
• Alcohol (e.g. HIV infection), alcoholism, smoking and UV light, can affect the course, duration, and clinical appearance of plaque psoriasis. Plaque psoriasis is often worse in the winter and improves in the summer.

• Plaque psoriasis may present at any age but most often in adolescents, young adults and those in middle age.
• The extent and duration of the disease is very variable.
• Plaque psoriasis most often causes itchy, circular-to-oval red plaques distributed over extensor body surfaces and the scalp.
• The plaques usually show scaling and peeling.
• New lesions often appear at sites of injury or trauma to the skin (Koebner reaction), which typically occurs 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 with adults.
• Up to 10-20% of patients with plaque psoriasis also experience psoriatic arthritis.
• Acute episodes of plaque psoriasis may evolve into more severe disease, e.g. pustular or erythrodermic psoriasis.

Signs

• Plaques: elevated lesions that vary in size from one to several centimeters. The number of lesions may range from few to many at any given time. The plaques are irregular to oval and are most often located on the scalp, trunk, and limbs, and mainly on extensor surfaces such as the elbows and knees. Smaller plaques may coalesce into larger lesions, especially on the legs and sacral regions. Fissuring within plaques can occur when lesions are present over joint lines or on the palms and soles.
• Psoriatic plaques are well defined and have sharply demarcated boundaries. Psoriatic plaques occasionally appear to be immediately encircled by a paler peripheral zone.
  
  
  
  
  
  
• The psoriatic lesions are a very distinctive rich, full, red color. When present on the legs, lesions sometimes carry a blue or violaceous tint.
• Psoriatic plaques typically have a dry, thin, silvery-white scale but the amount and thickness of the scale is variable. Removing the scale reveals a smooth, red, glossy membrane with tiny punctate bleeding points.
• Psoriatic plaques tend to be symmetrically distributed over the body.
• Nail changes are often seen, with pitting, onycholysis, subungual hyperkeratosis, or the oil-drop sign.

• Bowen disease
• Cutaneous T-Cell lymphoma
• Drug eruptions
• Lichen planus
• Discoid lupus erythematosus
• Dermatitis
• Pityriasis rosea
• Seborrheic dermatitis
• Syphilis
• Superficial basal cell carcinoma

• Diagnosis is usually made on clinical findings, and investigations are very rarely required.
• Skin biopsy may occasionally be required to confirm the diagnosis.

Topical therapy

• A number of topical treatments are available (eg, corticosteroids, coal tar, anthralin, calcipotriene, tazarotene).
• Emollients should be used to soften scaling and reduce any irritation
• For localised plaque psoriasis, e.g. on the elbows or knees, one or more of the following topical preparations can be tried. The sequence of choice will vary according to the extent and pattern of psoriasis, and patient preference:²
  • A tar-based cream, or a tar/corticosteroid mixture (most are relatively mild; stronger tar preparations tend to be messy)
  • A moderate potency topical corticosteroid (e.g. 0.05% clobetasone butyrate): stronger agents can be used on palms and soles or on the scalp. Use of topical steroids may lead to rebound exacerbation when treatment is discontinued.
  • A vitamin D analogue (e.g. Calcipotriol, calcitriol or tacalcitol - the latter two tend to be less irritant and are more suitable for face or flexures, but should still be used with caution)
  • Calcipotriol with betamethasone dipropionate as a combination product (note that long term data regarding relapse rates is not yet established)
  • A vitamin A analogue (tazarotene): tazarotene is clean and odourless. Irritation is common but it is minimised by applying tazarotene sparingly to the plaques and avoiding normal skin.
  • A dithranol preparation, usually used as a short-contact treatment (these are effective but more difficult to use, especially if there are many small lesions)
• For more widespread plaque psoriasis, the same treatments may be appropriate but dithranol is often impracticable to apply to multiple small lesions and will irritate flexures, and topical corticosteroids may be inappropriate for use in widespread psoriasis, particularly more potent agents if used on a long-term basis.

Phototherapy

• Phototherapy is a second line treatment and should only be used for extensive and widespread disease. Resistance to topical treatment is another indication for phototherapy:³
• Narrow-band UVB therapy offers superior efficacy with less risk of burning. UVB therapy is usually combined with one or more topical treatments. UVB is often combined with topical corticosteroids, calcipotriene, tazarotene, or simply bland emollients. UVB phototherapy is extremely effective for treating moderate-to-severe plaque psoriasis.
• The major drawback of this therapy is the time commitment required for treatments and the accessibility of the UVB equipment. Home ultraviolet therapy can overcome some of the problems of time and convenience but they are expensive.
• PUVA photochemotherapy uses the photosensitizing drug methoxsalen (8-methoxypsoralens) in combination with UVA irradiation to treat patients with more extensive 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.
• Excimer laser UVB therapy can deliver high-dose light to limited plaques.

Systemic agents

• Only used after both topical treatments and phototherapy have been unsuccessful and for patients with very active psoriatic arthritis or who have disease that is physically, psychologically, socially, or economically disabling.
• Methotrexate is useful in acute, generalised, pustular psoriasis, psoriatic erythroderma, psoriatic arthritis, and for extensive chronic plaque psoriasis in patients who are inadequately controlled by topical therapy alone.⁴
• Ciclosporin may be employed either as a maintenance treatment, using long term continuous therapy, or as a short course of treatment for 4 to 12 weeks, to induce remission, which might then be repeated later following relapse.⁵
• Hydroxycarbamide is a second line modality for the treatment of psoriasis and is usually reserved for cases where other second line agents have failed or are contraindicated.⁶
• 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.⁷

Biological therapies

• Biological therapies for psoriasis comprise two main groups:⁸
  • Agents targeting the cytokine tumour necrosis factor (TNF)-alpha (e.g. etanercept, infliximab, adalimumab)⁹
  • Agents targeting T cells or antigen-presenting cells (e.g. efalizumab, alefacept).
• Etanercept should be considered for treating adults with severe plaque psoriasis when other treatments have been ineffective or contraindicated. If there has been no definite improvement with etanercept after 12 weeks, the treatment should be stopped.¹⁰
• Efalizumab should be considered for treating adults with severe plaque psoriasis when other treatments have been ineffective or contraindicated, and etanercept treatment has been ineffective.¹⁰

• The quality of life may be severely affected by pruritus, dry and peeling skin, fissuring, and the adverse effects of therapy.
• Self-consciousness and embarrassment about appearance. May lead to significant anxiety and depression.
• Approximately 10-20% of all cases of plaque psoriasis are associated with psoriatic arthritis.
• 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, psoralen plus UVA [PUVA]-induced skin cancers with metastases) are the primary disease-related causes of death.

• Avoiding specific exacerbating factors may help prevent or minimize flare-ups but the cause of disease exacerbation is often unknown.