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Bayesian Methods for Evaluating Drug Safety with Real-World Evidence
Published in Harry Yang, Binbing Yu, Real-World Evidence in Drug Development and Evaluation, 2021
Psoriasis is a chronic autoimmune disease in which the growth cycle of skin cells is accelerated. Genetic and environmental factors induce immune responses mediated by several cytokines and chemokines, including interleukin-17 (IL-17) [27, 28]. IL-17 is a cytokine that controls cells and activates inflammation. For healthy individuals without psoriasis, these molecules stimulate the body's immune system into action only when there is a cut or a scrape, sending cells to the surface to fight infection and heal a wound. Psoriasis patients have 30 times more IL-17 than healthy people. Research has shown that stopping IL-17, or reducing it, may help clear psoriasis.
Dermatologic Disorders Causing Vulvar Disease
Published in William J. Ledger, Steven S. Witkin, Vulvovaginal Infections, 2017
William J. Ledger, Steven S. Witkin
Pemphigus vulgaris and pemphigus foliaceus are two pemphigoid autoimmune disorders resulting in intraepidermal blistering of the skin and mucus membranes. Autoantibodies from patients with these disorders predominantly react with desmogleins, which are glycoprotein components of the skin epidermis.16,17 This leads to loss of cohesion between keratinocytes in the epidermis resulting in blister formation. The transfer of these autoantibodies to mice induced pemphigus, while their removal prevented disease development.18 Why these autoantibodies develop and persist remains largely undetermined, although a very recent study highlighted the presence of abnormal B and T lymphocyte regulation, prevalence of anti-inflammatory cytokines, and enhanced interleukin-17 production in affected individuals.19 A British study reported that 51% of women with pemphigus vulgaris had lesions in their genital tract.20 Of these, 92% were on the labia majora, 28% on the labia minora, 36% in the vagina, and 15% on the cervix. Antibody recognition of these proteins triggers neutrophil recruitment, activation of the complement cascade, and the release of proteases that initiate pathological changes in the epidermis.21 Potential triggers for development of this specific autoimmunity in susceptible individuals include several members of the herpesvirus family as well as exposure to ultraviolet or x-irradiation or burns.21
Pediatric psoriasis
Published in M. Alan Menter, Caitriona Ryan, Psoriasis, 2017
Biological agents are highly effective options for recalcitrant psoriasis through inhibition of tumor necrosis factor-alpha (TNF-α; adalimumab, etanercept, infliximab), interleukin-12 /23 (ustekinumab),85 or interleukin-17 (secukinumab) (Table 15.1). Only etanercept has undergone a double-blind, randomized trial in U.S. children (n = 211)47; 57% of children receiving etanercept 0.8 mg/kg subcutaneously once weekly achieved 75% improvement in 12 weeks of therapy, compared to 11% receiving vehicle control. Five-year follow-up has shown safety and continued efficacy.86 Although primarily used for plaque psoriasis, TNF inhibitors have led to improvement for recalcitrant palmoplantar pustular and erythrodermic psoriasis. Other biologic agents have been described in trials outside the United States.87–96 Standard dosing of adalimumab is more efficacious than low dose (0.1–0.4 mg/kg/week) methotrexate over 16 weeks.94 Ustekinumab led to a PASI90 reduction of 61% after 12 weeks in a recent blinded, randomized trial in adolescents.95 Ustekinumab may also be the optimal therapy for CARD14-related psoriasis and pityriasis rubra pilaris. To date, secukinumab has not been tested in children.
Anti-IL17 treatment in childhood chronic rheumatic diseases
Published in Expert Opinion on Biological Therapy, 2023
Valerio Maniscalco, Ilaria Maccora, Flavio Girodo, Marta Tomaselli, Gaia Priolo, Edoardo Marrani, Maria Vincenza Mastrolia, Ilaria Pagnini, Gabriele Simonini
Interleukin-17 (IL-17) is a widely studied group of cytokines that plays a key role in the pathogenesis of several inflammatory chronic diseases, in adults as well as children. The first description reported IL-17 in 1993 in murine T cells and it was initially named cytotoxic T lymphocyte-associated antigen 8 (CTLA8) [1]. Six IL-17 isoforms have been currently described, from IL-17A to IL-17F [2]. IL-17 is mainly produced by lymphocyte T helper 17 (Th17), along with other cells of the innate and adaptive immune responses, including macrophages, dendritic cells, natural killer cells, γδ-T cells and CD8+ cells [3]. IL-17 production is a keynote step to protect against extracellular pathogens, such as fungi and bacteria and it acts by upregulating the expression of numerous inflammatory cytokines (e.g. IL-6, tumor necrosis factor [TNF]-α), chemokines, and inflammatory factors (e.g. acute-phase proteins and complement) [3,4].
Spotlight on the treatment armamentarium of concomitant psoriasis and inflammatory bowel disease: a systematic review
Published in Journal of Dermatological Treatment, 2022
Claudio Conforti, Caterina Dianzani, Iris Zalaudek, Michele Cicala, Paolo Persichetti, Roberta Giuffrida, Silviu-Horia Morariu, Nicoleta Neagu
The interleukin-17 family cytokines have a fundamental role in the pathogenesis of psoriasis and psoriatic arthritis. Secukinumab (SEC) and Ixekizumab (IXE), both monoclonal IgG4 antibodies directed against IL-17A, as well as brodalumab (BRO), a monoclonal antibody directed against IL-17 receptor, have been successfully used for the treatment of chronic plaque psoriasis and psoriatic arthritis (48). However, their use has been linked to the onset of paradoxical effects (49). Experimental colitis murine models revealed conflicting data on the role of the IL23–IL17 pathway: neutralization led to worsening or healing of intestinal inflammation (50). Recent publications have shown an increased rate of IBD in patients treated with IL-17 inhibitors (9,48,51–57). These are summarized in Table 2.
Ixekizumab and herpes zoster in an erythrodermic patient
Published in Baylor University Medical Center Proceedings, 2020
Corley C. Pruneda, Brett A. Austin, Daniel T. Wallis, Brent R. Paulger, Michelle B. Tarbox
Ixekizumab is an IL-17A antagonist approved by the US Food and Drug Administration for the treatment of moderate to severe plaque psoriasis in adults who are candidates for systemic therapy or phototherapy. It is also indicated for active psoriatic arthritis and was recently approved for active ankylosing spondylitis. Interleukin-17 is a pro-inflammatory cytokine that plays an important role in host defense against bacterial and fungal infections. It works by inducing granulocyte-colony stimulating factor production and producing chemokines that attract neutrophils to sites of infection.1 Absence of the gene encoding IL-17 has been associated with chronic mucocutaneous candidiasis.2 It has also been implicated as a key mediator of the inflammation in psoriasis. Adverse reactions reported in patients taking ixekizumab include injection site reactions, upper respiratory tract infections, nausea, and tinea infections.3 To the authors’ knowledge, herpes zoster has not been reported in the literature in a patient treated with an IL-17 antagonist. Here we describe a case of herpes zoster in an erythrodermic patient treated with ixekizumab.