Managing psoriasis: What’s best for your patient?

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Applied Evidence

Managing psoriasis: What’s best for your patient?

J Fam Pract. 2012 July;61(7):402-451

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References

1. Gelfand JM, Weinstein R, Porter SB, et al. Prevalence and treatment of psoriasis in the United Kingdom: a population-based study. Arch Dermatol. 2005;141:1537-1541.

2. Fortune DG, Richards HL, Griffiths CE. Psychologic factors in psoriasis: consequences, mechanisms, and interventions. Dermatol Clin. 2005;23:681-694.

3. Housman TS, Mellen BG, Rapp SR, et al. Patients with psoriasis prefer solution and foam vehicles: a quantitative assessment of vehicle preference. Cutis. 2002;70:327-332.

4. Pettey AA, Balkrishnan R, Rapp SR, et al. Patients with palmoplantar psoriasis have more physical disability and discomfort than patients with other forms of psoriasis: implications for clinical practice. J Am Acad Dermatol. 2003;49:271-275.

5. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis. Section 3. Guidelines of care for the management and treatment of psoriasis with topical therapies. J Am Acad Dermatol. 2009;60:643-659.

6. Kaufmann R, Bibby AJ, Bissonnette R, et al. A new calcipotriol/betamethasone dipropionate formulation (Daivobet) is an effective once-daily treatment for psoriasis vulgaris. Dermatology. 2002;205:389-393.

7. Koo JY, Martin D. Investigator-masked comparison of tazarotene gel q.d. plus mometasone furoate cream q.d. vs. mometasone furoate cream b.i.d. in the treatment of plaque psoriasis. Int J Dermatol. 2001;40:210-212.

8. Berger TG, Duvic M, Van Voorhees AS, et al. The use of topical calcineurin inhibitors in dermatology: safety concerns. Report of the American Academy of Dermatology Association Task Force. J Am Acad Dermatol. 2006;54:818-823.

9. Cornell RC, Stoughton RB. Correlation of the vasoconstriction assay and clinical activity in psoriasis. Arch Dermatol. 1985;121:63-67.

10. Lui H. Phototherapy of psoriasis: update with practical pearls. J Cutan Med Surg. 2002;6(suppl):17-21.

11. Walters IB, Burack LH, Coven TR, et al. Suberythemogenic narrow-band UVB is markedly more effective than conventional UVB in treatment of psoriasis vulgaris. J Am Acad Dermatol. 1999;40:893-900.

12. Stern RS, Laird N. The carcinogenic risk of treatments for severe psoriasis. Photochemotherapy follow-up study. Cancer. 1994;73:2759-2764.

13. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 5. Guidelines of care for the treatment of psoriasis with phototherapy and photochemotherapy. J Am Acad Dermatol. 2010;62:114-135.

14. Trehan M, Taylor CR. High-dose 308-nm excimer laser for the treatment of psoriasis. J Am Acad Dermatol. 2002;46:732-737.

15. Morison WL, Baughman RD, Day RM, et al. Consensus workshop on the toxic effects of long-term PUVA therapy. Arch Dermatol. 1998;134:595-598.

16. Spuls PI, Witkamp L, Bossuyt PM, et al. A systematic review of five systemic treatments for severe psoriasis. Br J Dermatol. 1997;137:943-949.

17. Murase JE, Lee EE, Koo J. Effect of ethnicity on the risk of developing nonmelanoma skin cancer following long-term PUVA therapy. Int J Dermatol. 2005;44:1016-1021.

18. Lowe NJ, Prystowsky JH, Bourget T, et al. Acitretin plus UVB therapy for psoriasis. Comparisons with placebo plus UVB and acitretin alone. J Am Acad Dermatol. 1991;24:591-594.

19. Torras H, Aliaga A, Lopez-Estebaranz JL, et al. A combination therapy of calcipotriol cream and PUVA reduces the UVA dose and improves the response of psoriasis vulgaris. J Dermatolog Treat. 2004;15:98-103.

20. Tanew A, Guggenbichler A, Honigsmann H, et al. Photochemotherapy for severe psoriasis without or in combination with acitretin: a randomized, double-blind comparison study. J Am Acad Dermatol. 1991;25:682-684.

21. Menter A, Korman NJ, Elmets CA, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 4. Guidelines of care for the management and treatment of psoriasis with traditional systemic agents. J Am Acad Dermatol. 2009;61:451-485.

22. Strober BE, Menon K. Folate supplementation during methotrexate therapy for patients with psoriasis. J Am Acad Dermatol. 2005;53:652-659.

23. Taler SJ, Textor SC, Canzanello VJ, et al. Cyclosporine-induced hypertension: incidence, pathogenesis and management. Drug Saf. 1999;20:437-449.

24. Menter A, Gottlieb A, Feldman SR, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: section 1. Overview of psoriasis and guidelines of care for the treatment of psoriasis with biologics. J Am Acad Dermatol. 2008;58:826-850.

25. Heydendael VM, Spuls PI, Opmeer BC, et al. Methotrexate versus cyclosporine in moderate-to-severe chronic plaque psoriasis. N Engl J Med. 2003;349:658-665.

26. Lloyd ME, Carr M, McElhatton P, et al. The effects of methotrexate on pregnancy, fertility and lactation. QJM. 1999;92:551-563.

27. Ellis CN, Fradin MS, Messana JM, et al. Cyclosporine for plaque-type psoriasis. Results of a multidose, double-blind trial. N Engl J Med. 1991;324:277-284.

28. Buccheri L, Katchen BR, Karter AJ, et al. Acitretin therapy is effective for psoriasis associated with human immunodeficiency virus infection. Arch Dermatol. 1997;133:711-715.

29. Lebwohl M, Bagel J, Gelfand JM, et al. From the Medical Board of the National Psoriasis Foundation: monitoring and vaccinations in patients treated with biologics for psoriasis. J Am Acad Dermatol. 2008;58:94-105.

30. Gordon KB, Vaishnaw AK, O’Gorman J, et al. Treatment of psoriasis with alefacept: correlation of clinical improvement with reductions of memory T-cell counts. Arch Dermatol. 2003;139:1563-1570.

31. Brown SL, Greene MH, Gershon SK, et al. Tumor necrosis factor antagonist therapy and lymphoma development: twenty-six cases reported to the Food and Drug Administration. Arthritis Rheum. 2002;46:3151-3158.

32. Fulchiero GJ, Jr, Salvaggio H, Drabick JJ, et al. Eruptive latent metastatic melanomas after initiation of antitumor necrosis factor therapies. J Am Acad Dermatol. 2007;56(suppl):S65-S67.

33. Leonardi CL, Kimball AB, Papp KA, et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 76-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 1). Lancet. 2008;371:1665-1674.

34. US Food and Drug Administration. FDA approves new drug to treat psoriasis. Sept. 25, 2009. Available at: http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm183851.htm. Accessed June 15, 2012.

35. Duchini A, Goss JA, Karpen S, et al. Vaccinations for adult solid-organ transplant recipients: current recommendations and protocols. Clin Microbiol Rev. 2003;16:357-364.

36. Mann DL, McMurray JJ, Packer M, et al. Targeted anticytokine therapy in patients with chronic heart failure: results of the Randomized Etanercept Worldwide Evaluation (RENEWAL). Circulation. 2004;109:1594-1602.

37. Griffiths CE, Strober BE, van de Kerkhof P, et al. Comparison of ustekinumab and etanercept for moderate-to-severe psoriasis. N Engl J Med. 2010;362:118-128.

38. Papp KA, Langley RG, Lebwohl M, et al. Efficacy and safety of ustekinumab, a human interleukin-12/23 monoclonal antibody, in patients with psoriasis: 52-week results from a randomised, double-blind, placebo-controlled trial (PHOENIX 2). Lancet. 2008;371:1675-1684.

Topicals aren’t working? Move on to phototherapy

Phototherapy is an option for patients with extensive disease or skin manifestations that are recalcitrant to topicals. It is efficacious, cost-effective, and lacks systemic immunosuppression. Ultraviolet (UV) A and B act on Langerhans cells, cytokines, and adhesion molecules, inhibiting epidermal proliferation and angiogenesis.¹⁰

Broadband UVB (BB-UVB) was first used during the 1950s, with crude tar or anthralin, but is rarely used today.

Narrow-band UVB (NB-UVB) (311-313 nm), developed in the 1980s, has largely replaced BB-UVB. In addition to providing more rapid clearing and resolution of psoriasis compared with BB-UVB, NB-UVB may have less phototoxicity.¹¹ Between 20 and 25 NB-UVB treatments, 2 to 3 times a week (in the office or at home) are usually required for significant improvement.

FAST TRACK

Narrow-band UVB therapy is a safe and effective option for patients with diffuse psoriasis.

Photocarcinogenesis is a concern but numerous studies, including a review of 3867 patients treated with NB-UVB with a median 5.5-year follow-up, found no significant association with cutaneous malignancies.¹² NB-UVB is considered safe during pregnancy and used as first-line therapy for pregnant patients.¹³

Targeted UVB therapy using a 308-nm excimer laser, another option, selectively targets psoriatic lesions, leaving normal skin untreated. This makes supraerythemogenic doses possible, which increases UVB’s efficacy. Long-term adverse effects and duration of remission have not been clearly established.¹⁴

Psoralen and UVA (PUVA), which uses oral or topical psoralens to sensitize the skin to UVA, has a slightly higher efficacy than NB-UVB, but with increased risk of squamous cell carcinoma (SCC) and possibly melanoma.¹⁵ Clearing can occur within 24 treatments, with remissions lasting 3 to 6 months;¹⁶ monthly maintenance has not been found to lengthen remission.¹³

Common adverse effects include erythema that peaks 48 to 96 hours after a treatment, pruritus, xerosis, irregular pigmentation, and gastrointestinal symptoms that can be reduced by decreasing psoralen and/or UVA doses.¹³ High cumulative doses of oral PUVA (>200 treatments) is associated with a dose-related increased risk of nonmelanoma skin cancer, particularly SCC, in the Caucasian population. This increased risk has not been demonstrated in patients treated with PUVA bath therapy, which is more common in Scandinavian countries.¹⁷ There is no consensus regarding the risk of melanoma.¹⁵

A careful risk-benefit analysis is needed before initiating phototherapy in patients who take photosensitizing drugs, are immunosuppressed, or have a photosensitivity disorder or a history of melanoma, atypical nevi, multiple melanoma risk factors, or multiple nonmelanoma skin cancers.¹³ Regardless of the type of UV therapy administered, eye protection with goggles is required to decrease the risk of UV-related cataract formation, and genital shielding is needed to prevent increased risk of tumors.¹³ Photoaging is a long-term effect.

CASE When questioned further about the challenges that Tom has had with controlling his symptoms, he admitted to being noncompliant. As a busy executive, he said he didn’t have time to use the topical corticosteroids regularly. Phototherapy could alleviate his cutaneous symptoms, but would not address his symptoms that were consistent with psoriatic arthritis.

Pairing therapeutic modalities decreases exposure
Combining therapeutic modalities like emollients and topical or oral retinoids with NB-UVB improves efficacy while reducing the number of treatment sessions and cumulative UVB dosage. If calcipotriene is used, it should be applied after phototherapy because it is degraded upon UVB exposure.¹⁸ Acitretin should be started 2 weeks prior to initiation of phototherapy, and its use accompanied by a 25% reduction in initial UV dosage.¹³

PUVA may also be combined with topical calcipotriene or retinoids.¹⁹ In both cases, the addition of the other agent typically decreases the duration of phototherapy, improves the clinical response, and reduces the risk of cancer.^13,20

Extensive disease? Consider a traditional systemic agent

Traditional systemic therapy is used to treat extensive disease ( FIGURE ), psoriasis refractory to topical agents, and debilitating disease on the palms, soles, or scalp. Biologics are a recent alternative, but traditional systemics have been utilized longer and have a more longstanding adverse effect and safety profile, are administered orally, and are much less expensive than biologics. Monitoring patients on systemic therapy is necessary ( TABLE 2 ).^21-24

Methotrexate (MTX), a competitive inhibitor of dihydrofolate reductase, is the most commonly prescribed traditional systemic psoriasis treatment.²¹ It is administered in a single weekly dose via tablet, parenteral solution, or intramuscular (IM) or subcutaneous (SC) injection.²⁵ A test dose (2.5 or 5 mg) is given initially and complete blood cell count is monitored within one week to evaluate for potential bone marrow toxicity. If none is observed, the dose may be increased to control the disease while minimizing adverse effects.²¹