INTRODUCTION
Psoriasis is a chronic inflammatory condition that affects 2% to 3% of the world’s population and can be challenging to treat.1,2 For patients with more extensive disease, difficult-to-treat areas (such as the scalp and palmoplantar surfaces), or greater reductions in quality of life, determining an optimal therapeutic regimen is a multifactorial and often challenging process. Biologics have altered the landscape of psoriasis treatment by providing effective and safe options for patients with moderate-to-severe psoriasis without the need for corticosteroids or other conventional immunosuppressive medications, which may cause liver, kidney, or bone marrow toxicity.
Although biologic therapies have significantly advanced psoriasis treatments, many unmet needs remain. Long-term treatment is required in up to 90% of cases because of the relapsing-remitting nature of the disease.3,4 Although biologics effectively target the inflammatory pathways driving psoriasis, some patients experience reduction or loss of therapeutic response over time.5 Such situations require a switch in biologic therapy, ideally to a drug with a different mechanism of action.5,6 However, given the number of biologics available for the treatment of psoriasis, the choice of therapy after treatment failure requires careful consideration from clinicians.7
The pathogenesis of psoriasis involves the (interleukin)-23– mediated differentiation of T cells into the helper T-cell subtype TH17, which then leads to production of IL-17.8 Interleukin-17 encompasses a total of 6 proteins (IL-17A to IL-17F) that drive inflammation in several cell types, including keratinocytes.8 This cycle of inflammation produces the painful, pruritic plaques seen in psoriasis, which commonly appear on the extensor surfaces of the limbs but also occur in areas such as the scalp, intertriginous areas, and palmoplantar surfaces.9
Although biologic therapies have significantly advanced psoriasis treatments, many unmet needs remain. Long-term treatment is required in up to 90% of cases because of the relapsing-remitting nature of the disease.3,4 Although biologics effectively target the inflammatory pathways driving psoriasis, some patients experience reduction or loss of therapeutic response over time.5 Such situations require a switch in biologic therapy, ideally to a drug with a different mechanism of action.5,6 However, given the number of biologics available for the treatment of psoriasis, the choice of therapy after treatment failure requires careful consideration from clinicians.7
The pathogenesis of psoriasis involves the (interleukin)-23– mediated differentiation of T cells into the helper T-cell subtype TH17, which then leads to production of IL-17.8 Interleukin-17 encompasses a total of 6 proteins (IL-17A to IL-17F) that drive inflammation in several cell types, including keratinocytes.8 This cycle of inflammation produces the painful, pruritic plaques seen in psoriasis, which commonly appear on the extensor surfaces of the limbs but also occur in areas such as the scalp, intertriginous areas, and palmoplantar surfaces.9
