New evidence concerning the pathomechanism and treatment of thyroid associated orbitopathy
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ArticleID
: 194
ArticleDOI
: 10.1186/1756-6614-8-S1-A6
ArticleCitationID
: A6
ArticleSequenceNumber
: 6
ArticleCategory
: Meeting abstract
ArticleFirstPage
: 1
ArticleLastPage
: 2
ArticleHistory
:
ArticleCopyright
Daroszewski; licensee BioMed Central Ltd.2015 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits : unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
RegistrationDate OnlineDate
: 2015–6–22 : 2015–6–22
Aff1
Department of Endocrinology, Diabetes and Isotope Therapy, Wroclaw Medical University, Poland Spring School of Thyroidology organized by the Polish Thyroid Association 2014: abstracts of invited lectures Spring School of Thyroidology organized by the Polish Thyroid Association 2014 Miedzyzdroje, Poland 23-24 May 2014 Publication of this supplement was funded by the Polish Thyroid Association. The Supplement Editors declare that they have no competing interests. Meeting abstracts Andrzej Lewinski Mariusz Stasiolek
Thyroid associated orbitopathy (TAO) is an immune-mediated inflammatory disorder that causes expansion of the orbital adipose tissue and muscles and deposition of glycosaminoglycans and collagen. No specific therapy has been established, and treatment still relies on high-dose I.V. glucocorticoids in the acute inflammatory phase of the disease and surgical procedures in a burnt-out state. However, the results of the medical treatment are unsatisfactory, since up to 20% of patients are unresponsive and another 20% experience disease relapses after therapy withdrawal. Therefore, as in other autoimmune diseases, new therapeutic options based on biological treatment are under experimental and clinical investigation. The efficacy of rituximab (RTX), has been reported since 2006. This humanized chimeric anti-CD-20 antibody blocks the activation and differentiation of B cells, since CD-20 protein is expressed on the surface of pre-B and mature B lymphocytes, but not on stem cells, pro-B lymphocytes and plasma cells. Therefore, treatment with RTX leads to specific elimination of B cells without affecting their regeneration or production of immunoglobulins by plasma cells. Preliminary studies in patients with TAO indicate that blocking of CD-20 significantly and positively affected the clinical course of disease by rapid reduction of inflammation and degree of proptosis. The number of CD-20+ cells was lower in orbital tissues than in periphery. RTX given locally as retrobulbar injections in patients resistant to glucocorticoid therapy resulted in a significant amelioration of the clinical symptoms. No side effects of that procedure were observed. The outcome of the first
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