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Chronic Autoimmune Urticaria

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Chronic Autoimmune Urticaria SPECIAL ARTICLE Chronic Autoimmune Urticaria Wardhana, E.A. Datau Department of Internal Medicine, Siloam International Hospitals. Siloam Hospitals Group’s CEO Office, Siloam Hospital Lippo Village 5th floor. Jl. Siloam no. 6, Karawaci, Indonesia. Correspondence mail: [email protected]. ABSTRAK Urtikaria kronik umum terjadi dan pasien dapat memiliki gejala dan tanda sementara seperti rasa gatal, kemerahan, dan pembengkakan atau edema jaringan dermis, yang dapat berlangsung lebih dari enam minggu. Salah satunya adalah urtikaria idiopatik kronik, dan di antaranya adalah urtikaria autoimun. Urtikaria autoimun kronik disebabkan oleh afinitas reseptor IgE (anti-FcεRI) yang tinggi, dan penyebab yang lebih jarang adalah autoantibody anti-IgE; selain itu, aktivasi komplemen juga memiliki peranan yang dapat mengakibatkan aktivasi sel mast dan basofil. Meskipun telah banyak kemajuan dalam memahami urtikaria autoimun kronik, kondisi ini tetap menjadi tantangan tersendiri, terutama dalam hal etiologi, pemeriksaan, dan tata laksananya. Kata kunci: kronik, autoimun, urtikaria. ABSTRACT Chronic urticaria is common and patients may present with transient eruption of itchy, eruthematous, edematous swellings of the dermis, which lasts more than six weeks. One type of chronic idiopathic urticaria, and part of it, is the chronic autoimmune urticaria. The chronic autoimmune urticaria is caused by high affinity of IgE receptors (anti-FcεRI) and less frequently by anti-IgE autoantibodies, also the role of complement activation, that leads to mast and basophil activation. Despite many recent advances in the understanding of chronic autoimmune urticaria, this condition remains a major challenge in the terms of its etiology, investigations, and management. Key words: chronic, autoimmune, urticaria. INTRODUCTION Urticaria is defined as intense, itching welts caused by allergic reactions to internal and external agents. The word of urticaria is derived from the latin word urtica, which means “nettle”, which are tooth-leaved palnts covered with hairs capable of secreting a stinging fluid 1,2 that immediately affects the skin on contact. A B Urticarial lessions resulting from localized edema Figure 1. A) Urticaria – annular configuration. B) Urticaria of upper dermis are called wheals. By definition, on the neck. acute urticaria resolves than six weeks, whereas the chronic urticaria (CU) lasts six weeks or Urticaria affects 15-25% of the population at more with continuous disease activity, but when least once in their life time. The chronic urticaria occuring intermitently over a period of more than is more common in adults, affecting mainly six weeks can be defined as episodic Figure( 1).1,3 middle-aged women, and is rare in children Acta Medica Indonesiana - The Indonesian Journal of Internal Medicine 165 Wardhana Acta Med Indones-Indones J Intern Med and adolescents.2 The CU, based on the cause, helper 2 cell (Th2)-type immunologic response, is devided into the CU caused by identifiable autoimmune disease are variable, although many cause in 5-10% of the cases (the chronic physical are associated with Th1 lymphocytes, but the urticaria including symtomatic dermatographism, data presented from skin biopsies of CU had a delayed pressure urticaria, cold urticaria, Th0 (virgin or naïve Th) phenotype because there aquagenic urticaria, solar urticaria, cholinergic were significant increases in interferon-gamma urticaria, vibratory urticaria vasculitis; and the (IFN-γ), interleukin 4 (IL-4), and interleukin other is the chronic vasculitis urticaria), the 5 (IL-5) mRNA+ cells. Alternatively, it is also chronic idiopathic urticaria in 50% of cases (up possible that there is a mixture of Th1/Th2 cell to 30% of chronic idiopathic urticaris have an types. Allergen induced late-phase reaction autoimmune basis), and the chronic autoimmune (LPR) resembling the immune responsiveness urticaria (CAU) in more than 30% of cases.1,3 of CU histologically, produce IL-4 and IL-5, but not IFN-γ.6,7 The Th0 arrive at each surveillance PATHOGENESIS stopover in a secondary lymphoid organ via the Genetic background is thought to be a bloodstream. In the case of lymph nodes and relevant factor in autoimmune diseases, including Peyer’s patches, the high endothelial venules CAU. A study in large population of CU patients (HEVs), which are specialized blood vessels, showed a marked increase in prevalence of the serve as the nidus of attraction for the T cells disease among the first degree relatives and to enter the tissue. The extravasation of the Th0 showing a family history of autologous serum through HEVs relies on the intercellular adhesion skin test (ASST), which suggests the presence molecules (ICAMs) that engage the integrin lymphocyte function-associated antigen-1 (LFA- of circulating autoantibodies, and the association 7 with autoimmune thyroiditis has long been 1). recognized, and anti-thyroglobulin or anti-thyroid The Th0 lymphocytes may be found in the peroxidase antibodies can be detected in 25-30% skin tissue of CU, since in the autoimmue diseases of these patients.4 No obvious explaination for there is thymic T cells hyporesponsiveness this association has been proposed. The recent or unresponsiveness (anergy) to the antigens observation that the DRB1*04-DQB1*0301 expressed in the thymic environment during halotype is significantly increased in these the early immune cells’ positive and negative patients with Hashimoto’s thyroiditis, which selection and in induction of self-tolerance.8 The may indicate a common genetic background. Th0 lymphocytes need at least two signals for An association with Grave’s disease is less their proliferation and differentiation into effector common.2,4 Nevertheless, there is some evidence cells: signal 1 is always antigen, and signal 2 is of genetic predisposition, since particular major provided by costimulators that are expressed on histocompability complex (MHC) alleles may antigen-presenting cells (APC). The best-defined contribute to the autoimmunity because they are costimulator for T cells are two related proteins inefficient at displaying self antigens, leading to called B7-1 (CD80) and B7-2 (CD86). These B7 defective negative selection of T cells, or because proteins, which usually come from microbes, are peptide antigens presented by these MHC alleles recognized by a receptor called CD28, which is may fail to stimulate regulatory T cells. There is expressed on virtually all T cells, Signals from increased prevalence of MHC class I-Bw4 and CD28 on T cells binding on APCs work together MHC class II- DRB1*04 (DR4) and its associated with signals generated by binding of T cell allele, DQ*0302 (DQ8) genotype found in receptor (TCR) and coreceptor to peptide-MHC patients with in vivo and in vitro histamine- complexes on the same APCs.5,8 releasing activity.4,5 The CD28-mediated signaling is essential for The mechanisms involved in the regulation initiating the response of Th0 lymphocytes. The T and activation of immune cells in CAU have lymphocytes with receptors for the self antigens not been well investigated. Studies of the are able to recognize the antigens and thus receive pathogenesis of CU indicate that a subpopulation prolonged signals from their antigen receptors, of patients have a cutaneous autoimmune disease but the T cells do not receive strong costimulation associated with antibody to the IgE receptor.6 because there is no accompanying innate immune Whereas atopic allergy is a well-defined T response.5 Under this condition, the TCR may 166 Vol 44 • Number 2 • April 2012 Chronic Autoimmune Urticaria lose their ability to transmit activating signals complement dependence of the reaction, because (aberrant signals).9 IgG1 and IgG3 fix the classical complement The TCR α and β chain from the ligand- pathway.14,15 binding subunit which recognized antigenic peptides bound to MHC complex molecules. The signaling process is provided by γ, δ, and ε polypeptides of the CD3 complex as well as the ζ chain heterodimer and involves two principal signaling pathways.10 The first pathway depends on the stimulation of protein-tyrosine kinase (PTK) activity and involves at least three PTKs, Fyn, Lck, and ζ-chain associated protein kinase, which appear to form a cooperative kinase network. The second pathway, which depends upon the activity of PTKs, involves the induction of inositol phospholipid turnover which leads to 10,11 protein kinase C (PKC) activation. Figure 2. Aberrant regulation of the p21Ras pathway in The signaling on TCR activates serine/ lymphocytes of patients with CIU: possible mechanisms threonine kinase belonging to the mitogen- leading to autoimmune disease. Genetically determined aberrant p21Ras signaling interferes with thymic T-cell activated protein kinase (MAP kinase) or selection (1), leading to a release of self-aggressive T cells extracellular signal-regulated kinase (ERK) (2). Alternatively, exposure to an unknown environmental family. This molecular information is transmitted trigger (3) results in an aberrant signaling in B and T cells (4) and disrupts immune balance. T cell–assisted (5) production as signal from activated PTKs through serine/ of anti-FcεRI autoantibodies (auto Abs) by B cells (6) and a threonine kinases in the cytoplasm to reach direct interaction of autoimmune T cells with mast cells (7) 9 transcription factors in the nucleus. The activation lead to autoimmune chronic urticaria. of TCR will translocate human son-of-seven- less (hSOS) into the inner surface of the plasm membrane and
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