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      The 2016 European Thyroid Association/European Group on Graves' Orbitopathy Guidelines for the Management of Graves' Orbitopathy


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          Graves' orbitopathy (GO) is the main extrathyroidal manifestation of Graves' disease, though severe forms are rare. Management of GO is often suboptimal, largely because available treatments do not target pathogenic mechanisms of the disease. Treatment should rely on a thorough assessment of the activity and severity of GO and its impact on the patient's quality of life. Local measures (artificial tears, ointments and dark glasses) and control of risk factors for progression (smoking and thyroid dysfunction) are recommended for all patients. In mild GO, a watchful strategy is usually sufficient, but a 6-month course of selenium supplementation is effective in improving mild manifestations and preventing progression to more severe forms. High-dose glucocorticoids (GCs), preferably via the intravenous route, are the first line of treatment for moderate-to-severe and active GO. The optimal cumulative dose appears to be 4.5-5 g of methylprednisolone, but higher doses (up to 8 g) can be used for more severe forms. Shared decision-making is recommended for selecting second-line treatments, including a second course of intravenous GCs, oral GCs combined with orbital radiotherapy or cyclosporine, rituximab or watchful waiting. Rehabilitative treatment (orbital decompression surgery, squint surgery or eyelid surgery) is needed in the majority of patients when GO has been conservatively managed and inactivated by immunosuppressive treatment.

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          Most cited references 117

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          Graves' ophthalmopathy.

           S Bahn (2010)
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            Shared decision making: really putting patients at the centre of healthcare

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              Clinical activity score as a guide in the management of patients with Graves' ophthalmopathy.

              Approximately 35% of patients with Graves' ophthalmopathy do not respond to immunosuppressive treatment. A possible explanation for this finding is that only patients with active ophthalmopathy respond to immunosuppressive treatment, whereas patients with fibrotic end stage disease do not. To distinguish between these two groups and to predict the outcome of immunosuppressive treatment, we developed a clinical activity score (CAS) based on four of the five classical signs of inflammation and tested its efficacy in a double-blind, prospective study. The CAS was determined by an opthalmologist before, on the day of, and after the start of either oral prednisone or retrobulbar irradiation in 43 patients with moderate to severe Graves' ophthalmopathy. The therapeutic outcome was determined by a second ophthalmologist unaware of the CAS stores given. Success of treatment was defined as an improvement in NOSPECS class or grade. Responders (22) and non-responders (21) did not differ in age, sex, duration or severity of their Graves' ophthalmopathy. The pretreatment CAS, however, was significantly higher in responders than in non-responders. Twelve of 22 responders and three of 21 non-responders had a CAS > or = 4 (55% vs 14%; P or = 4 had a similar duration of Graves' ophthalmopathy as patients with a CAS < 4. The clinical activity score has a high predictive value for the outcome of immunosuppressive treatment in Graves' ophthalmopathy. Disease activity, and not disease duration, is the prime determinant of therapeutic outcome.

                Author and article information

                European Thyroid Journal
                S. Karger AG
                March 2016
                02 March 2016
                : 5
                : 1
                : 9-26
                aDepartment of Clinical and Experimental Medicine, University of Insubria, Endocrine Unit, Ospedale di Circolo, Varese, Italy; bDepartment of Ophthalmology, Hospital Saint Luc, Catholic University of Louvain, Brussels, Belgium; cOphthalmology Department, Aristotle University of Thessaloniki, Thessaloniki, Greece; dZentrum für Augenheilkunde, Universitätsklinikum Essen, Essen, and eDepartment of Medicine I, Johannes Gutenberg University (JGU) Medical Center, Mainz, Germany; fDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy; gDepartment of Endocrinology, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK; hGraves' Orbitopathy Center, Endocrinology, Fondazione Ca' Granda IRCCS, University of Milan, Milan, Italy; iDepartment of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
                Author notes
                *Prof. Luigi Bartalena, Department of Clinical and Experimental Medicine, University of Insubria, Endocrine Unit, Ospedale di Circolo, Viale Borri 57, IT-21100 Varese (Italy), E-Mail luigi.bartalena@uninsubria.it
                443828 PMC4836120 Eur Thyroid J 2016;5:9-26
                © 2016 European Thyroid Association Published by S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 5, References: 134, Pages: 18


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