Psoriasis in Children

Psoriasis in ChildrenA Guide to its Diagnosis and Management

Joyce Leman and David BurdenDepartment of Dermatology, Western Infirmary, Glasgow, Scotland

Contents Abstract . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6731. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 674

1.1 Prevalence and Age of Onset . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6741.2 Clinical Features . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 674

2. Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6752.1 Elimination of Triggering and Exacerbating Factors . . . . . . . . . . . . . . . . . . . . . . . . 6752.2 Topical Treatments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675

2.2.1 Emollients . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6762.2.2 Topical Corticosteroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6762.2.3 Tar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6762.2.4 Anthralin (Dithranol) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6762.2.5 Vitamin D Analogues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6762.2.6 Topical Retinoids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 677

2.3 Phototherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6772.4 Systemic Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 677

2.4.1 Retinoids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6782.4.2 Methotrexate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6782.4.3 Cyclosporin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 678

3. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 679

Abstract Psoriasis often presents in childhood. The diagnosis may be challenging if thedisease is mild or the presentation is atypical. All of the forms recognised in adultsare encountered in childhood (plaque, guttate, erythrodermic and pustular). Gutt-ate and flexural forms are particularly common in children.

Successful management requires education of the child and parents regardingthe course of the disease and treatment options. Environmental triggers shouldbe sought out and eliminated where possible. Most patients respond to topicaltreatment with emollients, coal tar, anthralin (dithranol) or calcipotriol. Treatmentis tailored according to patient age, extent and distibution of psoriasis. For thosewho fail to respond, daycare or inpatient care is appropriate. Phototherapy withUVB may be combined with topical agents. Systemic therapy is required in aminority, usually those with resistant or erythrodermic disease, pustular psoriasisand arthropathic psoriasis. Retinoids are probably the systemic agent of choice.There are few data regarding the use of methotrexate or cyclosporin in childhoodpsoriais.

REVIEW ARTICLE Paediatr Drugs 2001; 3 (9): 673-6801174-5878/01/0009-0673/$22.00/0

© Adis International Limited. All rights reserved.

1. Introduction

Psoriasis is a chronic inflammatory scaling con-dition of the skin, which quite often presents inchildhood. In some series of patients it accounts for4% of dermatoses encountered in childhood andadolescence.[1] The precise aetiology and patho-genesis remain enigmatic; however, it is likely thatthere is interplay between genetic and environmen-tal factors. Psoriasis plaques are characterised bykeratinocyte hyperproliferation, vascular endothe-lial proliferation and inflammatory cell infiltration.T-cells play a central role. The cytokine profile isT helper (Th)-1 like, characterised by interleukin(IL)-2 and interferon (INF)-γ. The disease courseis unpredictable and is characterised by relapses andremissions. In most cases the disease is relativelymild and easy to control. In a minority, the diseasepresents a challenging management problem.

All of the clinical variants of psoriasis describedin adults (plaque, guttate, erythrodermic and pus-tular) are recognised in childhood. Different formsmay occur in the same patient at different times.

Non-pustular varieties of psoriasis may be sub-divided by age of onset.[2] Type 1 psoriasis has anage at onset <40 years, is often familial and isstrongly associated with the histocompatibility lo-cus HLA Cw6 allele. This contrasts with those af-fected in later life in whom the disease is moreoften sporadic, is not associated with the Cw6 alleleand tends to be less severe. Childhood psoriasis isby definition type 1.

1.1 Prevalence and Age of Onset

Estimates regarding disease prevalence varyfrom 0.1 to 3%.[3] In 2% of cases the disease startsprior to the age of 2 years and 10% are diagnosedbefore the age of 10 years.[4] Congenital and nae-void forms have been reported, but are rare.[5,6] Inmany instances there is a positive family history.[7]

The lifetime risks are 4, 28 and 65% if neither, oneor both parents are affected.[8]

1.2 Clinical Features

The characteristic lesion in psoriasis is a sharply

demarcated, deep red plaque with adherent, silveryscale. Making the diagnosis of psoriasis in infancycan be challenging as the disease is often limited inits extent and the appearance may be atypical. Thenapkin area is often the first site to be affected; thecharacteristic appearance is a well-defined red areadevoid of scale.[4] Napkin psoriasis must be distin-guished from the more common causes of a rash inthe napkin area, such as irritant contact dermatitisand candidal infection. Napkin seborrhoeic derma-titis is a particular diagnostic problem as it mayappear very similar to napkin psoriasis and a sig-nificant proportion of affected children developpsoriasis in adult life.[9]

Plaque psoriasis is the most common variant en-countered in children. Plaques, which are typically5 to 10cm in diameter, are often symmetrically dis-tributed on extensor aspects of the knees and el-bows. The scalp is the most frequently affected site;seborrhoeic eczema and tinea capitis may need tobe considered in the differential diagnosis.[10] Fa-cial involvement appears to be more common inchildren than adults.[11,12]

Nail changes such as superficial pits (the mostcommon finding), oil spots, onycholysis and sub-ungal hyperkeratosis are seen in 7 to 40% of ado-lescents <18 years of age.[13] Onycholysis is oftenmistaken for onychomycosis and sometimes inap-propriately treated with antifungal preparations.

Guttate psoriasis refers to the rapid develop-ment of small plaques of psoriasis (0.5 to 1cm dia-meter) over the face, trunk and proximal limbs. It isoften preceded by an upper respiratory tract infec-tion and we would recommend culturing a throatswab and measuring the serum antistreptolysin Otitre. It has been suggested that treating the associ-ated infection, be it respiratory or cutaneous, mayimprove psoriasis[11,14,15] but evidence from con-trolled trials is lacking.[16] There is a tendency forthis variety of psoriasis to resolve spontaneously,although a substantial proportion of patients willgo on to develop chronic plaque disease.[17] Pityri-asis rosea and discoid eczema can cause diagnosticconfusion.

Erythrodermic and pustular psoriasis are rare in

674 Leman & Burden

© Adis International Limited. All rights reserved. Paediatr Drugs 2001; 3 (9)

children. Erythroderma may follow the introduc-tion of systemic therapies such as lithium. Pustularpsoriasis in children tends to follow a more benigncourse than in adults.[18-20] In contrast to the situa-tion in adults, male children are more commonlyaffected. The pustules are sterile and superficial,and may be localised or generalised. General mal-aise, fever and anorexia are commonly associated.Pustular psoriasis may be precipitated by infec-tions, UVB radiation, oral and topical corticoste-roids and vaccination. Many infants with general-ised pustular psoriasis have no history of psoriasisvulgaris but 30% have a history of seborrhoeic ornapkin dermatitis.[20]

Psoriatic arthropathy, an inflammatory seroneg-ative arthritis, may predate, coincide with, or post-date the diagnosis of cutaneous psoriasis. This con-dition is distinct serologically and clinically fromjuvenile rheumatoid arthritis and juvenile ankylos-ing spondylitis.[21]

2. Treatment

Treatment must be tailored to disease severity,location, and patient age. Compliance, which oftenreflects parental motivation in younger children, isalso an important issue. A positive approach byphysicians and parents is essential. Successfultreatment begins with educating the parents andchild about the nature and natural history of psori-asis (see table I).

2.1 Elimination of Triggering andExacerbating Factors

Streptococcal infections are associated particu-larly with a flare of guttate psoriasis and to a lesserextent, plaque psoriasis. The organism is usuallydetected in the upper respiratory tract but there areoccasional reports of the development of guttatepsoriasis following streptococcal perianal derma-titis.[22] It is known that these organisms secretesuper antigens which enhance the T-cell response.

Infection with HIV is associated with flaring ofpsoriasis and the skin condition is better controlledwhen the patient starts antiretroviral therapy.

Psychological stress may be a relatively moreimportant trigger in childhood compared with adultdisease.[11,23] The Koebner or isomorphic phenom-enon (psoriasis developing in an area of trauma) iscommon in this age group.[24] The trauma may re-sult from irritation from a soiled nappy in the nap-kin area. Exacerbations secondary to drugs or al-cohol are less common in children than adults. Thepossibility that factors such as stress, infection andtrauma could be contributing to flares or ongoingactivity should be considered.

2.2 Topical Treatments

Most of the agents used in childhood psoriasisare well tried and tested in adult disease but theiruse in children has, for the most part, been empir-ical. In most patients the treatment can be kept sim-ple and should not unduly interfere with normaldaily activities. Thought must be given to the prac-ticality of any regimen prescribed. From the outsetit must be made clear that the realistic objective isto control rather than to cure the disease. It is worthestablishing from the parents and child which as-pects of the condition cause the most distress.Some children are concerned only by the scaling,whereas others are troubled by severe itch. In olderchildren and adolescents cosmetic considerations

Table I. Site specific treatment

Clinical presentation Suitable treatment options

Scalp Potent topical corticosteroidapplication

Vitamin D analogues

Keratolytics (e.g. salicyclic acid)

Coal tar ointment

Nails (limited response totopical treatment)

Potent topical corticosteroid lotion tonail fold

Intralesional corticosteroids (painful)

Facial Mild topical corticosteroids

Coal tar cream

Flexures and genitals Moderate potency topicalcorticosteroids

Palms/soles Potent topical corticosteroids

Keratolytics (e.g. salicylic acid)

Coal tar (may apply under occlusion)

Diagnosis and Management of Psoriasis 675


become more important, thus, treatment should betailored to address these specific concerns.

All of the preparations discussed below are suit-able for home use. Demonstration of application byskilled dermatology nurses in the outpatient clinicmay be helpful. If the disease is extensive, or provingrefractory to treatment, supervision in a daycaresetting or admission to an inpatient care facilitymay be indicated.

2.2.1 EmollientsFor some, the disease is so mild that regular lib-

eral application of an emollient, with its antipru-ritic and descaling properties, is sufficient. Thesepreparations are considered well tolerated and arerelatively inexpensive.

2.2.2 Topical CorticosteroidsTopical corticosteroids have antiproliferative

and anti-inflammatory properties. They reduce ery-thema and scaling, and are particularly useful ifitch is a dominant symptom. They are the treatmentof choice in flexural disease and are widely usedon the face and scalp. These sites are particularlysusceptible to irritation from other topical prepara-tions. Topical corticosteroids have high patient ac-ceptability as they do not stain the skin and arerelatively odourless.

Topical corticosteroids are frequently used incombination with other agents such as calcipotriolon stable plaques.[25] Application of topical corti-costeroids under occlusion enhances penetration,thereby potentiating their action. In general, theleast potent topical corticosteroid preparationshould be used for the shortest possible time to pre-vent tachyphylaxis and long-term sequelae such asstriae and telangiectases. Extensive application ofpotent corticosteroids can rarely lead to suppres-sion of the hypothalamic pituitary adrenal axis.Abrupt discontinuation of topical corticosteroidscan lead to a rebound flare of disease and theyshould, therefore, be gradually withdrawn.

2.2.3 TarTars have a well-established place in the treat-

ment of psoriasis.[4] Tars have an antiproliferativeand antipruritic effect. Coal tar is the most fre-

quently prescribed tar but ichthyol and cade oil arealso used. The unpleasant smell and tendency tostain has limited their use. Coal tar is not as irritat-ing as some other modalities of topical treatmentand can, therefore, be applied to small plaque pso-riasis without concerns about irritating unaffectedperilesional skin. It is also suitable for use on themore sensitive skin of the face or genital area. Re-cently, concerns have been expressed about the car-cinogenicity of coal tar; however, at present thereis little evidence that this is of relevance in the clin-ical situation.

Tar is frequently used in combination with othermodalities such as UVB (Goekerman regimen) fortreating plaque and guttate psoriasis.

2.2.4 Anthralin (Dithranol)This synthetic hydroxy anthrone is concentrated

in the mitochondria where it undergoes oxidationand produces oxygen radicals.[26,27] In a study ofchildren aged 5 to 10 years, remission was achievedusing dithranol (up to 1%) in 47 of 58 children(81%).[28] However, its use is limited by the pro-pensity to irritate healthy skin and to stain the skinand clothing. Irritation makes dithranol unsuitablefor use on the face, flexures and genitalia. It shouldnot be used in erythrodermic or pustular psoriasis.Anthralin is particularly useful on thick plaqueswith a large surface area. Application should beunder parental supervision for younger children.Particular care must be given to protecting the sur-rounding healthy skin, for example, with a greasyemollient. The preparations are just as effective ifapplied for a short duration and this forms the basisof the frequently prescribed short contact dithranoltherapy. Dithranol is applied daily for 30 to 45 min-utes at a low concentration (0.1 to 0.25%) and theconcentration is increased on a weekly basis to thehighest tolerable concentration (often 2 to 3%).Dithranol is available commercially in a creambase suitable for home use. For inpatients anddaycare treatment, it is more effective in Lassar’spaste.

2.2.5 Vitamin D AnaloguesVitamin D and some of its derivatives are known

to stimulate differentiation and inhibit DNA syn-

676 Leman & Burden


thesis and cell proliferation in cultured keratino-cytes.[29] Vitamin D may also have immunomodu-latory effects,[30] and its use is restricted by its ef-fect on calcium homeostasis. Calcipotriol is asynthetic analogue of vitamin D3 designed to havea lesser effect on calcium balance.[31] It is consid-ered clean and odourless by patients and compli-ance tends to be good. Facial irritation is reportedin a minority of patients either when directly ap-plied to the face or transferred accidentally whentreating other areas. In contrast to other topicaltherapies, calcipotriol has been relatively wellevaluated in children. In a UK multicentre openstudy of 66 children aged between 3 and 14 years,calcipotriol 50 μg/g was applied twice daily (up to45 g/week/m2) for up to 8 weeks. In 65% of patients,psoriasis was cleared or markedly improved, and astandardised measure of disease activity [the pso-riasis area and severity index (PASI)] was reducedsignificantly. There was no disturbance of serum cal-cium levels.[32] A subsequent international double-blind parallel group study in 77 children aged be-tween 2 and 14 years compared calcipotriol 50 μg/gtwice daily and placebo for 8 weeks. This con-firmed the tolerability of the treatment. Althoughthe PASI fell more in the treated than the controlgroup (by 52 vs37%), this was not significant.[33]

The long-term tolerability and efficacy of calci-potriol was recently reported from Korea in a smallopen study.[34] 12 children received calcipotriol 50μg/g (up to 100 g/week). The treatment was foundto be effective and, although no abnormalities inserum calcium were detected, there was a fall inmean 1, 25 dihydroxyvitamin D3 levels, leadingthe authors to suggest monitoring vitamin D levelsduring prolonged treatment.[34] Calcipotriol 50μg/g is currently licensed for use in children in theUK at a maximum dose of 50 g/week in those >6years and 75 g/week in those >12 years.

Tacalcitol is another vitamin D analogue whichis commercially available for the treatment of pso-riasis. There are currently no published data on itstolerability and efficacy in children.

2.2.6 Topical RetinoidsTazarotene is a receptor specific topical retinoid

which is licensed for use in psoriasis in adults.[35]

It has not been studied in children to our knowl-edge. In adults, local irritation has been a commonadverse effect which may be ameliorated by alter-nating treatment with a topical corticosteroid.

2.3 Phototherapy

Many patients report improvement in their pso-riasis after sunny holidays. Phototherapy is the useof UVB radiation for therapeutic benefit. There is,however, concern about the long-term effects ofrepeated courses of phototherapy in terms of photo-carcinogenesis and skin photoaging.[36] Parentsand children should, therefore, give informed con-sent. UVB is usually prescribed on a 3 times/weekbasis; however, the initial dose is based on an as-sessment of the individual’s photosensitivity (ide-ally the minimal erythema dose, the dose which pro-duces barely perceptible erythema). Subsequentdoses are increased incrementally. CombiningUVB radiation and topical therapy, such as tar orcalcipotriol, is well tolerated and efficacious in sta-ble plaque disease. There have been anecdotal re-ports of exacerbation of acute guttate cases if UVBis given early in the disease course.[37] TLO1 (nar-row band UVB) fluorescent lamps emit a narrowUVB band at 311 ± 2nm. Its use in children hasbeen extrapolated from studies in adults whichsuggest efficacy equal to that of psoralen plus UVA(PUVA), but probably with less carcinogenic po-tential.[38] Some authors have suggested that longerremissions and a lower incidence of burning maybe expected with TLO1 in adults compared to treat-ment with broadband UVB.[39,40] PUVA therapy isnot generally suitable for young children.

2.4 Systemic Therapy

The most frequently used systemic drugs forpsoriasis in adults include retinoids (particularlyacitretin), methotrexate and cyclosporin. There isa paucity of clinical trials assessing the efficacy ortolerability of any of these agents in the paediatricage group. Treatment with such agents is reserved



for pustular or erythrodermic disease, psoriatic ar-thropathy or severe disease resistant to other thera-peutic modalities. Full counselling of, and informedconsent from, parents is essential. They must beaware of possible adverse effects and the need forcontinued monitoring. The decision to introducethese potentially toxic agents into the therapeuticregimen should be made by a dermatologist expe-rienced in their use.

2.4.1 RetinoidsMost experience has been reported with retin-

oids; acitretin (0.25 to 0.6 mg/kg) appears to be thedrug of choice. There is quite extensive clinicalexperience with the use of these agents in the treat-ment of inherited disorders of keratinisation andthe ichthyoses.[41] Nevertheless, the literature inpsoriasis is restricted to case reports and very smallcase series.[42-44] It has been suggested that erythro-dermic disease responds to lower doses of retinoidsthan pustular psoriasis.[45] Measurements of base-line lipid profile and liver enzymes are essential.These should be repeated at one-month and then atthree-monthly intervals. It is imperative that womenof child-bearing age are counselled about the abso-lute requirement to avoid pregnancy during treat-ment and for 2 years after cessation of the drug.Most patients can expect some adverse effects suchas dryness of the skin and mucous membranes, andmyalgia, especially after exercise. Children seemto tolerate oral retinoids better than adults.[45]

There has been some suggestion that retinoids maybe involved in premature epiphyseal closure. Someauthorities advocate a bone scan every 12 to 18months.[46]

2.4.2 MethotrexateMethotrexate is a folic acid antagonist, which

binds to dihydrofolate reductase thereby interfer-ing with DNA synthesis. Recent work has sug-gested that methotrexate may have a direct effecton T-lymphocytes.[47]

The tolerability and efficacy of methotrexate inthe treatment of childhood psoriasis is yet to beestablished. The evidence which is available comeslargely from a few studies involving small numbersof patients.[48,49] Methotrexate has been used suc-

cessfully in 7 children aged between 3 and 16 yearswith erythrodermic, generalised pustular psoriasisor psoriatic arthropathy. They tolerated doses of 0.2to 0.4 mg/kg with no detectable biochemical or hae-matological upset. Gastrointestinal upset was com-mon, but folic acid ameliorated their symptoms.[48]

Nausea and headache are common adverse ef-fects. Bone marrow suppression is an early dose-dependant adverse effect. The risk of hepatotoxic-ity is thought to be related to the total cumulativedose. Baseline full blood count, liver enzymes andrenal function should be established and then mon-itored throughout the treatment. Assays are checkedweekly initially, then monthly and eventually threemonthly. The lack of sensitivity of elevated liverenzymes in detecting early methotrexate hepato-toxicity is a cause for concern. Some guidelinesrecommend monitoring by repeated liver biop-sies.[50] Noninvasive techniques such as dynamichepatic scintigraphy and serial measurement of se-rum pro collagen 111 N terminal peptide are underinvestigation.[51] There are several important druginteractions with methotrexate (particularly non-steroidal anti-inflammatories, antibacterials such ascotrimoxazole, and anticonvulsants such as pheny-toin) of which the prescribing physician should beaware.

2.4.3 CyclosporinCyclosporin is a potent immunosuppressant

which inhibits T-lymphocyte production of IL2.There is considerable experience using this drug totreat adults with psoriasis and for treating childrenwith other conditions, e.g. atopic eczema.[52,53] How-ever, the only published literature in childhoodpsoriasis to date is a single case report.[54] A9-year-old boy with generalised pustular psoriasis wassuccessfully treated with 3 mg/kg/day cyclosporin-modified (Neoral®). The use of cyclosporin in thepaediatric transplant population suggests that theymay require a relatively higher dose than in adults.[55]

This agent is more suited to short-term use inachieving remission than to long-term maintenancetherapy.

678 Leman & Burden


3. Conclusions

The impact of psoriasis on the affected childvaries according to age, emotional and intellectualdevelopment, disease severity, and sites affected.Parental and medical attitudes can have a majorimpact on the disability caused by the disease. Par-ents can be reassured that psoriasis does not gen-erally affect life expectancy. From the outset itshould be stressed that psoriasis can usually becontrolled with topical agents. Treatment is sup-pressive rather than curative and is not known toaffect the natural history of disease.

The introduction of second-line agents such asretinoids and methotrexate is reserved for those se-verely affected and should only be undertaken byexperienced dermatologists with adequate facili-ties for monitoring. Further studies are required toassess the long-term tolerability of systemic thera-pies and phototherapy.

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Correspondence and offprints: Dr Joyce Leman, Departmentof Dermatology, Western Infirmary, Dumbarton Road,Glasgow, G11 6NT, Scotland.

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Psoriasis in Children

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