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Graves' Orbitopathy


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Swelling of tissues within the inextensible bony orbital cavity leads to an increase in intraorbital pressure. This has mechanical consequences which account for most of the signs and symptoms of GO.

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      Early Inflammatory Changes

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      De novo Adipogenesis

      Increased Production of Glycosaminoglycans

      Lid retraction, the most common ocular sign, may result from excessive sympathetic activity within Müller’s muscle as well as retraction of the levator muscle.

      Additional manifestations may worsen the clinical presentation:

      •Excessive exposure of the cornea due to lid retraction and/or proptosis, especially in cases of lidlag, may lead to keratitis and, if not treated properly, to a cornea ulcer or even perforation. There is a risk of a central cornea ulcer when the Charles Bell phenomenon is impaired due to restriction of the upper duction.

      •Impairments in vision may result from optic neuropathy. However, an impression of visual impairment may have many other causes: keratitis, photophobia, orbital pain, excessive tearing, mild diplopia and severe lid oedema, which should be recognised as such. Dysthyroid optic neuropathy usually results from the compression of the optic nerve by the enlarged posterior segment of the rectus muscles at the orbital apex. Coronal imaging demonstrates the apical crowding resulting from muscle enlargement and the loss of the perinerve lining. In these cases, surgical decompression or glucocorticoids usually lead to visual recovery. Dysthyroid optic neuropathy may also result from stretching the optic nerve or ischaemia, a mechanism which is difficult to demonstrate.

      So far, what really triggers GO – and indeed Graves’ hyperthyroidism (GH) itself – is unknown.

      Minimal symptoms/signs of GO are very common in GH as suggested by the presence of mild symptoms upon meticulous clinical examination and orbit imaging as well as the exaggerated increase in intraocular pressure in the upper gaze. However, full-blown GO is present in only 25–50% of the patients with GH.

      Therefore, there are two questions:

      1.What triggers GO?

      2.Why is GO more prominent or severe in some patients than in others?

      GO onset is not related to hyperthyroidism per se as it can precede,