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      Chronic urticaria and thyroid pathology

      research-article
      a , b , a , , a , a , a
      The World Allergy Organization Journal
      World Allergy Organization
      Autoimmunity, Chronic urticaria, Histamine, Levothyroxine, Urticaria, Thyroid disease, ATAbs, anti-thyroid autoantibodies, AAbs, autoantibodies, AD, autoimmune diseases, AE, angioedema, ASST, autologous serum skin test, ATD, autoimmune thyroid disease, TGAbs, anti-thyroglobulin antibodies, TPOAbs, anti-thyroid peroxidase antibodies, AMA, antithyroid microsomal antibody, BAT, basophil activation test, CU, chronic urticaria, CAU, chronic autoimmune urticaria, CSU, chronic spontaneous urticaria, DAMPs, damage-associated molecular patterns, FcεRIa, high affinity IgE receptor, GD, Graves' disease, ICU, inducible chronic urticaria, IFN-γ, gamma interferon, IgE, Immunoglobulin E, IgG, Immunoglobulin G, IL, Interleukin, NSAH, non-sedating antihistamines, PAF, platelet activating factor, PAMPs, pathogen-associated molecular patterns, TG, thyroglobulin, HT, Hashimoto's thyroiditis/autoimmune thyroiditis, TNF-α, tumor necrosis factor alpha, Treg, regulatory T cells, TSH, thyroid stimulating hormone, TSHR, thyroid stimulating hormone receptor, T4L, free thyroxine, TLR, Toll-like receptors, UAS, urticaria activity score, VEGF, vascular endothelial growth factor

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          Abstract

          Urticaria is defined as the sudden appearance of erythematous, itchy wheals of variable size, with or without angioedema (AE) (swelling of the deeper layers of the skin). Its classification depends on time course of symptoms and the presence of eliciting factors. When it lasts less than 6 weeks it is classified as acute urticaria (AU), and if the symptoms persist for more than 6 weeks, it is classified as chronic urticaria (CU). Current International Guidelines also classify CU as chronic spontaneous urticaria (CSU) and inducible urticarial, according to the absence or presence of environmental triggering factors. CSU is defined as urticaria and/or angioedema in which there is no evidence of a specific eliciting factor. CSU is associated with autoimmunity in 30–45% of the cases, sharing some immunological mechanisms with other autoimmune diseases, and is associated with autoimmune thyroid disease (ATD) in about 4.3%–57.4% patients. Several studies suggest that adequate therapy with anti-thyroid drugs or levothyroxine in early stages of ATD and CSU, may help to remit the latter; but there is still a lack of double-blind, placebo-controlled studies that support this hypothesis in patients without abnormal thyroid hormone levels. The objective of this review is to describe the pathophysiology of chronic spontaneous urticaria and its association with autoimmune thyroid disease.

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          Most cited references43

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          The EAACI/GA²LEN/EDF/WAO Guideline for the Definition, Classification, Diagnosis and Management of Urticaria. The 2017 Revision and Update

          This evidence- and consensus-based guideline was developed following the methods recommended by Cochrane and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) working group. The conference was held on 1 December 2016. It is a joint initiative of the Dermatology Section of the European Academy of Allergology and Clinical Immunology (EAACI), the EU-founded network of excellence, the Global Allergy and Asthma European Network (GA²LEN), the European Dermatology Forum (EDF) and the World Allergy Organization (WAO) with the participation of 48 delegates of 42 national and international societies. This guideline was acknowledged and accepted by the European Union of Medical Specialists (UEMS). Urticaria is a frequent, mast cell-driven disease, presenting with wheals, angioedema, or both. The lifetime prevalence for acute urticaria is approximately 20%. Chronic spontaneous urticaria and other chronic forms of urticaria are disabling, impair quality of life and affect performance at work and school. This guideline covers the definition and classification of urticaria, taking into account the recent progress in identifying its causes, eliciting factors and pathomechanisms. In addition, it outlines evidence-based diagnostic and therapeutic approaches for the different subtypes of urticaria.
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            Diagnosis and classification of Graves' disease.

            Graves' disease (GD) is an autoimmune disorder involving the thyroid gland, typically characterized by the presence of circulating autoantibodies that bind to and stimulate the thyroid hormone receptor (TSHR), resulting in hyperthyroidism and goiter. Organs other than the thyroid can also be affected, leading to the extrathyroidal manifestations of GD, namely Graves' ophthalmopathy, which is observed in ~50% of patients, and Graves' dermopathy and acropachy, which are quite rare. Presumably, the extrathyroidal manifestations of GD are due to autoimmunity against antigens common to the thyroid and other affected organs. Although its exact etiology remains to be completely understood, GD is believed to result from a complex interaction between genetic susceptibility and environmental factors. Clinically, GD is characterized by the manifestations of thyrotoxicosis as well as by its extrathyroidal features when present, the latter making the diagnosis almost unmistakable. In the absence of ophthalmopathy, the diagnosis is generally based on the association of hyperthyroidism and usually diffuse goiter confirmed with serum anti-TSHR autoantibodies (TRAbs). Hyperthyroidism is generally treated with anti-thyroid drugs, but a common long term treatment strategy in patients relapsing after a course of anti-thyroid drugs (60-70%), implies the use of radioactive iodine or surgery. Copyright © 2014 Elsevier B.V. All rights reserved.
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              The potential pharmacologic mechanisms of omalizumab in patients with chronic spontaneous urticaria.

              In patients given a diagnosis of chronic spontaneous urticaria (CSU), there are no obvious external triggers, and the factors that initiate the clinical symptoms of wheal, flare, and itch arise from within the patient. Most patients with CSU have an autoimmune cause: some patients produce IgE autoantibodies against autoantigens, such as thyroperoxidase or double-stranded DNA, whereas other patients make IgG autoantibodies against FcεRI, IgE, or both, which might chronically activate mast cells and basophils. In the remainder of patients with CSU, the nature of the abnormalities has not yet been identified. Accumulating evidence has shown that IgE, by binding to FcεRI on mast cells without FcεRI cross-linking, can promote the proliferation and survival of mast cells and thus maintain and expand the pool of mast cells. IgE and FcεRI engagement can also decrease the release threshold of mast cells and increase their sensitivity to various stimuli through either FcεRI or other receptors for the degranulation process. Furthermore, IgE-FcεRI engagement potentiates the ability of mast cells to store and synthesize de novo inflammatory mediators and cytokines. Administration of omalizumab, by virtue of its ability to deplete IgE, attenuates the multiple effects of IgE to maintain and enhance mast cell activities and hence reduces the ability of mast cells to manifest inflammatory mechanisms in patients with CSU.
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                Author and article information

                Contributors
                Journal
                World Allergy Organ J
                World Allergy Organ J
                The World Allergy Organization Journal
                World Allergy Organization
                1939-4551
                06 March 2020
                March 2020
                06 March 2020
                : 13
                : 3
                : 100101
                Affiliations
                [a ]Centro Regional de Alergia e Inmunología Clinica, Hospital Universitario “Dr. José Eleuterio González”, Ave. Gonzalitos y Madero, s/n, Colonia Mitras Centro, CP. 64460, Monterrey, Nuevo Leon, Mexico
                [b ]Allergy and Clinical Immunology Department, Centro Medico Docente La Trinidad, Allergy Service, Clinica El Avila, 6a. Transversal Urb. Altamira, Piso 8, Consultorio 803, Caracas, 1060, Venezuela
                Author notes
                []Corresponding author. dra.dmrangel@ 123456yahoo.com
                Article
                S1939-4551(20)30004-1 100101
                10.1016/j.waojou.2020.100101
                7063156
                32180891
                fb50a1bb-8631-42d6-969d-40ef76f9acda
                © 2020 Published by Elsevier Inc. on behalf of World Allergy Organization.

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

                History
                : 11 October 2018
                : 27 November 2019
                : 31 December 2019
                Categories
                Article

                Immunology
                autoimmunity,chronic urticaria,histamine,levothyroxine,urticaria,thyroid disease,atabs, anti-thyroid autoantibodies,aabs, autoantibodies,ad, autoimmune diseases,ae, angioedema,asst, autologous serum skin test,atd, autoimmune thyroid disease,tgabs, anti-thyroglobulin antibodies,tpoabs, anti-thyroid peroxidase antibodies,ama, antithyroid microsomal antibody,bat, basophil activation test,cu, chronic urticaria,cau, chronic autoimmune urticaria,csu, chronic spontaneous urticaria,damps, damage-associated molecular patterns,fcεria, high affinity ige receptor,gd, graves' disease,icu, inducible chronic urticaria,ifn-γ, gamma interferon,ige, immunoglobulin e,igg, immunoglobulin g,il, interleukin,nsah, non-sedating antihistamines,paf, platelet activating factor,pamps, pathogen-associated molecular patterns,tg, thyroglobulin,ht, hashimoto's thyroiditis/autoimmune thyroiditis,tnf-α, tumor necrosis factor alpha,treg, regulatory t cells,tsh, thyroid stimulating hormone,tshr, thyroid stimulating hormone receptor,t4l, free thyroxine,tlr, toll-like receptors,uas, urticaria activity score,vegf, vascular endothelial growth factor

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