Psoriasis is a chronic inflammatory skin disease whose main pathological manifestations are inflammation, epidermis hyperproliferation, altered epidermis maturation, and changes in blood vessels. The prevalence of this disease ranges from 0.51% to 11.43% in various countries. Pathogenesis of psoriasis is a combination of irregularities of the immunological system, a vulnerability associated with autoantigen psoriasis, and several environmental factors.
In recent years, the use of biological therapy in psoriasis has increased as a result of advances in understanding the pathophysiology of psoriasis disease. Biological agents currently approved for the treatment of moderate to severe plaque psoriasis include inhibitorTNF-α (adalimumab, etanercept, infliximab), inhibitor IL-17 (ixekizumab, brodalumab, secukinumab), inhibitor IL-12/IL-23 (ustekinumab), and inhibitor IL-23 (guselkumab, tildrakizumab). Each drug has its unique effectiveness and safety profile.
Inhibitor interleukin represents a new group of biologic agents with greater specificity to treat psoriasis. In theory, these agents should be more effective and safer than conventional therapies and inhibitor TNF-α, as they selectively target inflammatory pathways considered the most specific and important in the pathogenesis of psoriasis. Secukinumab is a human monoclonal antibody that selectively neutralizes IL-17A, a cytokine involved in the development of psoriasis. Secukinumab has demonstrated long-lasting effectiveness and safety in the manifestations of psoriasis, including on the nails, scalp, palms, soles, and psoriasis arthritis.
Psoriasis is a chronic inflammation of the skin with the characteristic form of erythematous plaque firmly, thick scale, layered, and silvery-white. Disorders in the innate and adaptive skin immune response are responsible for the development of inflammation in psoriasis. Psoriasis vulgaris is the most common overview consisting of 85% to 90% of all cases. This manifestation is a well-demarcated erythematous plaque closed to silvery scales that can reach a diameter of several centimetres.
Diagnosis of psoriasis is generally based on the clinical picture. If the clinical examination and the anamnesis are not enough to establish a diagnosis, then a biopsy can be done. Psoriasis exhibits characteristic histopathological changes in almost every type of skin cell. Psoriasis is characterized by epidermal acanthosis, hyperkeratosis, and parakeratosis, the extends of epidermal rete ridges. In the dermis, the blood vessels are dilated, and winding reaches the end of the dermis papilla.
Management of psoriasis can be classified as topical, systemic, or phototherapy. Systemic therapy consists of methotrexate, acitretin, biologic agents (adalimumab, etanercept, infliximab, ixekizumab, secukinumab, and ustekinumab), cyclosporin A, hydroxyurea, 6-thioguanine, cellcept, and sulfasalazine. Some parameters should be considered in the selection of treatment, including the characteristics of the disease such as the severity and location of skin lesions, the patient’s risk factor including age, history of failed treatment, and the characteristics of care such as effectiveness and safety issues. Some parameters can serve as the basis for consideration of biological agent selection.
There are three main classes of biological agents in the treatment of psoriasis. They are inhibitor TNFα, inhibitor IL-17, and inhibitor IL-23. Secukinumab is a fully human, fully derived from human antibodies anti-IL-17A IgG1 monoclonal antibody (antibodies made by identical immune cells that are all clones of unique stem cells) that selectively bind and neutralize IL-17A. Interleukin-17A has an important role in the proinflammatory cytokine in the pathogenesis of psoriasis. It can activate keratinocytes by causing hyperproliferation and excess production of antimicrobial peptides, cytokines, and chemokines, which activates other immune cells, leading to the inflammation of psoriasis. The binding of IL-17A by secukinumab inhibits interactions with IL-17 receptor, which will inhibit the release of other proinflammatory cytokines, chemokines, and mediators of tissue damage and reduce IL-17A contributions to this inflammatory disease.
Author: dr.Sylvia Anggraeni,Sp.KK
Details of this study can be viewed in our article at :
https://e-journal.unair.ac.id/BIKK/article/view/20013
SECUKINUMAB THERAPY IN PSORIASIS MANAGEMENT
Ira Yunita, Sylvia Anggraeni
