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      Catamenial dermatoses associated with autoimmune, inflammatory, and systemic diseases: A systematic review ,,

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          Abstract

          Background

          Sex hormones are important in female sexual physiology, growth, and homeostasis. Through skin receptors, sex hormones contribute to the dermatologic pathology known as catamenial dermatoses.

          Objective

          This study aims to summarize the literature on catamenial dermatoses and menses-induced exacerbations of chronic dermatoses.

          Methods

          This systematic review used the PRISMA method. PubMed was searched using the terms “menses” and “skin” in July 2018, and an assessment was conducted of the relevant literature on skin diseases related to non-pathologic menstruation, such as polycystic ovarian syndrome. Pathology associated with androgenetic acne was excluded from the study.

          Results

          A total of 102 studies with 1269 female patients were included. The most commonly reported primary catamenial dermatoses were autoimmune progesterone dermatitis and autoimmune estrogen dermatitis. The most commonly reported chronic skin disorders exacerbated by menses were psoriasis, Behcet’s disease, and eczematous dermatoses.

          Conclusion

          Physicians should be aware of the nature of catamenial dermatoses and their presentation with normal sexual physiology. Patients with chronic dermatoses should be appropriately counseled on menstruation-related exacerbations. Further research needs to be conducted to determine the interplay between immune regulation and sex hormones in catamenial dermatoses and to elucidate effective therapies.

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          Most cited references114

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          Estrogen receptors in immunity and autoimmunity.

          Due to the female predominance of autoimmune diseases, the role of gender and sex hormones in the immune system is of long-term interest. Estrogen's primary effects are mediated via estrogen receptors alpha and beta (ER α/β) that are expressed on most immune cells. ERs are nuclear hormone receptors that can either directly bind to estrogen response elements in gene promoters or serve as cofactors with other transcription factors (i.e., NFkB/AP1). Cytoplasmic ER and membrane associated ER impact specific kinase signaling pathways. ERs have prominent effects on immune function in both the innate and adaptive immune responses. Genetic deficiency of ERα in murine models of lupus resulted in significantly decreased disease and prolonged survival, while ERβ deficiency had minimal to no effect in autoimmune models. The protective effect of ERα in lupus is multifactoral. In arthritis models, ERα agonists appears to mediate a protective effect. The modulation of ERα function appears to be a potential target for therapy in autoimmunity.
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            Immunology and the menstrual cycle.

            Sex and gender differences in disease prevalence, pathogenesis and modulation have been frequently reported. The menstrual cycle represents the opportunity to study the physiological effect of hormonal fluctuations in vivo on the immune function and chronic disease modulation. Reports on the effect of the cycle on immune cell numbers and activity fluctuations are scarce, but recent publications demonstrate an increasing interest in the subject. The menstrual cycle might affect immune cell numbers and modulate their activity throughout the 4-week cycle, as demonstrated in the case of regulatory T cells. The implications of these fluctuations are particularly relevant in the field of chronic diseases affecting women of reproductive age. In fact, baseline inflammation and immune cell activation in association with other mechanisms, such as regulation of receptor expression, modulation of muscular contraction and behavioral aspects might explain the menstrual-associated fluctuations described in chronic and acute diseases. In the following review the current knowledge about the modulatory effects of the menstrual cycle on both immune cells and systemic diseases, such as autoimmune diseases, asthma, diabetes, cardiac arrhythmia and schizophrenia, is reported. Most of these diseases display worsening of symptoms premenstrually or during menses due to physiologic effects on the target tissue mediated by progesterone and estrogen fluctuations and, thus, display paradigmatic changes potentially relevant to numerous other conditions. Copyright © 2011 Elsevier B.V. All rights reserved.
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              Estrogen alters thresholds for B cell apoptosis and activation.

              Estrogen is thought to contribute to the increased frequency of autoimmune disorders occurring in females, but a molecular basis for its effects on autoimmunity remains to be elucidated. We have shown previously that estrogen leads to the survival and activation of autoreactive cells in the naive repertoire. To identify the molecular pathways involved in B cell tolerance, we sought to identify genes that are differentially regulated by estrogen in mouse B cells. Several genes involved in B cell activation and survival, including cd22, shp-1, bcl-2, and vcam-1, were upregulated by estrogen in B cells. We found that overexpression of CD22 and SHP-1 in B cells decreased B cell receptor signaling. Estrogen receptors alpha and beta are expressed on B cells and are functional, since they can directly upregulate expression of CD22, SHP-1, and Bcl-2. Estrogen treatment protected isolated primary B cells from B cell receptor-mediated apoptosis. These results suggest that estrogen induces a genetic program that alters survival and activation of B cells in a B cell-autonomous fashion and thus skews the naive immune system toward autoreactivity.
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                Author and article information

                Contributors
                Journal
                Int J Womens Dermatol
                Int J Womens Dermatol
                International Journal of Women's Dermatology
                Elsevier
                2352-6475
                25 October 2019
                December 2019
                25 October 2019
                : 5
                : 5
                : 361-367
                Affiliations
                [a ]Georgetown University, School of Medicine, Washington, D.C., United States
                [b ]University of California, Irvine, Department of Dermatology, Irvine, CA, United States
                [c ]University of California, Irvine, School of Medicine, Irvine, CA, United States
                Author notes
                [* ]Corresponding author. nmesinko@ 123456uci.edu
                Article
                S2352-6475(19)30107-8
                10.1016/j.ijwd.2019.09.008
                6938828
                31909158
                3bf35b8e-89f0-4356-9850-a40d773a2079
                © 2019 Published by Elsevier Inc. on behalf of Women's Dermatologic Society.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 17 April 2019
                : 8 September 2019
                : 26 September 2019
                Categories
                Article

                catamenial,menses,menstruation,menstrual cycle,autoimmune,progesterone,estrogen,dermatoses

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