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      Systemic Immune-Inflammation Index (SII) Predicts Increased Severity in Psoriasis and Psoriatic Arthritis

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          Abstract

          Background: Psoriasis is a common chronic inflammatory dermatosis. Systemic immune inflammation index (SII) is an inflammation-based biomarker, which has been shown to be an effective prognostic factor in diseases with an inflammation-related etiology. Objectives: The aim of the present study was to investigate the potential efficacy of SII as a prognostic factor in patients with psoriasis and psoriatic arthritis. Materials and methods: This is a study developed based on the analysis of the medical records of patients with psoriasis. The study retrospectively evaluated the records of the participants for complete blood count results. The SII was calculated by the formula: neutrophil x platelet/lymphocyte. Neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR) and platelet-lymphocyte ratio (PLR) were determined. Results: SII was significantly higher in patients with psoriasis than in controls (578.1 vs. 396, p<0.001). The differences between the median NLR (2.2 vs. 1.5, p<0.001), MLR (0.25 vs. 0.21, p<0.001) and the mean red cell distribution width coefficient of variation (13.8 vs. 12.8, p<0.001) values of patient and control group were significant. SII was higher in patients with moderate/severe psoriasis than patients with mild psoriasis (687.3 vs. 506.6, p=0.034). A positive correlation was observed between SII and PASI (p<0.001; r=0.37). SII was higher in patients with arthritis than patients without (672.1 vs. 548.2, p=0.018). Conclusion: This is the first study to prove that SII might serve as an independent prognostic indicator for patients with psoriasis and psoriatic arthritis.

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          Most cited references21

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          Psoriasis Pathogenesis and Treatment

          Research on psoriasis pathogenesis has largely increased knowledge on skin biology in general. In the past 15 years, breakthroughs in the understanding of the pathogenesis of psoriasis have been translated into targeted and highly effective therapies providing fundamental insights into the pathogenesis of chronic inflammatory diseases with a dominant IL-23/Th17 axis. This review discusses the mechanisms involved in the initiation and development of the disease, as well as the therapeutic options that have arisen from the dissection of the inflammatory psoriatic pathways. Our discussion begins by addressing the inflammatory pathways and key cell types initiating and perpetuating psoriatic inflammation. Next, we describe the role of genetics, associated epigenetic mechanisms, and the interaction of the skin flora in the pathophysiology of psoriasis. Finally, we include a comprehensive review of well-established widely available therapies and novel targeted drugs.
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            Immunology of psoriasis.

            The skin is the front line of defense against insult and injury and contains many epidermal and immune elements that comprise the skin-associated lymphoid tissue (SALT). The reaction of these components to injury allows an effective cutaneous response to restore homeostasis. Psoriasis vulgaris is the best-understood and most accessible human disease that is mediated by T cells and dendritic cells. Inflammatory myeloid dendritic cells release IL-23 and IL-12 to activate IL-17-producing T cells, Th1 cells, and Th22 cells to produce abundant psoriatic cytokines IL-17, IFN-γ, TNF, and IL-22. These cytokines mediate effects on keratinocytes to amplify psoriatic inflammation. Therapeutic studies with anticytokine antibodies have shown the importance of the key cytokines IL-23, TNF, and IL-17 in this process. We discuss the genetic background of psoriasis and its relationship to immune function, specifically genetic mutations, key PSORS loci, single nucleotide polymorphisms, and the skin transcriptome. The association between comorbidities and psoriasis is reviewed by correlating the skin transcriptome and serum proteins. Psoriasis-related cytokine-response pathways are considered in the context of the transcriptome of different mouse models. This approach offers a model for other inflammatory skin and autoimmune diseases.
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              Psoriasis pathogenesis and the development of novel targeted immune therapies.

              Psoriasis is caused by a complex interplay between the immune system, psoriasis-associated susceptibility loci, autoantigens, and multiple environmental factors. Over the last 2 decades, research has unequivocally shown that psoriasis represents a bona fide T cell-mediated disease primarily driven by pathogenic T cells that produce high levels of IL-17 in response to IL-23. The discovery of the central role for the IL-23/type 17 T-cell axis in the development of psoriasis has led to a major paradigm shift in the pathogenic model for this condition. The activation and upregulation of IL-17 in prepsoriatic skin produces a "feed forward" inflammatory response in keratinocytes that is self-amplifying and drives the development of mature psoriatic plaques by inducing epidermal hyperplasia, epidermal cell proliferation, and recruitment of leukocyte subsets into the skin. Clinical trial data for mAbs against IL-17 signaling (secukinumab, ixekizumab, and brodalumab) and newer IL-23p19 antagonists (tildrakizumab, guselkumab, and risankizumab) underscore the central role of these cytokines as predominant drivers of psoriatic disease. Currently, we are witnessing a translational revolution in the treatment and management of psoriasis. Emerging bispecific antibodies offer the potential for even better disease control, whereas small-molecule drugs offer future alternatives to the use of biologics and less costly long-term disease management.
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                Author and article information

                Journal
                Curr Health Sci J
                Curr Health Sci J
                CHSJ
                Current Health Sciences Journal
                Medical University Publishing House Craiova
                2067-0656
                2069-4032
                Oct-Dec 2020
                31 December 2020
                : 46
                : 4
                : 352-357
                Affiliations
                [1 ]Ankara Bilkent City Hospital
                Author notes
                Corresponding Author: Ahu Yorulmaz, Ankara Bilkent City Hospital ahuyor@ 123456gmail.com
                Article
                2020.4.05
                10.12865/CHSJ.46.04.05
                7948012
                33717509
                f31d5dfb-b929-4fdd-a54f-9c79be32861e
                Copyright © 2014, Medical University Publishing House Craiova

                This is an open-access article distributed under the terms of a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International Public License, which permits unrestricted use, adaptation, distribution and reproduction in any medium, non-commercially, provided the new creations are licensed under identical terms as the original work and the original work is properly cited.

                History
                : 02 November 2020
                : 09 December 2020
                Categories
                Original Paper

                psoriasis,psoriatic arthritis,systemic immune-inflammation index,severity,prognosis

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