Adalimumab Plus Narrowband Ultraviolet B Light Phototherapy for the Treatment of Moderate to Severe Psoriasis

April 2011 | Volume 10 | Issue 4 | Original Article | 366 | Copyright © 2011

Jerry Bagel MDa,b

aPsoriasis Treatment Center of Central New Jersey, East Windsor, NJ bThe College of Physicians and Surgeons of Columbia University, New York, NY

Abstract

Background: Combining systemic agents with phototherapy is becoming a standard of care for patients with moderate to severe psoriasis. The combination of adalimumab and phototherapy has not been previously explored.
Methods: In this 24-week single-arm open-label study, adults with moderate to severe psoriasis received adalimumab 40 mg every other week and narrowband (NB)-UVB phototherapy three times a week for 12 weeks and then were followed for 12 weeks without treatment. Response to therapy was determined using the Psoriasis Area and Severity Index (PASI), Body Surface Area (BSA) affected and Physician’s Global Assessment (PGA) of psoriasis.
Results: Twenty patients were enrolled with mean baseline scores of 17.0 for PASI, 21.2 for BSA and 3.5 for PGA. Half (10/20) of the patients achieved PASI 75 response by week 4. At the end of treatment at week 12, 19 (95%) patients achieved PASI-75, 15 (75%) patients achieved PASI-90 and 11 (55%) patients achieved PASI-100. Seventeen (85%) patients were clear or almost clear (PGA score ≤1). Mean baseline PASI, BSA and PGA scores improved by 95 percent, 93 percent and 80 percent, respectively. Disease improvement was observed through the end of follow up period at week 24. No serious adverse events were noted.
Conclusion: Concurrent use of adalimumab and NB-UVB phototherapy was clinically effective and well tolerated in patients with moderate to severe psoriasis. This combination regimen represents a new treatment option for clinical practice and warrants further investigation in controlled clinical trials.

J Drugs Dermatol. 2011;10(4):366--371.

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INTRODUCTION

Psoriasis is a chronic immunologically driven inflammatory disease characterized by infiltration of the skin with activated T cells and by abnormal keratinocyte proliferation and differentiation, resulting in marked inflammation and thickening of the epidermis. Psoriasis affects 1-3 percent of the world population, making it one of the most prevalent inflammatory immunological diseases.1, 2 There are several clinical subtypes of psoriasis: plaque, guttate, erythrodermic, inverse and pustular. Plaque psoriasis is the most common type of psoriasis affecting up to 90 percent of psoriasis sufferers.1, 2 It presents as raised silvery scale, which can cover large areas, with underlying erythema, itching and discomfort. A significant proportion of patients with plaque psoriasis also have psoriatic arthritis.3, 4

Currently incurable, psoriasis is treated with a plethora of topical and systemic agents and photo(chemo)therapy. Traditional therapies for moderate to severe psoriasis include phototherapy, methotrexate, oral retinoids and cyclosporin. Patients whose skin lesions and concurrent symptoms cannot be adequately controlled with one therapeutic modality may receive combination therapy with systemic agents and phototherapy.5

Combination regimens that utilize a systemic agent with light therapy and/or a topical agent are becoming the standard of care in the United States 6 and Europe,7 confirming the observation of Lebwohl et al.8 in 2004 that the use of two or more therapies to treat patients with moderate to severe psoriasis seems to be the rule rather than the exception.

Injectible immunomodulatory agents, the so-called “biologics,” such as alephacept, etanercept, efalizumab and adalimumab have also become candidates for use in combination psoriasis regimens. Alefacept interferes with leukocyte function antigen (LFA)-3/CD2 interaction by suppressing the activation of T-lymphocytes,9 etanercept interferes with the natural activity of tumor necrosis factor (TNF)-α in the body by mimicking the p75 TNF receptor 10 and efalizumab interferes with the binding of LFA-1 to intercellular adhesion molecule-1 (ICAM- 1),11 thereby inhibiting the adhesion of leukocytes to other cell types. Adalimumab is a recombinant human immunoglobulin (IgG1) monoclonal antibody specific for tumor necrosis factor (TNF). Adalimumab binds with high affinity and specificity to soluble TNF-α and neutralizes the biological function of TNF-α by blocking its interaction with the p55 and p75 cell surface TNF

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