CME: Psoriasis: Finding the right approach for your patients


Psoriasis can be hard to diagnose and treat in children and teenagers. Early therapy and thorough patient and parent education are the keys to a favorable outcome.


Psoriasis: Finding the right approach for your patients

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Choose article section...LEARNING OBJECTIVES Who gets psoriasis and why The many forms of psoriasis Treating psoriasis: Some caveats Topical therapy: For mild and moderate cases Ultraviolet therapy: Benefits and risks For severe cases: A systemic approach Don't forget patient education ACCREDITATION CONTINUING MEDICAL EDUCATION CREDIT HOW TO APPLY FOR CME CREDIT FACULTY DISCLOSURES CME REGISTRATION AND EVALUATION FORM

By Nancy Chen, MD, and Bari B. Cunningham, MD

Psoriasis is common but sometimes hard to diagnose and treat in children and teenagers. Early, effective therapy and thorough patient and parent education are the keys to a favorable outcome.

Psoriasis is a common skin disorder that can begin at any age. Therapy may range from recommending a bland emollient for a mild case to systemic immunosuppressive therapy for a patient with severe, refractory disease. Treating severe juvenile psoriasis challenges pediatricians and dermatologists because there are few evidence-based studies on the effectiveness of systemic medications in this age group.



After reviewing this article the physician should be able to:


Addressing the psychosocial implications of psoriasis is particularly important for children and adolescents. Medical care should begin with education regarding the chronicity of the disease and its tendency to fluctuate in severity. Treatment needs to be individualized, depending on the degree of involvement, previously failed treatments, and lifestyle issues. Early, effective therapy may favorably influence the child's physical and psychosocial development.

Who gets psoriasis and why

The prevalence of psoriasis in the general population is estimated to be 1% to 3%, with lower frequency in Japanese, African-Americans, and Native Americans.1,2 Roughly one third of patients have their first outbreak in childhood or adolescence: The disease is diagnosed in infancy in 2%; in childhood in 10%; and during adolescence in 25%.1 Several population studies have shown that approximately 35% of psoriasis patients have a family history of the disease2­4; children with psoriasis are more likely to have a family history of the disease than patients who develop it as adults.5,6

Although the etiology of psoriasis is multifactorial, many studies have implicated genetic and environmental factors. Distinct HLA markers have been associated with different forms of psoriasis. Haplotypes Cw6 and DR7, for example, are linked to early-onset psoriasis, whereas the Bw13 haplotype is associated with milder psoriasis but a higher likelihood of antecedent streptococcal infection.3,7,8 Despite known associations, the linkage between heritable factors and disease manifestation remains incompletely understood.

The many forms of psoriasis

Psoriasis presents in a number of morphologic forms, including plaque psoriasis, guttate psoriasis, pustular psoriasis, erythrodermic psoriasis, seborrheic psoriasis, tinea amiantacea, and juvenile psoriatic arthritis. Commonly affected anatomic areas include the scalp, elbows, knees, and intergluteal and periumbilical regions. The lesions, particularly if mild, may be difficult to distinguish from tinea corporis and nummular eczema.

Infants may have lesions in the diaper region or other flexural locations, such as the axilla and antecubital fossae, that can be mistaken for seborrheic dermatitis. In a study of 72 children who were initially given a diagnosis of infantile seborrheic dermatitis and followed for as long as 13 years, 27% were eventually determined to have psoriasis (19% had keratosis pilaris, 19% had no lesions at follow-up, and the remainder had a variety of skin disorders, including atopic dermatitis, xerosis, and ichthyosis vulgaris).9

Psoriasis is notoriously difficult to diagnose when it appears in infancy or early childhood. On average, the correct diagnosis is not made until 11 months after presentation.10 When faced with an infant with red patches and plaques in intertriginous regions, consider candidiasis, seborrheic dermatitis, psoriasis, and contact or irritant dermatitis.

Psoriasis fluctuates in severity, with periodic "flares." External trauma may exacerbate it—a phenomenon known as the Koebner reaction. Table 1 lists some other common triggers of psoriasis.


Common triggers of psoriasis


Streptococcal infection (often occult)

Systemic corticosteroids


Medications (lithium, gold, antimalarials, ß-blockers)


Itching is the most common symptom of psoriasis. In one study, itching occurred in 72% of 305 Kuwaiti children with the disease.3

Plaque psoriasis is the most common clinical presentation. The typical lesions are thick, well-demarcated, erythematous plaques covered with thick, silvery, mica-like scales resulting from accelerated epidermal turnover (Figures 1 and 2). The scales are attached mostly in the center of the lesion. Plaques often demonstrate punctate bleeding when the scales are removed—the so-called Auspitz sign, which is caused by capillary proliferation in the superficial papillary dermis.




The scalp is the most frequently affected site in children. Plaques also may localize to a surgical scar, reflecting the Koebner reaction, or to the elbows and knees because these areas are often traumatized, especially in children.

Guttate psoriasis is common in childhood and presents as raindrop-shaped papules ranging in size from 1 mm to 1 cm, scattered over the trunk and proximal extremities (Figure 3). The face is less likely to be involved than with other forms of psoriasis, and the palms and soles are usually spared. Guttate psoriatic lesions may resemble those of pityriasis rosea, pityriasis lichenoides et varioliformis acuta, secondary syphilis, and tinea corporis.



Children with guttate psoriasis are likely to have had an antecedent streptococcal infection of the upper respiratory tract. Recurrent streptococcal pharyngotonsillitis may exacerbate psoriasis, particularly in children, and lead to a guttate disease pattern. The correlation between streptococcal infection and psoriatic onset and flare has been postulated to result from the structural similarity between human keratin and the M6 streptococcal protein. This antigenic mimicry allows activation and expansion of streptococcal-specific T-cells in the skin, leading to the flare of psoriasis. In support of this hypothesis, guttate psoriasis may remit after adenotonsillectomy and may be accompanied by a decrease in circulating IgM antikeratin antibody.11

Streptoccoccus proteins and exotoxins also may act as a "superantigen." In this case, microbially encoded proteins simultaneously stimulate large numbers of T-cell clones, leading to T-cell proliferation, release of cytokines, and a psoriatic flare.12 A throat culture for streptococci, and occasionally an antistreptolysin titer, are recommended for children with guttate psoriasis. Empiric antistreptococcal therapy may be beneficial in acute cases.

Pustular psoriasis, which occurs in both localized and generalized (von Zumbusch) forms, is rarely seen in children. The localized form usually runs a chronic course characterized by sterile pustules without systemic symptoms (Figure 4). In contrast, generalized pustular psoriasis is marked by widespread eruption of tender, discrete, sterile pustules and is often associated with fever, malaise, and anorexia.11­15 Both variants are often misdiagnosed as bacterial folliculitis, impetigo, or candidal infection. Treatment of generalized pustular psoriasis is often challenging and may require systemic retinoids, topical corticosteroids, and hospitalization.



Erythrodermic psoriasis. Psoriasis can progress to erythema and exfoliation involving the entire skin. The condition is rare in children. Patients typically have less scaling than those with plaque psoriasis. Occasionally, erythrodermic psoriasis may be provoked by external factors, including systemic corticosteroids, stress, coexisting dermatologic diseases, and medications such as gold therapy, lithium, ß-blockers, and antimalarial drugs.16 The differential diagnosis includes atopic dermatitis, drug eruption, seborrheic dermatitis, and generalized contact dermatitis.

Seborrheic psoriasis, also known as sebopsoriasis and seborrhiasis, is characterized by greasy, soft, salmon-colored lesions resembling seborrhea in combination with well-demarcated erythematous plaques covered by adherent silvery scales (Figure 5). It is commonly seen on the head and neck. Whereas classic seborrhea of the scalp tends to be confined to the hairline, psoriasis often extends to the retroauricular and preauricular regions, forehead, and external auditory canals.



Tinea amiantacea (pityriasis amiantacea) produces thick, crusted lesions that occur mainly on the scalp. They are often misdiagnosed as tinea capitis because of their scaly appearance or as pediculosis because of the "pseudonit" appearance of crusted hair shafts (Figure 6). Unlike tinea capitis, however, tinea amiantacea does not involve hair loss. It can be differentiated from lice infestation by microscopic examination of the hair shaft, which shows concretions of scale, not true nits, adhering to the hair, and by the absence of live lice.



Juvenile psoriatic arthritis can be a challenge to recognize, especially if cutaneous psoriasis is absent or of subtle presentation. The intergluteal fold, umbilicus, and scalp are good places to examine carefully for milder cutaneous manifestations. Diagnosis is often delayed because the condition bears similarities to juvenile rheumatoid arthritis.

The most common presentation of this type of psoriasis is a monoarticular, often acute, arthritis of the knee. Juvenile psoriatic arthritis tends to occur in children with a strong family history of the condition and is often associated with the HLA haplotype B27, especially when it takes the form of spondyloarthritis. Onset is bimodal, with a first peak incidence between 2 and 4 years of age (affecting more girls than boys) and a second peak between 11 and 12 years of age (affecting slightly more boys). The Vancouver criteria for classifying childhood psoriatic arthritis includes not only the presence of psoriasis, arthritis, and positive family history, but also dactylitis, nail pitting, antinuclear antibodies, and uveitis (Table 2).17,18


Diagnostic criteria for juvenile psoriatic arthritis


Onset of arthritis prior to 16 years of age with psoriasis


Arthritis with three of four minor criteria for psoriasis (nail pits, dactylitis, psoriasis-like rash, family history of psoriasis)


Arthritis with two minor criteria

Adapted from Vancouver criteria, in Southwood TR, Petty RE, Malleson PN, et al18


Nail abnormalities. Nail pitting is common in psoriasis patients. Pitting usually appears as small, irregularly spaced depressions measuring approximately 1 mm in diameter (Figure 7). Other nail changes associated with psoriasis include yellow-brown discoloration, onychodystrophy, subungual hyperkeratosis, and onycholysis. Treatment of nail abnormalities is challenging, and the condition may respond only to systemic therapy, such as methotrexate.



Treating psoriasis: Some caveats

A wide variety of topical and systemic therapies are used to treat psoriasis (Table 3). Because only a limited number of comparative, blinded, placebo-controlled trials have involved children, many treatments are extrapolated from evidence-based studies in adults.


Recommended treatments for pediatric psoriasis

Type of psoriasis
Localized pustular
Generalized pustular
Oral antibiotics
Retinoids, systemic


Another problem in treating children is that the importance of parental education and patient compliance is often overlooked. Thorough treatment should include verbal guidance and written information regarding the chronicity and unpredictable course of the disease, the fact that it sometimes resolves spontaneously, and the importance of early treatment. A written, preprinted treatment plan, which can be individualized, is helpful and can improve compliance.

Topical therapy: For mild and moderate cases

Most children with mild or moderate psoriasis can be managed with topical therapy. A combination of two or three different agents may be necessary. The benefit of emollients such as plain petrolatum, Eucerin, and Aquaphor are often overlooked, and their effects underestimated. Keratolytics such as urea (10% to 20%) and salicylic acid (6%) can effectively exfoliate and hydrate the skin, especially in combination with a topical steroid. If the patient does not improve with topical therapy and the physician is not comfortable treating psoriasis with ultraviolet phototherapy or systemic agents, referral to a dermatologist is indicated.

Corticosteroids are the workhorse agents for psoriasis in children. Applied alone or in combination with vitamin D3 analogues, they have few side effects when used at low potency and for limited duration.

The risk of systemic adverse effects is much greater in infants than in older children because infants have a higher ratio of body surface area to mass. These effects include tachyphylaxis, irreversible striae, reversible atrophy, and acneiform lesions on the face, chest, back, and perioral and periocular regions. Several studies have described possible suppression of the pituitary-adrenal axis, which leads to irreversible growth retardation, as a result of percutaneous absorption of the topical steroid in children on chronic steroid therapy.19 When used appropriately and for a limited time, however, topical corticosteroids are safe and effective for treating psoriasis.

Anthralin is a synthetic compound derived from chrysarophanic acid, which is an extract of the Vouacopoua araroba tree. Its mechanism of action has not been worked out, but it is thought to decrease cell turnover. It also exerts strong anti-inflammatory effects by inhibiting neutrophil and monocyte functions. A main advantage of this therapy is its lack of long-term side effects, which allows reintroduction of the medication as often as needed. Anthralin can, however, discolor hair, clothing, and surrounding skin and often causes irritant dermatitis when applied at a concentration that exceeds instructions. For plaque psoriasis, a low concentration of 0.05% to 1% anthralin incorporated into petrolatum or zinc paste can be applied once daily for 30 minutes. The application time can be slowly increased as tolerated.

Coal tar is one of the oldest effective therapies for both plaque and guttate psoriasis and is widely available in over-the-counter antipsoriatic products. It does not irritate the skin like anthralin and vitamin D3 analogues and does not cause long-term side effects. The main disadvantage of coal tar is its unappealing odor, which usually leads to poor adherence among children. Liquid carbonis detergent (LCD), a 20% crude coal tar solution, has a less offensive odor and less tendency to stain skin and clothing than other coal tar preparations.

Vitamin D3 analogues, which were first used to treat psoriasis because of their antiproliferative effects on keratinocytes and their ability to induce in vitro terminal differentiation, also can alter lymphocytic activation and decrease the inflammatory response. Several studies critically evaluated one such analogue, calcipotriol (also called calcipotriene), in children after its safety and efficacy in adults was established. The studies found calcipotriol ointment to be a safe and effective treatment of childhood psoriasis.20­25

Retinoids. Tazarotene is the newest topical retinoid agent for treating psoriasis. As with all retinoids, a tendency to irritate skin limits its usefulness. Applying it in combination with a potent topical corticosteroid may reduce irritation. No evidence-based studies of topical retinoids for treating psoriasis in children have been conducted. For now, tazarotene is worth recommending for plaque psoriasis, particularly if lesions are not located in sensitive intertriginous regions.

Ultraviolet therapy: Benefits and risks

Both ultraviolet A (UVA) and ultraviolet B (UVB) phototherapy are used to treat psoriasis.

UVA. Psoralen plus UVA (PUVA) is a form of photochemotherapy that combines an orally administered photosensitizing agent (psoralen) with high-intensity UVA light at ranges of 320 nm to 400 nm. The interaction between psoralen and UVA results in conjugation of psoralen to DNA and subsequent inhibition of DNA synthesis, which decreases the turnover rate of epidermal cells. Although this regimen is effective in adults, its use in children has not been well established because of known long-term effects such as cataracts, premature actinic changes, and possible development of cutaneous cancers.

Recent epidemiologic studies have indicated that exposure to the sun during childhood can increase the lifetime risk of developing basal cell carcinoma and that cumulative exposure to ultraviolet light correlates with a higher incidence of squamous cell carcinoma.25,26 Stern and colleagues, following 26 patients who were started on PUVA before 15 years of age, found that one developed two basal cell carcinomas before 21 years of age.26,27 Although the authors did not report any squamous cell carcinomas or melanomas, PUVA should be reserved for children with severe psoriasis that does not respond to other treatments.

UVB phototherapy has been a mainstay of psoriasis treatment in adults for decades. Its use in children has been limited by concern over safety and the long-term risk of cutaneous malignancy.28­32 Several recent studies have demonstrated the efficacy and safety of UVB phototherapy in children. Tay and colleagues, for example, treated 10 psoriatic children with UVB, all of whom responded within 20 weeks without serious side effects.33 At this time, UVB is considered a safe and effective therapy for psoriasis if its duration is limited. In view of the lack of long-term follow-up data, patients and their parents should be advised of the possible risks of photoaging and skin cancer.

Narrow-band UVB, also called selective UVB therapy, is a safer alternative to traditional broad-band UVB. Narrow-band UVB clears lesions more quickly, burns less, and, on average, extends the duration of remission. Burning and blistering may develop even with this theoretically safer method, however.34

Narrow-band UVB is particularly suited for children with the plaque or guttate variant of psoriasis because it has a safer side effect profile. It is used alone or in combination with a topical regimen.35

Advantages of narrow-band UVB over PUVA include lack of pain and nausea associated with treatment, no need for eye protection, and a lower risk of treatment-induced cancer.36 Despite recent reports that narrow-band UVB has efficacy comparable to PUVA for adults with moderate or severe psoriasis, PUVA remains the mainstay of therapy in severe disease.36

For severe cases: A systemic approach

Systemic therapy is recommended only for patients with severe psoriasis or acute flares associated with generalized or pustular forms of the disease.

Methotrexate is commonly used to treat adult psoriatics with severe or recalcitrant disease. Its use in children is limited to the most severe, refractory cases. In one report, seven severely psoriatic children between 3.5 and 16 years of age were treated with methotrexate for a mean of 38.8 weeks. Their disease was controlled in six to 10 weeks at a dosage of 0.2 to 0.4 mg/kg/wk. Slow tapering of medication preceded complete withdrawal. None showed evidence of laboratory abnormalities or an adverse effect on growth or on development of secondary sex characteristics. Three children experienced vomiting and nausea that were controlled with metoclopramide.37

Children with generalized or pustular psoriasis that is unresponsive to topical therapy can be started on methotrexate at 0.2 to 0.4 mg/kg/wk, along with folic acid at 1 mg/d or 5 mg twice weekly to ease gastrointestinal side effects without loss of methotrexate efficacy. For nonadherent patients, weekly intramuscular injection of methotrexate can be given in the doctor's office or clinic.

Common adverse effects of methotrexate include—in addition to nausea—anorexia, fatigue, and alopecia. Leukopenia and thrombocytopenia may signal bone marrow toxicity and can be reversed with folinic acid. A complete blood count, hepatic panel, and serum chemistry panel (chem 10) are recommended as a baseline, monthly, and, eventually, every three months.

Hepatotoxicity is a major concern with methotrexate. Liver biopsy is indicated after each cumulative dose of 1.5 g to monitor for structural liver damage. Also, several classes of medications are contraindicated during methotrexate therapy because they enhance the drug's toxicity by altering protein binding, decreasing renal excretion, or increasing hepatotoxicity (Table 4).


Prescribing recommendations for methotrexate

0.2–0.4 mg/kg/wk as a single dose or divided into 3 equal doses given 12 hr apart along with folic acid 1 mg qd or 5 mg twice weekly
Lab tests
Baseline: urinalysis, complete blood count (CBC) liver function tests (LFT), chem 10 (serum chemistries) At time treatment begins: monthly, until a stable methotrexate (MTX) dose is attained, for 2 mo CBC, LFT, chem 10 Maintenance: every 3 mo: CBC, LFT, chem 10
Liver biopsy
After every cumulative dose of 1.5 g
Drug interactions
Agents that increase risk for hepatotoxicity of MTX acitretin, isotretinoin Agents that decrease MTX clearance or increase blood level of MTX: aminoglycosides, amoxicillin, barbiturates cisplatin, NSAIDs, phenytoin, probenecid, sulfonamides Psoriasis-aggravating medications: chloroquine, lithium
Sulfonamides, NSAIDS, retinoids


Retinoids. Derivatives of vitamin A—such as isotretinoin, etretinate, and its principal metabolite, acitretin—are effective treatments for psoriasis38 but are used to treat it very rarely (only in severe cases refractory to other treatments) because of their teratogenicity and side effects. Isotretinoin is preferred for its shorter half-life and favorable metabolism. Etretinate and acitretin are not recommended for children and adolescents because of concern over prolonged teratogenicity (the drugs can remain in the body for up to three years).

In young children, retinoids may lead to premature epiphyseal closure.39 Because orthopedic changes seen in adults on retinoid therapy, such as diffuse idiopathic skeletal hyperostosis (DISH), also may occur in children, long bone radiographs are recommended every 12 to 18 months. Other side effects of retinoids include dry lips (cheilitis), dry eyes and mouth, and generalized dryness of the skin. Alopecia, muscle and joint pain, and gastrointestinal effects occur less often. Serum lipids and liver enzymes sometimes become elevated and should be monitored with monthly serologic testing.

The teratogenic potential of retinoids cannot be overemphasized and should be discussed thoroughly with female adolescent patients. Warn them to avoid conception for one month before treatment, during treatment, and for three years after treatment with acitretin.40 We require sexually active girls and women to agree to use two forms of birth control while they are taking any systemic retinoid, regardless of what morphologic variant of psoriasis is being treated.

Don't forget patient education

Childhood psoriasis is a common cutaneous disorder that does not reduce life expectancy, but may nevertheless have a devastating psychosocial impact on patients. Successful management depends not only on effective medical therapy but on patient and family education to address accompanying psychosocial issues. Information for patients, families, and medical professionals about medical and psychosocial aspects of psoriasis and how it is treated is available at , the National Psoriasis Foundation's Web site, or from the NPF at 6600 SW 92nd Avenue, Suite 300, Portland, OR 97223-7195; phone: 503-244-7404 or 800-723-9166; fax: 503-245-0626; e-mail:

1. Abel EA, DiCicco LM, Orenberg EK, et al: Drugs in exacerbation of psoriasis. J Am Acad Dermatol 1986;15:1007

2. Farber EM, Nall ML: Natural history of psoriasis in 5,600 patients. Dermatologica 1974;148:1

3. Nanda A, Al-Fouzan AS, El-Kashlan M, et al: Salient features and HLA markers of childhood psoriasis in Kuwait. Clin Exp Dermatol 2000;25:147

4. Swanbeck G, Inerot A, Martinsson T, et al: A population genetics study of psoriasis. Br J Dermatol 1994;131:32

5. Raychaudhuri SP, Gross J: A Comparative study of pediatric-onset psoriasis with adult-onset psoriasis. Pediatr Dermatol 2000;17(3):174

6. Bernard JD: Clinical difference in juvenile vs. adult-onset psoriasis. Br J Dermatol 1996;135:501

7. Henseler T: The genetics of psoriasis. J Am Acad Dermatol 1997;37:S1

8. Perlman SG: Psoriatic arthritis in children. Pediatr Dermatol 1984;1:283

9. Menni S, Piccinno R, Baietta S, et al: Infantile seborrheic dermatitis: Seven-year follow-up and some prognostic criteria. Pediatr Dermatol 1989;6(1):13

10. Pruszkowski A, Bodemer C, Fraitag S, et al: Neonatal and infantile erythrodermas. Arch Dermatol 2000; 136(7):875

11. McMillin BD, Maddern BR, Graham WR: A role for tonsillectomy in the treatment of psoriasis? ENT J 1999;78(3):155

12. Nickoloff B, Sron-Smith T: Superantigens, autoantigens, and pathogenic T cells in psoriasis. J Invest Dermatol 1998;110(4):459

13. Zelickson BD, Muller SA: Generalized pustular psoriasis in childhood: Report of thirteen cases. J Am Acad Dermatol 1991;24(pt 1):186

14. Farber M, Nall L: Pustular psoriasis. Cutis 1993;51:29

15. Gong J, Chen Z, Hu Z: Evaluation of the effectiveness of childhood generalized pustular psoriasis treatment in thirty cases. Pediatr Dermatol 1998;15(2):144

16. Farber EM, Nall L: Erythrodermic (exfoliative) psoriasis. Cutis 1993;51:79

17. Roberton DM, Cabral DA, Malleson PN, et al: Juvenile psoriatic arthritis: Follow-up and evaluation of diagnostic criteria. J Rheumatol 1996;23:166

18. Southwood TR, Petty RE, Malleson PN, et al: Psoriatic arthritis in children. Arthritis Rheum 1989; 32:1007

19. Patel L, Clayton PE, Jenney MEM, et al: Adult height in patients with childhood-onset atopic dermatitis. Arch Dis Child 1997;76:505

20. Perez A, Chen TC, Turner A, et al: Pilot study of topical calcitriol (1,25-dihydroxyvitamin D3) for treating psoriasis in children. Arch Dermatol 1995;131:961

21. Darley CR, Cunliffe WJ, Ferguson J, et al: Safety and efficacy of calcipotriol ointment (Dovonex) in treating children with psoriasis vulgaris. Br J Dermatol 1993;129(S42):33

22. Saggese G, Federico G, Battini R: Topical application of 1,25-dihydroxyvitamin D3 (calcitriol) is an effective and reliable therapy to cure skin lesions in psoriatic children. Eur J Pediatr 1993;152:389

23. Oranje AP, Marcoux D, Svensson A, et al: Topical calcipotriol in childhood psoriasis. J Am Acad Dermatol 1997;36(2, pt1):203

24. Park SB, Suh DH, Youn JI: A pilot study to assess the safety and efficacy of topical calcipotriol treatment in childhood psoriasis. Pediatr Dermatol 1999;16(4):321

25. Gallagher RP, Hill GB, Bajdik CD, et al: Sunlight exposure, pigmentation factors, and risk of nonmelanocytic skin cancer. I. Basal cell carcinoma. Arch Dermatol 1995;131:157

26. Gallagher RP, Hill GB, Bajdik CD, et al: Sunlight exposure, pigmentation factors, and risk of nonmelanocytic skin cancer. II. Squamous cell carcinoma. Arch Dermatol 1995;131:164

27. Stern RS, Laird N: The carcinogenic risk of treatments for severe psoriasis: Photochemotherapy follow-up study. Cancer 1994;73:2759

28. Stern RS, Nichols KT: Therapy with orally administered methoxsalen and ultraviolet A radiation during childhood increases the risk of basal cell carcinoma. J Pediatr 1996;129(6):915

29. Meunier L, Bata-Csorgo Z, Cooper KD: In human dermis, ultraviolet radiation induces expansion of a CD36+ CD11b+ CD1-macrophage subset by infiltration and proliferation; CD1+ Langerhans-like dendritic antigen-presenting cells are concomitantly depleted. J Invest Dermatol 1995;105:782

30. Krueger JG, Wolfe JT, Nabeya RT, et al: Successful ultraviolet B treatment of psoriasis is acompanied by a reversal of keratinocyte pathology and by selective depletion of intraepidermal T cells. J Exp Med 1996;182:2057

31. Kang K, Hammerberg C, Meunier L, et al: CD11b+ macrophages that infiltrate human epidermis after in vivo ultraviolet exposure potentially produce IL-10 and represent the major secretory source of epidermal IL-10 protein. J Immunol 1994;153:5256

32. Cai JP, Harris K, Falanga V, et al: VUB therapy decreases the adhesive interaction between peripheral blood mononuclear cells and dermal microvascular endothelium and regulates the differential expression of CD 54, VCAM-1 and E-selectin in psoriatic plaque. Br J Dermatol 1996;134:7

33. Tay VK, Morelli JG, Weston WL: Experience with UVB phototherapy in children. Pediatr Dermatol 1996;13:406

34. Calzavara-Pinton PG, Zane C, Candiago E, et al: Blisters on psoriatic lesions treated with TL-01 lamps. Dermatology 2000;200(2):115

35. Brands S, Brakman M, Bos JD, et al: No additional effect of calcipotriol ointment on low-dose narrowband UVB phototherapy in psoriasis. J Am Acad Dermatol 1999;41:991

36. Tanew A, Radakovic-Fijan S, Schemper M, et al: Narrow-band UV-B phototherapy vs. photochemotherapy in the treatment of chronic plaque-type psoriasis. Arch Dermatol 1999;135:519

37. Kumar B, Shar S, Handa S, et al: Methotrexate in childhood psoriasis. Pediatr Dermatol 1994;11(3):271

38. Lacour M, Mehta-Nikhar B, Atherton DJ, et al: An appraisal of acitretin therapy in children with inherited disorders of keratinization. Br J Dermatol 1996;134:1023

39. Judge MR, McDonald A, Black MM: Pustular psoriasis in childhood. Clin Exp Dermatol 1993;18:97

40. Soriatane [package insert]. Nutley, N.J., Roche Laboratories, 1997

DR. CHEN is a resident in the department of medicine, division of dermatology, Children's Hospital and Health Center and School of Medicine, University of California, San Diego.
DR. CUNNINGHAM is attending dermatologist and assistant clinical professor of pediatrics and medicine, division of pediatric and adolescent dermatology, Children's Hospital and Health Center and School of Medicine, University of California, San Diego.


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Date of publication: August 2001
Title: "Psoriasis: Finding the right approach for your patients"
Author: Nancy Chen, MD, and Bari B. Cunningham, MD

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A. Slightly modify what I currently do.
B. Make a major change in what I currently do.
C. Follow a procedure; use a technique/technology that is completely new to me.
D. Follow a procedure; use a technique/technology that I currently use but for a different purpose.
E. None of the above, but some change.
F. Not considering any changes.

4. Please describe any change(s) you plan to make in your practice as a result of this activity: ________



5. How committed are you to making these changes? 5 (very committed) 4   3   2   1  (not at all committed)

6. Other comments __________________________________________________________________


Circle A or B, and enclose payment if required.

A. I am a paid subscriber to Contemporary Pediatrics, so no payment is due.

The subscriber number above my name on the mailing label is: ___ ___ ___ ___ ___ ___ ___ ___

(Example: _1_ _2_ _3_ _4_ _5_ _6_ _7_ _8_ ).

If you do not know your subscriber number, please call 1-800-432-4570.

B. I am not yet a paid subscriber, so I am enclosing $20 to cover the cost of processing my CME application.

[ ] I am enclosing a check (payable to JMC/CME).

[ ] Please charge my Mastercard or Visa (circle type of card),

account number: ___ ___ ___ ___-___ ___ ___ ___-___ ___ ___ ___-___ ___ ___ ___ ,

expiration date: ___ ___ /___ ___

                                                              Signature (required)


Nancy Chen, Bari Cunningham. CME: Psoriasis: Finding the right approach for your patients. Contemporary Pediatrics 2001;8:86.

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