Thyroid eye disease (TED) is a serious, progressive, and debilitating autoimmune disease with
only a limited window of activity, lasting up to 3 years, after which damage can be irreversible.1,2

A unique challenge: TED is a distinct disease that threatens vision 

TED, also called Graves’ orbitopathy, is a rare autoimmune disease most often seen in patients with Graves’ disease, but is distinct from Graves’ itself.1,2 A diagnosis of TED may even precede a finding of Graves’ and can serve as an early warning sign of impending thyroid dysfunction.2 Importantly, TED can also occur in Hashimoto’s hypothyroidism or even in euthyroid patients, so hyperthyroidism shouldn't be considered a defining risk factor.1

Because TED is a separate pathology from Graves’ disease, interventions aimed at reducing hyperthyroidism do not modify the course of TED.2 In fact, no currently available therapies are disease modifiers of TED. Accordingly, TED should be assessed, monitored, and managed as its own pathology.

TED progression includes inflammation, fibrosis, and fat proliferation in and around the orbit, creating long-term damage.1 The consequences can include irreversible disfigurement and can permanently impair vision.

Leading risk factors

Environment

Smoking increases
risk of disease and
exacerbates progression2

Age

Increasing age3,4

Gender

Women: Disease is more frequent1
Men: Disease tends to be more severe5

Thyroid dysfunction treatment

Radioactive iodine2

Annual incidence1

Men Men

3 out of 100,000 men

Women Women

16 out of 100,000 women

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References:
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  2. Mamoojee Y, Pearce SHS. Natural History. In: Wiersinga WM, Kahaly GJ (eds): Graves’ Orbitopathy: A Multidisciplinary Approach – Questions and Answers. Basel, Karger. 2017:93-104.
  3. Bartley GB. The epidemiological characteristics and clinical course of ophthalmopathy associated with autoimmune thyroid disease in Olmsted County, Minnesota. Tr Am Ophth Soc. 1994;92:477-588.
  4. Laurberg P, Berman DC, Pedersen IB, Andersen S, Carlé A. J Clin Endocrinol Metab. 2012;92(7):2325-2332.
  5. Perros P, Crombie AL, Matthews JN, Kendall-Taylor P. Age and gender influence the severity of thyroid-associated ophthalmopathy: a study of 101 patients attending a combined thyroid-eye clinic. Clin Endocrinol (Oxf). 1993;38(4):367-372.
  6. Tsui S, Naik V, Hoa N, et al. Evidence for an association between thyroid-stimulating hormone and insulin-like growth factor 1 receptors: a tale of two antigens implicated in Graves’ disease. J Immunol. 2008;181:4397-4405.
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  8. Kilicarsan R, Alkan A, Ilhan MM, et al. Graves’ ophthalmopathy: the role of diffusion-weighted imaging in detecting involvement of extraocular muscles in early period of disease. Br J Radiol. 2015;88(1047):20140677.
  9. Smith TJ, Hegedüs L. Graves’ disease. N Engl J Med. 2016;375:1552-1665.
  10. Villadolid MC, Yokoyama N, Isumi M, et al. Untreated Graves’ disease patients without clinical ophthalmopathy demonstrate a high frequency of extraocular muscle (EOM) enlargement by magnetic resonance. J Clin Endocrinol Metab. 1995;80(9):2830-2833.
  11. Rootman DB, Golan S, Pavlovich P, Rootman J. Postoperative changes in strabismus, ductions, exophthalmometry, and eyelid retraction after orbital decompression for thyroid orbitopathy. Ophthal Plast Reconstr Surg. 2017;33:289-293.
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  18. Mitchell AL, Goss L, Mathiopoulou L, et al. Diagnosis of Graves' orbitopathy (DiaGO): Results of a pilot study to assess the utility of an office tool for practicing endocrinologists. J Clin Endocrinol Metab. 2015;100(3):E458-E462.
  19. Ponto KA, Pitz S, Pfeiffer N, Hommel G, Weber MM, Kahaly GJ. Quality of life and occupational disability in endocrine orbitopathy. Dtsch Arztebl Int. 2009;106:283-299.
  20. Park JJ, Sullivan TJ, Mortimer RH, Wagenaar M, Perry-Keene DA. Assessing quality of life in Australian patients with Graves' ophthalmopathy. Br J Ophthalmol. 2004;88:75-78.
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