INTRODUCTION
Psoriasis
Psoriasis is a chronic, immune-mediated, inflammatory disease that affects the skin (including the scalp, hands, and feet) and the nails. It affects between 1.5–5% of the population in developed countries,1 with the most common symptoms reported by patients being pain, itch, and bleeding of skin lesions.2 Plaque psoriasis is the most common form of the disease, affecting 80–90% of patients, characterized by well-demarcated erythematous plaques.2 Psoriasis greatly affects patients’ quality of life (QoL) and psychological wellbeing, and can also be associated with joint disease, cardiovascular disease, inflammatory bowel disease (IBD), and depression. The exact cause of psoriasis is unknown; however, it is widely accepted that affected individuals may have a genetic predisposition involving immune-related genes, the interplay of which leads to a dysregulation of the adaptive and innate immune systems.3,4 The resulting changes in cytokine mediators lead to hyperproliferation and abnormal differentiation of epidermal keratinocytes, lymphocyte infiltration, and vascular changes, manifesting as lesions on the skin.2 Due to the chronic nature of the condition, patients require regular assessments to monitor disease severity and treatment effectiveness. Recently, a European consensus group defined treatment goals for moderate–severe psoriasis. Accordingly, a goal in psoriasis treatment is to reduce cutaneous signs and symptoms by at least 75%, as measured by the Psoriasis Area Severity Index (PASI), and to guarantee a good quality of life (QoL), as measured by a dermatology life quality index (DLQI) score of ≤5.5-7 Topical therapies are suggested for patients with limited disease. If the psoriasis is unresponsive to topical therapies, or if the disease is more extensive, then phototherapy (eg, psoralen ultraviolet A [PUVA], ultraviolet B [UVB]), oral therapies (eg, methotrexate, cyclosporine A, acitretin) or biological therapies (eg, anti-tumor necrosis factor [TNF] drugs) are recommended.2 The introduction of biologic agents has greatly improved disease management in patients with moderate–severe chronic psoriasis.5 While there are numerous biologic agents currently approved for the treatment of moderate–severe plaque psoriasis, in this article we will be proving an in-depth clinical review of originator adalimumab.
Adalimumab Mechanism of Action and Rationale for Use in Psoriasis
Tumor necrosis factor alpha (TNF-α), a pro-inflammatory cytokine, plays an important role in the pathogenesis of psoriasis.8,9 Patients with psoriasis have increased levels of TNF-α in their skin and serum, which significantly correlate with the severity of disease.2 Upon successful treatment of psoriasis, levels of TNF-α are reduced to normal.2 Adalimumab is a recombinant, fully human, monoclonal antibody against TNF-α. It binds with high affinity and specificity to TNF-α and blocks its interaction with both p55 and p75 cell-surface TNF receptors, neutralizing the biological
