gms | German Medical Science

27th International Congress of German Ophthalmic Surgeons

15. to 17.05.2014, Nürnberg

Key note lecture: Graves orbitopathy, the local disease and treatment

Meeting Abstract

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  • Haraldur Sigurdsson - Landspitali University, Hospital, Reykiavik, Island

27. Internationaler Kongress der Deutschen Ophthalmochirurgen. Nürnberg, 15.-17.05.2014. Düsseldorf: German Medical Science GMS Publishing House; 2014. DocH 4.4

doi: 10.3205/14doc016, urn:nbn:de:0183-14doc0160

Published: May 5, 2014

© 2014 Sigurdsson.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Outline

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There are many elements of Graves’s disease that we understand and can therefore treat, but in spite of research and cooperation between scientists, there are still a lot of things we don’t understand. We tend to agree on that there is a cross reactivity between thyroid and orbital antigens, with formation of autoantibody that mimics the action of TSH, that triggers the Thyroid Eye Disease (TED).The immune mechanism in the orbit appears mainly to be orchestrated by resident immune cells. Also TED is a self-limiting disease lasting approximately 2 years or so, because the orbit does not have the lymphoid tissue for lymphoid neogenesis. An important question is therefore are we dealing with a systemic disease or a local orbital disease? If it is a local disease what do we know about the fat and the muscles in the orbit? The orbital fat is most volumes in the orbit and this is the tissue we remove or displace with surgery in TED patients. We know the adipocytes in the orbit are of different size and also that the adipocytes of the orbital fat are different from subcutaneous and omentum fat, also being biologically different. The fat of TED patients have been compared to normal controls and found to be different. We know that the fat seems to play a much bigger role in TED in children compared to adults. Autoantibodies of the muscles of the orbit have been described but none found to be very specific. The reason why medial and inferior rectus is more often affected is still foggy. The immunology of TED is complex. It was thought that T cell would infiltrate the orbit, activate fibroblasts, which would then activate genes that regulate or dysregulate adipocytes and myofibroblasts. Rituximab which affects the B cells helps TED patients; the immunology process is obviously more complex than we thought. And if we are dealing with a local disease in the orbit, why are we not keener to use local treatment, like intraorbital steroids? It is well documented what the distribution of steroids injected into orbits of animals is like. No good comparative studies how to use intraorbital steroids in TED have been done in humans but clinical papers have showed promising results. The use of local biologic drugs have not been described.