COMPLETE HOW TO TREAT QUIZZES ONLINE ( to earn CPD or PDP points.

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1 HTT_017 JAN18_13. pdf Page 17 10/ 01/ 13, 2: 32 PM How to Treat PULL-OUT SECTION COMPLETE QUIZZES ONLINE ( to earn CPD or PDP points. inside Epidemiology Clinical features Living with psoriasis Differential diagnoses Investigations Management The authors DR ANNE HOWARD head of dermatology, Western Hospital, Footscray; and visiting dermatologist, Royal Melbourne, Royal Children s and Women s Hospitals and Skin and Cancer Foundation, Melbourne, Victoria. DR SARAH GAMBONI dermatology fellow, the Women s Hospital, Melbourne; dermatology research fellow, Occupational Dermatology Research and Education Centre, Skin and Cancer Foundation, Melbourne; and medical registrar, the Alfred Hospital, Melbourne, Victoria. Background PSORIASIS can be a physically and emotionally painful and debilitating condition. Its effect on quality of life can often be underestimated. This non-contagious skin condition causes much distress because of its disfiguring skin manifestations. It is a common, chronic, inflammatory and proliferative condition, which is influenced by both genetic and environmental factors. The disease can be widely variable in body distribution, duration and frequency of flares. The most common type is psoriasis vulgaris (chronic plaque psoriasis), which affects 80-90% of those with the disease. 1 cont d next page 18 January 2013 Australian Doctor 17

2 AD_018 JAN18_13. pdf Page 18 10/ 01/ 13, 10: 46 AM Epidemiology OBTAINING accurate figures for the epidemiology and morbidity of psoriasis can be difficult, as diagnostic criteria have never been validated. The prevalence of psoriasis vulgaris is estimated to be between 1.5-3% in Western countries. 2,3 Substantial racial variations occur, with those of non-caucasian background having a lower prevalence of disease. Chinese, West Africans and Japanese have a low prevalence of disease, while there is a very low or absent prevalence in Inuits, Latin American Indians and Samoans. 2,3 Climate appears to affect psoriasis, with those living further from the equator having higher rates of disease. 4 Incidence in a year has been estimated to be 60 individuals per 100,000 per year. 5 seems to have a bimodal age of onset, with early disease typically occurring between the ages of 16 and 30, with some cases occurring even earlier in childhood. 2,3 Earlier onset predicts a more severe, longer-lasting disease, and is usually associated with a positive family history of psoriasis. Late onset is usually between years of age. There is equal incidence in males and females, but females usually have earlier onset of disease. Risk factors is associated with both genetic and environmental risk factors, which can interact and cause disease. The following are the recognised risk factors for the condition. Genetics Susceptibility to psoriasis may be associated with a family history of the disease via a polygenic trait. The bimodal peak in age of onset suggests two pathogenetically different subtypes. Type I, which is hereditary, is strongly HLA associated, (particularly HLA-Cw6), associated with early onset and is more likely to be severe. Other HLA subtypes frequently associated with psoriasis include HLA- B13, HLA-B17 and HLA-Bw57. Type II is sporadic, HLA unrelated, of late onset and usually mild. Trauma Physical trauma is a major factor in the development of lesions, as rubbing and scratching stimulate the psoriatic proliferative process. This results in psoriasis occurring at the site of an injury, known as the Koebner phenomenon. This occurs as an all-or-none insult at multiple sites, meaning that if psoriasis occurs at one site of injury it does so at all sites. Interestingly, there is also a reverse Koebner phenomenon, whereby an injury sustained at the site of an already existing psoriatic lesion may clear existing lesions, again in an all-or-none pattern. Traumatic insults can occur via physical, chemical, electrical, surgical, infective and inflammatory means. The lag time between the trauma and appearance of skin lesions is usually 2-6 weeks. Infection Preceding or concurrent streptococcal infection (particularly of the throat) may precipitate guttate psoriasis, and may be important in psoriasis vulgaris. Additionally, HIV infection has been noted to be associated with psoriasis and psoriatic arthropathy. As features of HIV develop, psoriasis has been shown to become more severe. 6 Stress Stress is well known to stimulate flares and can severely exacerbate psoriasis. It may be associated in as many as 40% of cases in adults and more in children. On another level, psoriasis itself has a detrimental effect on quality of life. Stress management programs can aid in the treatment of psoriasis and shorten exacerbation periods. Drugs Drugs can either trigger or exacerbate psoriasis. The most significant are lithium salts and antimalarials, which may both cause severe reactions, as well as interferon, ACEIs, beta-adrenergic antagonists, NSAIDs and the rapid withdrawal of systemic corticosteroids. These drugs may all cause flares in existing psoriasis and trigger a subsequent psoriasiform drug eruption. Alcohol, smoking and obesity The association between alcohol, cigarettes and psoriasis has long been suspected. While alcohol does not appear to induce psoriasis, it may exacerbate pre-existing disease. Heavy drinkers are known to exhibit more extensive and inflamed disease. Smokers who smoke more than 15 cigarettes a day have been found to display more significant exacerbations of palmoplantar pustulosis, a pustular form of psoriasis. 7 Additionally, it is controversial whether obesity is a consequence of psoriasis or precedes its development. 8 Sunlight Despite usually being beneficial, in a small number of patients sunlight may actually exacerbate psoriasis. These patients may present with a polymorphic light eruption where psoriasis occurs as a secondary phenomenon or it may manifest independently as severely photosensitive psoriasis. Endocrine factors There may be a role for hormonal factors in the development of psoriasis. In women, there is a peak in the development of psoriasis around puberty. During pregnancy, psoriasis may improve and then deteriorate again during the postpartum period. Additionally, hypocalcaemia may be a triggering factor for generalised pustular psoriasis. Interestingly, although active vitamin D 3 analogues improve psoriasis, abnormal vitamin D 3 levels do not induce the condition. Aetiology occurs as a result of interplay between epidermal damage and innate and acquired immunity. The persistence of psoriatic lesions is thought to be due to an ongoing autoreactive immune response. Lesional psoriatic skin shows several features. Epidermal hyperproliferation with loss of differentiation occurs when there is an increase in the proliferating cell compartment in the basal and suprabasal levels of the epidermis with an increase of about seven times the normal number of cycling cells. 9 This process is influenced by multiple growth factors, particularly transforming growth factoralpha (TGF-alpha), which acts as an autocrine (substance secreted by a cell and acting on surface receptors of the same cell) mediator of events. Angiogenesis, through dilation and proliferation of dermal blood vessels also occurs, whereby there is a fourfold increase in superficial, but not deep endothelial microvasculature. Epidermal keratinocytes, with the aid of vascular endothelial growth factor (VEGF) produce an expanded superficial dermal vasculature. Finally, through the induction of inflammatory mediators there is accumulation of inflammatory cells, particularly neutrophils and T lymphocytes to the lesional dermis and epidermis. Molecular genetics plays a role, with at least nine chromosomal loci linked to psoriasis. PSORS1 on chromosome 6p is the major psoriasis genetic determinant, likely accounting for 35-50% of the heritability of the disease. 10 T lymphocytes play an important role in the development of plaque psoriasis with the early influx of T cells into expanding lesions and the increased antigen presentation in psoriatic plaques. A subset of T cell, known as Th17, is thought to be the predominant mediator. Additionally, the innate immune system is suspected to be dysregulated in psoriasis. Innate immune mechanisms lead to antigen-driven T cell expansion and activation. A pathogenic model has been suggested in which aberrations in the stratum corneum trigger activation of innate immune mechanisms, leading to recruitment and activation of Th17 cells, which provide effector cytokines to cause epidermal hyperproliferation and a proinflammatory state. 11 Clinical features PSORIASIS may present with a spectrum of cutaneous manifestations, but lesions share the trademark features of erythema, thickening and silvery-white scale. These macroscopic findings reflect the microscopic features of elongated dilated capillaries close to the skin surface, epidermal acanthosis, plus cellular infiltrates and abnormal keratinisation. The size of lesions may vary from tiny papules to more than 20cm in diameter. They are sharply demarcated with outlines that are usually circular, oval or polycyclic (indicating a conglomeration of several smaller lesions). Sometimes, a pale blanching ring, known as Woronoff s ring, will surround the lesion. The presence of the Koebner phenomenon will be evident from the pattern of psoriatic lesions. During exacerbations of psoriasis, lesions will often become itchy. Inflamed lesions may also be slightly tender. Pinpoint papules surrounding existing psoriatic plaques indicate that the patient is in an unstable phase of the disease. Furthermore, expanding psoriatic lesions are recognisable by an active edge with more intense erythema. The involution of a plaque usually starts in its centre, resulting Figure 1: Chronic plaque psoriasis on the knees. in annular psoriatic lesions. Chronic plaque psoriasis Chronic plaque psoriasis is characterised by well-demarcated, erythematous, papulosquamous lesions. There is usually a symmetric distribution of scaly plaques with varied degree of body surface involvement. The predominant Figure 2: Guttate psoriasis on the arms. sites are the scalp, elbows, knees (figure 1) and presacrum, as well as the hands and feet. The genitalia may be involved in up to 45% of patients. The course of the disease is chronic, and plaques may persist for months to years at the same location. Complete remission may occur for varied periods depending on the patient. Guttate psoriasis In guttate psoriasis, there will be a multitude of small, widely disseminated papules and plaques (figure 2). The condition is more commonly observed in children and adolescents and often occurs after an URTI. cont d page Australian Doctor 18 January

3 AD_020 JAN18_13. pdf Page 20 10/ 01/ 13, 10: 46 AM from page 18 Erythrodermic psoriasis In erythrodermic psoriasis, nearly all the body surface is involved (figure 3). There is generalised erythema and scaling. Onset can be gradual or acute. Differentiating psoriatic erythroderma from other causes of erythroderma such as eczema or drug-induced erythroderma is done by observing plaques in classic distribution, nail changes and facial sparing. Generalised pustular psoriasis In generalised pustular psoriasis there are obvious macroscopic pustules. Four distinct patterns are observed. Von Zumbusch pattern Von Zumbusch pattern is a generalised eruption starting abruptly with erythema and pustules. The skin is painful and may be associated with fevers and generally feeling unwell. After several days the pustules usually resolve and extensive scaling is observed. Annular pattern Annular pattern is characterised by annular lesions, with erythema and scaling, and pustules at the advancing edge. Lesions expand outwards over hours to days, while healing occurs centrally. Exanthematic type In the exanthematic type, acute eruptions of small pustules abruptly appear and disappear over a few days. The condition usually occurs after an infection or as a result of some medications, for example, lithium. The differential diagnosis is pustular drug eruption, known as acute generalised exanthematous pustulosis. Localised pattern In the localised pattern, pustules appear within or at edge of existing psoriatic plaques. Pustulosis of the palms and soles Pustulosis of the palms and soles is characterised by sterile pustules on the palmoplantar surfaces interspersed with yellow-brown macules and scaly erythematous plaques (figure 4). Pustules remain localised to palmoplantar surfaces and disease course is chronic. Figure 3: Erythrodermic psoriasis. Figure 4: Pustulosis of the soles, showing extensive scaling and yellow-brown macules. Figure 5: Scalp psoriasis. Figure 6: Flexural psoriasis. Figure 7: Nail psoriasis showing proximal pitting. Figure 8: Onycholysis and oil spot sign. Other sites of involvement Scalp psoriasis The scalp is a common site for psoriasis. There can be either individual lesions, or complete confluence of the scalp. This differs from the undefined areas of involvement of seborrhoeic dermatitis. Psoriatic lesions may appear on the periphery of the face (figure 5), behind the ears and the upper neck. Flexural psoriasis Flexural psoriasis lesions are shiny, pink to red, sharply demarcated thin plaques with less scale than chronic plaque psoriasis (figure 6). Sites of involvement are the axillae, inguinal crease, intergluteal cleft, inframammary region and retroauricular folds. Triggers for flexural psoriasis include localised dermatophyte, candida or bacterial infections. Nail psoriasis Nail involvement occurs frequently, with fingernails more often affected than toenails. Nail involvement is associated with an increased likelihood of psoriatic arthritis. The nail matrix involvement leads to proximal pitting (figure 7). Nail-bed involvement can lead to onycholysis and the typical yellowish oil spot sign (figure 8). Subungual hyperkeratosis can be prominent. Living with psoriasis PSORIASIS is a very unpredictable disease. It is impossible to say with certainty how long the disease will last and whether or when a relapse will occur. Environmental factors, such as sunlight and hot weather, are generally beneficial for patients with the condition, while stress can be detrimental. Unfortunately, relapse appears to be the rule, no matter how well lesions are treated and with what method. Nevertheless, with the advent of the new biologics, severe cases are being maintained for longer periods in remission. Comorbidities is becoming increasingly recognised as a multisystem chronic inflammatory disorder with associated comorbidities. These may develop before or after the psoriasis. There are probably shared genetic factors, but also it is postulated that the cytokines produced by the inflamed psoriatic skin can act on these other organs. Extracutaneous disorders associated with psoriasis include: Psoriatic arthritis. Obesity. Metabolic syndrome. Cardiovascular, cerebrovascular and peripheral vascular disease. Autoimmune diseases. Eye disease: panuveitis, scleritis, episcleritis. Nonalcoholic fatty liver disease. Chronic obstructive pulmonary disease. Obstructive sleep apnoea. Psychiatric disorders. Alcohol abuse. It is increasingly apparent that treating comorbidities is important in managing the patient s overall condition for example, losing weight may reduce the severity of the psoriasis. 20 Australian Doctor 18 January

4 AD_021 JAN18_13. pdf Page 21 10/ 01/ 13, 10: 24 AM Differential diagnoses WHEN investigating suspected psoriasis, differential diagnoses need to be borne in mind. There are several conditions that can be mistaken for psoriasis. Seborrhoeic dermatitis Lesions are brighter in colour, less well defined and covered with dull or branny scale. Eczema With eczema, there may be lesions with a psoriasiform appearance, especially on the legs, or in the form of hyperkeratotic eczema of the palms. Lichen planus Lichen planus can be difficult to distinguish when the two diseases alternate or coexist, especially with the existence of hypertrophic lesions on the legs, penile lesions and palmar pathology. Signs favouring lichen planus include violaceous colour, glistening surface and presence of oral changes. Lichen simplex Lichen simplex may closely resemble psoriasis, particularly on the scalp and near the elbows. Features to distinguish lichen simplex are intensified skin markings, ill-defined edges Lichen planus can be difficult to distinguish when the two diseases alternate or coexist. and extreme itching. The elbows also tend not be affected. Pityriasis lichenoides chronica This condition may resemble guttate psoriasis, but lesions tend to be less evenly scattered, are brownish red or orange-brown and capped with opaque soft mica-like scale. Candidiasis Candidiasis produces a glistening, deep red colour, particularly in the flexures, but scaling tends to be confined to the edge and small satellite pustules and papules are usually present outside the main area. Tinea cruris Tina cruris has a well-defined, often polycyclic edge. Scaling may be absent if corticosteroids have been applied. Investigations Biopsy A BIOPSY can be taken from any part of the lesion. There are typical histopathological features of psoriasis, which can differentiate it from lichen planus and fungal infections. Sometimes there is some overlap with eczema, especially if the psoriatic lesions are itchy and excoriated. Biomarkers There are no conclusive biomarkers for uncomplicated psoriasis. ESR and CRP may be inconsistently elevated or unaffected. Slight hyperuricaemia and low folate levels may be observed as a result of increased epidermopoiesis. Occasionally, IgA deficiency and monoclonal IgG gammopathy may be observed. Identification of valid biomarkers of disease severity and response to therapy would be a major advancement in research. Area and Severity Index (PASI) The percentage of body surface area involved in psoriasis does not reflect the severity of the individual lesions with respect to erythema, induration and scaling, so instead the Area and Severity Index (PASI) was developed as an instrument to grade the severity of Table 1: Calculation of the Area and Severity Index Severity of psoriatic lesions (0 = none, 1 = slight, 2 = moderate, 3 = severe, 4 = very severe) Head Trunk Upper limbs Lower limbs Erythema Induration Scaling Total score = TS Area of psoriatic involvement 0 = none, 1 = <10%, 2 = 10-30%, 3 = 30-50%, 4 = 50-70%, 5 = 70-90%, 6 = % Degree of involvement = DI Multiply TS TS DI TS DI TS DI TS DI DI Correction factor for area of involvement = CF TS DI CF A B C D A + B + C + D = total PASI Adapted from table 8.2, Calculation of the Area and Severity Index (PASI), from Bolognia JL 13 disease. The PASI score is calculated from the body surface area involved in each of four anatomical areas head, upper extremities, trunk and lower extremities, in addition to the scores for erythema, induration (hardening) and scaling. PASI ranges from 0 (no disease) to 72 (maximal disease) (table 1). About 25-30% of patients are scored as having moderate to severe disease. 12 Management TREATMENT for psoriasis is very much directed towards the individual and depends upon age, sex, occupation and personality as well as the type, extent and duration of the condition. When choosing the most appropriate treatment modality, the patient s general, physical and psychological health needs to be considered. Table 2: Summary of treatment modalities for psoriasis Type of psoriasis Plaque mild, moderate Plaque widespread Guttate Treatment options in order of common use Tars, topical corticosteroids, calcipotriol, dithranol, tazarotene Dithranol, tars, topical corticosteroids, phototherapy, methotrexate, acitretin, cyclosporin, biological agents Penicillin, tars, topical corticosteroids, phototherapy, calcipotriol Mild to moderate topical corticosteroids Topical treatments Topical therapy is first-line for most patients with stable plaque psoriasis. Typically, a combination of topical agents can be used (eg, emollients, a tar preparation and a topical corticosteroid or calcipotriol and a topical corticosteroid). It is a very individual decision as to what cream or creams are used, how often, in what order and how frequently, and common sense should dictate this. An older person who finds it hard to apply creams can probably only use them once a day whereas an anxious young person could put creams on many times a day. Emollients Emollient creams or ointments provide soothing relief for scaling and irritation. Sorbolene or aqueous cream (often with some glycerol or glycerine) are commonly used as they are reasonably priced and well tolerated. There are large numbers of moisturising creams available however, so it can often be a case of trial and error to find the one the patient likes. Perfumes are not such a problem in psoriasis in contrast to eczema, so such creams can be used and may be applied frequently. Keratolytics Keratolytics soften and lift scale. Flexural Erythrodermic Palmoplantar pustular Palmoplantar hyperkeratotic Scalp mild Scalp severe Nail Genital The most commonly used compound is 5% salicylic acid mixed with ointment or cream base. Ten per cent lactic acid or 10% urea may also be used. Tar Coal tar is effective for its antiinflammatory and anti-pruritic effects. One of the benefits of tar is that it is a generally safe treatment, with folliculitis being the most common side effect. Nevertheless, patients may be deterred by its colour and odour. Coal tar solution is usually prepared as LPC (liquor picis carbonis) in combination with aqueous cream or ointment and/or salicylic acid. A common recipe is LPC 6%, salicylic acid 5% in aqueous cream or Hospitalisation, baths, emollients, methotrexate, acitretin, cyclosporin, biological agents Tars, topical corticosteroids, tetracyclines, acitretin, calcipotriol, phototherapy, methotrexate, cyclosporin Topical keratolytics, tars, calcipotriol, acitretin Tar shampoo, topical corticosteroid lotions Tar or dithranol pomades, tar shampoo, systemic therapy Calcipotriol, potent topical corticosteroids, intralesional corticosteroids, systemic therapy Topical corticosteroids, tars Adapted from table 4.20, Therapeutic Guidelines white soft paraffin. Dithranol (anthralin) The anti-proliferative effect of dithranol makes it one of the most effective topical treatments for thick plaque psoriasis. Disadvantages of its use are that it stains clothes permanently and skin transiently. It can also burn unaffected skin and is unsuitable for use on the face, flexures or genitals. It is often used in combination with a topical corticosteroid. It is most often used nowadays as short contact treatment for minutes. A typical recipe would be dithranol 0.25%, salicylic acid 5% in aqueous cream or white soft paraffin applied to the scalp or knees for 30 minutes, then washed off and topical steroid applied afterwards. Topical corticosteroids Topical corticosteroids are the most commonly used therapy for psoriasis for their anti-inflammatory and anti-mitotic effects. More potent preparations are used to treat thicker plaques for 4-6 weeks and pulse treatment is advocated to minimise side effects and loss of efficacy from continuous treatment. Pulse treatment could involve applying the stronger topical steroid, such as betamethasone dipropionate (Diprosone OV) two days a week, and using a milder one such as mometasone (Elocon) on the other days. Topical steroids are best for sites such as the palms and flexures where other preparations may be irritating. In the flexures, psoriasis is usually not thick, and milder steroids, such as methyl prednisolone or hydrocortisone, are best. Vitamin D analogues Topical synthetic vitamin D 3 analogues such as calcipotriol are effective against psoriasis by regulating proliferation and differentiation of keratinocytes, and by shifting the Th1 cytokine profile of plaques towards a Th2 cytokine profile. Nowadays a combination calcipotriol cortisone preparation (Daivobet) is commonly used as first-line treatment for plaque psocont d next page 18 January 2013 Australian Doctor 21

5 AD_022 JAN18_13. pdf Page 22 10/ 01/ 13, 10: 26 AM from previous page riasis. It is not messy and preparation maintains efficacy over time, unlike topical steroids by themselves. Daivobet can be applied once a day, with a keratolyticmoisturiser preparation used at other times of the day. Vitamin D and its analogues have the potential to affect systemic calcium homeostasis, causing hypercalciuria and hypercalcaemia, therefore dosing should not exceed 100g per week. Other side effects include erythema and irritation. Topical calcineurin inhibitors Tacrolimus and pimecrolimus may be effective in treating psoriasis affecting the face, neck, flexures and genitalia. Advantages over topical corticosteroids are that they are selective, unlikely to be absorbed systemically and do not produce skin atrophy, making them more suitable for long-term use. They are not on the PBS for psoriasis and must be given on a private prescription. Tacrolimus is usually only available from compounding pharmacies. UV phototherapy The benefits of sunlight for skin conditions has been recognised for centuries. Controlled phototherapy is used mainly for its immunomodulatory and antiinflammatory effects. Pretreatment with acitretin can make phototherapy more efficacious. Ultraviolet B (UVB) Broadband and narrowband UVB therapy at wavelengths of nm and 311nm respectively involves exposing the patient s skin to carefully monitored doses of UVB radiation. Nowadays, most clinicians use narrowband UVB, which gives superior results and has not been associated with an increase in melanoma incidence. Treatment regimens are dependent on the patient, including any adverse effects and clinical response. Side effects include significant erythema, blistering and hyperpigmentation if dosing is not correct. In the long term, there may be an increase in nonmelanoma skin cancer, so patients need to be monitored. Psoralen ultraviolet A (PUVA) PUVA involves using a photosensitising compound, psoralens before UVA exposure and is a more potent form of phototherapy. Psoralens can be administered orally to cause generalised photosensitivity or topically for localised effects. Side effects include nausea, erythema and blistering. Patients need to be careful in natural sunlight as they will be sensitised for the remainder of the day after treatment. Long-term use of PUVA (more than 150 treatments) can lead to an increased risk of skin malignancy such as squamous cell carcinoma and melanoma. Systemic therapy Systemic therapy is indicated when psoriasis is widespread, severe or causing disfigurement or disability. These drugs generally have antiproliferative, anti-inflammatory or immunosuppressive Table 3: Biological drugs used for the treatment of psoriatic disease Drug Type Target Adalimumab Human monoclonal antibody TNF alpha Ustekinumab Humanised monoclonal IL-12 and IL-23 antibody Etanercept Soluble TNF alpha receptor TNF alpha Infliximab Chimeric monoclonal antibody TNF alpha TNF alpha Adapted from table 4.2, Therapeutic Guidelines effects. The main systemic drugs (discussed below) are usually combined with topical and/or phototherapy. Sequential and rotational therapies are often used. Methotrexate Methotrexate is the most commonly prescribed oral anti-psoriasis drug. It inhibits DNA synthesis by competitive inhibition of dihydrofolate reductase and as a result may exert an antimitotic action on the epidermis. The usual dose is mg/kg (average 15mg) orally one day per week. 15 Clinical response is slow. It can take a month or more to see much effect and maximal effect may take 3-6 months. It may be very helpful for arthritis too. Possible side effects include nausea, pancytopenia and increased liver enzymes, which can be combated with the concomitant use of folic acid supplementation, 5mg orally once or twice weekly. Side effects occur more commonly in the elderly and in patients with impaired renal function, so dosing should be adjusted accordingly. Methotrexate also interacts with many drugs which can alter its pharmacokinetics, including inducing toxicity. Potential drug interactions need to be checked before prescribing new medications to the patient. FBC, renal tests and LFTs should also be monitored regularly. Methotrexate is an immunosuppressive drug, so long-term use may increase risk of infections and malignancy. Acitretin Acitretin is a vitamin A analogue and has effects on epithelial differentiation and proliferation as well as anti-inflammatory effects. It may be used as monotherapy in the treatment of palmoplantar and hyperkeratotic psoriasis at a dose of up to 0.5mg/kg orally, once daily. Additionally, it can be used to increase the efficacy of phototherapy with narrowband ultraviolet B (UVB) therapy or psoralen and ultraviolet A (PUVA) therapy in cases of pustular, erythrodermic and atypical presentations of psoriasis. The main concern with acitretin is its teratogenicity and hence pregnancy must be avoided during its use and for two years following cessation of treatment. Other side effects include cheilitis, hair shedding, photosensitivity, elevated liver enzymes and elevated serum lipids. Regular monitoring blood tests are needed. Cyclosporine The mechanism of action of cyclosporine in psoriasis is not completely understood, but its The benefits of sunlight for skin conditions has been recognised for centuries. actions as an immunosuppressant are likely related to its inhibitory effects on T-cell activation. Usual doses are mg/kg orally, twice daily (to a maximum of 5mg/kg/ day). 15 Cyclosporine can be a very effective drug in the control of psoriasis, however, it does not produce long remissions and recurrence follows discontinuation. Extended periods of use are not recommended as long-term side effects include hypertension, impaired renal function, hirsutism, gingival hyperplasia and the development of neoplasia (skin squamous cell carcinoma and lymphoma). Significant drug interactions can also occur, and hence potential side effects should be noted before prescribing any new medications. Biological therapies Biological drugs are the most recent addition to the treatment regimen of psoriasis. These drugs are expensive and strict eligibility criteria apply for subsidy under the PBS. They are given by injection or infusion. The biologics target the activity of T lymphocytes through binding to interleukins, which activate the T cells (eg, IL-12 and 23 [ustekinumab]) or the proinflammatory cytokine TNF alpha (infliximab, etanercept, adalimumab), which are thought to be involved in the pathophysiology of psoriasis. 16 Risks of taking these drugs include the possibility of reactivation of latent infection (including tuberculosis) and induction of malignancy. They can be extremely effective and improve quality of life enormously for patients with severe disease. New biological drugs are currently being developed. References 1. Freedberg I. Fitzpatrick s Dermatology in General Medicine. 6th edition. McGraw- Hill, New York, Burns T, et al (editors). Rook s Textbook of Dermatology. 8th edition. Wiley-Blackwell, West Sussex, Wolff K, Johnson RA. Fitzpatrick s Color Atlas and Synopsis of Clinical Dermatology. 6th edition. McGraw-Hill, New York, Barker JNWN. Genetic aspects of psoriasis. Clinical and Experimental Dermatology 2001; 26: Mallon E, et al. HLA-C and guttate psoriasis. British Journal of Dermatology 2000; 143: Duvic M, et al. Acquired immunodeficiency syndromeassociated psoriasis and Reiter s syndrome. Archives of Dermatology 1987; 123: Naldi L, et al. Association of early-stage psoriasis with smoking and male alcohol consumption: evidence from an Italian case-control study. Archives of Dermatology 1999; 135: Herron MD, et al. Impact of obesity and smoking on psoriasis presentation and management. Archives of Dermatology 2005; 141: Naldi L, et al. Study Group of the Italian Group for Epidemiological Research in Dermatology. Family history of psoriasis, stressful life events, and recent infectious disease are risk factors for a first episode of acute guttate psoriasis: results of a case-control study. Journal of the American Academy of Dermatology 2001; 44: Trembath RC, et al. Identification of a major susceptibility locus on chromosome 6p and evidence for further disease loci revealed by a two stage genome-wide search in psoriasis. Human Molecular Genetics 1997; 6: Nestle F, et al.. New England Journal of Medicine 2009; 361: Schon BW.. New England Journal of Medicine 2005; 352: Bolognia JL, et al (editors) Dermatology. 3rd edition. Elsevier Saunders, Philadelphia, Dermatology Expert Group. Therapeutic Guidelines Dermatology. Version 4: Therapeutic Guidelines Ltd, Melbourne, Conclusion PSORIASIS is a common skin disease that can seriously disrupt a person s quality of life. Understanding of aetiological factors involved with the condition has increased over the past decade, but still no cure is available. Treatment is aimed at control of the disease such that it causes minimal disruption. The development of new biologic drugs may herald an improvement in quality of life for psoriasis patients. cont d page Australian Doctor 18 January

6 AD_024 JAN18_13. pdf Page 24 10/ 01/ 13, 10: 27 AM Case studies Figure 9: Thick scaly psoriatic plaques on the knee. Case 1 A 28-YEAR-old woman presents with an annoying rash on her elbows and knees (figure 9). On questioning she says she has bad dandruff, which consists of discreet scaly patches on the scalp. She has well-defined pink patches on the elbows and knees with coarse scale. A clinical diagnosis of psoriasis is made. A skin biopsy could have been undertaken to support this. There are no helpful blood tests, and with mild psoriasis in a young person it is probably not worthwhile looking for the metabolic syndrome. The patient is initially treated with frequent emollients on the elbows and knees. For this purpose, the patient uses sorbolene cream and a topical combination calcipotriol and topical steroid (Daivobet) once or twice a day is prescribed. The patient returns after 12 weeks. Some areas have improved but parts of the rash remain. Intralesional steroid is then prescribed for these stubborn areas. For the patient s scalp, Daivobet scalp solution at night washed out in the morning is prescribed. A coal tar cream (eg, 6% LPC, 5% salicylic acid in aqueous cream) can be alternated with this. Tar shampoo can be helpful too. The patient is told that this is a condition that can be controlled, not cured, and relapses are common. Case 2 An obese 62-year-old man presents with a widespread, red, scaly rash on his arms, legs and lower back, that has come on gradually over the past six months. It is not very itchy, but uncomfortable, making him very embarrassed. On questioning, he also reveals he has widespread plaques on his scalp and has a painful rash in the groin. He has type 2 diabetes, hypertension and smokes about 12 cigarettes a day. There is a family history of psoriasis. This man obviously needs all his medical problems managed optimally as well as his skin disease. His diabetes and hypertension need adequate control and his smoking and obesity need to be tackled in a co-ordinated way. His skin disease requires a combination of topical and physical treatments, and very likely an oral agent, so he may need referral to a dermatologist. The patient is advised to use emollients on the affected areas. Topical combination calcipotriol and topical steroid (Daivobet) to extensor areas is prescribed, along with a mild topical steroid for the groin, with an anticandidal agent too as secondary candida is common. Physical therapy with narrow-band UVB and probably an oral retinoid, such as acitretin, could be helpful. It is also important to ensure ongoing monitoring of his liver function and lipids. How to Treat Quiz 18 January 2013 INSTRUCTIONS Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points. We no longer accept quizzes by post or fax. The mark required to obtain points is 80%. Please note that some questions have more than one correct answer. ONLINE ONLY for immediate feedback 1. Which TWO statements are correct regarding the epidemiology of psoriasis? a) The most common type of psoriasis is pustular psoriasis b) The prevalence of psoriasis vulgaris is estimated to be from 1.5% to 3% of the population in Western countries c) There is a high incidence of psoriasis in the Chinese population d) Climate appears to affect psoriasis, with those living further from the equator having higher rates of disease 2. Which THREE statements are correct regarding the epidemiology of psoriasis? a) The incidence of psoriasis in the population in a year has been estimated to be 60 individuals per 100,000 per year b) seems to have a bimodal age of onset, with early disease typically occurring between ages 16 and 30 or even much earlier in childhood c) The bimodal peak in age of onset suggests two pathogenetically different subtypes. Type 1, which is hereditary, is strongly HLA associated, particularly HLA-Cw6 d) Males have a significantly higher incidence of psoriasis than females 3. Which THREE statements are correct regarding risk factors for psoriasis? a) Physical trauma such as rubbing and scratching can cause development of psoriatic lesions b) Preceding or concurrent streptococcal infection (particularly of the throat) may precipitate guttate psoriasis c) Stress is known to stimulate flares and may be associated with about 5% of cases in adults d) Various drugs such as interferon, ACEIs, beta-adrenergic antagonists and NSAIDs can either cause or exacerbate psoriasis 4. Which THREE of the following are histological features of psoriasis lesions? a) Epidermal hyperproliferation b) Angiogenesis c) Accumulation of inflammatory cells d) Vacuolated upper keratinocytes with hypergranulosis 5. Which THREE statements are correct regarding the clinical appearance of psoriasis? a) The characteristic clinical appearance of psoriasis is erythema, thickening and silverywhite scale b) Pinpoint papules surrounding existing psoriatic plaques indicate that the lesions are responding to treatment and are resolving c) Guttate psoriasis appears as a multitude of small, widely disseminated papules and plaques d) The characteristic annular lesions with central healing form one of the patterns of generalised pustular psoriasis 6 Which THREE statements regarding scalp, flexural and nail psoriasis are correct? a) Psoriatic lesions rarely appear on the scalp and the upper neck b) Triggers for flexural psoriasis include localised dermatophyte, candida or bacterial infections c) Fingernails are more often affected than toenails in nail psoriasis d) Nail involvement is associated with an increased likelihood of psoriatic arthritis 7. Which THREE skin conditions may be confused with psoriasis? a) Seborrhoeic dermatitis b) Pityriasis lichenoides chronica c) Laugier Hunziker syndrome d) Candidiasis 8. Which TWO statements regarding biomarkers, assessment of severity and topical psoriasis treatment are correct? a) ESR and CRP are reliable biomarkers for psoriasis b) The Area and Severity Index (PASI) has been developed as an instrument to grade the severity of disease c) Coal tar is effective for its anti-inflammatory and anti-pruritic effects d) Dithranol is the most appropriate topical treatment for use on the face, flexures and genitals 9. Which THREE statements are correct regarding treatment for psoriasis? a) Topical synthetic vitamin D3 analogues such as calcipotriol may affect systemic calcium homeostasis b) Pretreatment with acitretin can make phototherapy more efficacious c) Phototherapy with UVB is contraindicated for treatment of psoriasis because of the increased risk of melanoma d) Long-term use of PUVA (more than 150 treatments) can lead to an increased risk of skin malignancy such as squamous cell carcinoma and melanoma 10. Which TWO statements are correct regarding systemic therapy and biologicals? a) Systemic therapy is usually combined with topical and/or phototherapy, and sequential and rotational therapies are often used b) The maximal effect from methotrexate is seen within a month of starting therapy c) Acitretin is safe in pregnancy but can cause cheilitis, hair shedding, photosensitivity and affects liver enzymes and serum lipids d) Biologicals target the activity of T lymphocytes through binding to interleukins, which activate the T cells, or the proinflammatory cytokine TNF alpha CPD QUIZ UPDATE The RACGP requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the triennium. You can complete this online along with the quiz at Because this is a requirement, we are no longer able to accept the quiz by post or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online. Editor: Dr Barbara Tink howtotreat@reedbusiness.com.au NEXT WEEK Rheumatoid arthritis is a systemic disease that can potentially affect much more than joints. Treatment of this condition involves an appreciation of the spectrum of the condition and its complications. The next How to Treat aims to facilitate GPs ability to be involved in shared care for rheumatoid arthritis patients. The authors are Associate Professor Mark Arnold, associate professor of medicine, Northern Clinical School, Sydney University, VMO rheumatologist, Royal North Shore Hospital, St Leonards and consultant rheumatologist, Orthopaedic and Arthritis Specialist Centre, Chatswood; and Dr Anna Finniss, consultant general medicine physician and rheumatologist at Royal North Shore Hospital, St Leonards; consultant general medicine physician, Mona Vale Hospital, Mona Vale and consultant rheumatologist, Orthopaedic and Arthritis Specialist Centre, Chatswood, NSW. 24 Australian Doctor 18 January