About Thyroid Eye Disease

Thyroid Eye Disease (TED) or Graves' orbitopathy is a heterogeneous autoimmune disease with variability in duration and symptom presentation1,2

TED evolves from the progressive phase to the fibrotic phase.1,3-5*

*Content was drawn from: Bhatti MT, Dutton JJ. Thyroid eye disease: therapy in the active phase. J Neuroophthalmol. 2014;34(2):186-197.4

Progressive phase (Active)1,3-5

  • Often characterized by inflammation (including pain, redness, and swelling) and changing symptomatology
  • Fibrotic damage can begin during the progressive phase of TED

Fibrotic phase (Inactive)1,3,4,6-8

  • Stabilization of inflammation and clinical manifestations
  • Irreversible damage may already have occurred
  • Once TED is in the fibrotic phase, surgery may be the only option, and in some cases is unsuccessful

The critical time for intervention is during the progressive phase, before permanent damage may occur.3-5,9,10


The debilitating and vision-threatening consequences of TED11,12:

62-icon 62-icon

of patients with TED experience Proptosis13†

51-icon 51-icon

of patients with TED experience Diplopia14‡

6-to-9-icon 6-to-9-icon

of patients with TED experience Compressive Optic Neuropathy15-17†§

(can be sight-impairing and/or cause blindness)

The impact of TED on psychological health12,18-20:

63 percent 63 percent

of patients with TED experience psychosocial distress caused by a change in appearance19||

52 percent 52 percent

of patients with TED experience loss of self-confidence due to TED20¶

45 percent 45 percent

of patients with TED experience emotional distress such as feeling anxious18#

†Based on an incidence cohort of 120 patients with Graves’ orbitopathy in Olmsted County, Minnesota, who were diagnosed between 1976 and 1990.13,15

‡Based on a cross-sectional follow-up study carried out from 1998 to 2000 of 168 patients with Graves’ orbitopathy who had started radiotherapy and/or prednisone treatment between 1982 and 1992.14

§Based on a retrospective study of 1463 cases seen at the University of British Columbia Orbital Clinic between September 1976 and March 1986.16

||Based on a modified Graves’ Ophthalmopathy Quality of Life (GO-QOL) survey completed by 128 patients with TED.19

¶Based on the responses of 250 patients with TED on a questionnaire about their quality of life, occupational disability, and use of psychotherapy.20

#Based on a prospective and controlled descriptive study of 102 consecutive patients to assess the psychosocial morbidity of TED, using internationally validated self-reporting questionnaires.18


A multidisciplinary team is optimal to co-manage this complex disease7,21

  • TED co-management often includes an endocrinologist working with a subspecialty ophthalmologist who treats TED. This is most commonly an oculoplastic surgeon or neuro-ophthalmologist, but may vary depending on your area 3,21,22
  • Find a co-management partner for your patients with Thyroid Eye Disease

INDICATION AND IMPORTANT SAFETY INFORMATION

IMPORTANT SAFETY INFORMATION

Warnings and Precautions

Infusion Reactions: TEPEZZA may cause infusion reactions. Infusion reactions have been reported in approximately 4% of patients treated with TEPEZZA. Reported infusion reactions have usually been mild or moderate in severity. Signs and symptoms may include transient increases in blood pressure, feeling hot, tachycardia, dyspnea, headache, and muscular pain. Infusion reactions may occur during an infusion or within 1.5 hours after an infusion. In patients who experience an infusion reaction, consideration should be given to premedicating with an antihistamine, antipyretic, or corticosteroid and/or administering all subsequent infusions at a slower infusion rate.

Preexisting Inflammatory Bowel Disease: TEPEZZA may cause an exacerbation of preexisting inflammatory bowel disease (IBD). Monitor patients with IBD for flare of disease. If IBD exacerbation is suspected, consider discontinuation of TEPEZZA.

Hyperglycemia: Increased blood glucose or hyperglycemia may occur in patients treated with TEPEZZA. In clinical trials, 10% of patients (two-thirds of whom had preexisting diabetes or impaired glucose tolerance) experienced hyperglycemia. Hyperglycemic events should be managed with medications for glycemic control, if necessary. Monitor patients for elevated blood glucose and symptoms of hyperglycemia while on treatment with TEPEZZA. Patients with preexisting diabetes should be under appropriate glycemic control before receiving TEPEZZA.

Adverse Reactions

The most common adverse reactions (incidence ≥5% and greater than placebo) are muscle spasm, nausea, alopecia, diarrhea, fatigue, hyperglycemia, hearing impairment, dysgeusia, headache, and dry skin.

INDICATION

TEPEZZA is indicated for the treatment of Thyroid Eye Disease.

Please see Full Prescribing Information for more information.

INDICATION AND IMPORTANT SAFETY INFORMATION

IMPORTANT SAFETY INFORMATION

Warnings and Precautions

Infusion Reactions: TEPEZZA may cause infusion reactions. Infusion reactions have been reported in approximately 4% of patients treated with TEPEZZA. Reported infusion reactions have usually been mild or moderate in severity. Signs and symptoms may include transient increases in blood pressure, feeling hot, tachycardia, dyspnea, headache, and muscular pain. Infusion reactions may occur during an infusion or within 1.5 hours after an infusion. In patients who experience an infusion reaction, consideration should be given to premedicating with an antihistamine, antipyretic, or corticosteroid and/or administering all subsequent infusions at a slower infusion rate.

Preexisting Inflammatory Bowel Disease: TEPEZZA may cause an exacerbation of preexisting inflammatory bowel disease (IBD). Monitor patients with IBD for flare of disease. If IBD exacerbation is suspected, consider discontinuation of TEPEZZA.

Hyperglycemia: Increased blood glucose or hyperglycemia may occur in patients treated with TEPEZZA. In clinical trials, 10% of patients (two-thirds of whom had preexisting diabetes or impaired glucose tolerance) experienced hyperglycemia. Hyperglycemic events should be managed with medications for glycemic control, if necessary. Monitor patients for elevated blood glucose and symptoms of hyperglycemia while on treatment with TEPEZZA. Patients with preexisting diabetes should be under appropriate glycemic control before receiving TEPEZZA.

Adverse Reactions

The most common adverse reactions (incidence ≥5% and greater than placebo) are muscle spasm, nausea, alopecia, diarrhea, fatigue, hyperglycemia, hearing impairment, dysgeusia, headache, and dry skin.

INDICATION

TEPEZZA is indicated for the treatment of Thyroid Eye Disease.

Please see Full Prescribing Information for more information.

REFERENCES:

1. Douglas RS, Kahaly GJ, Patel A, et al. Teprotumumab for the treatment of active thyroid eye disease. N Engl J Med. 2020;382(4):341-352. 2. Bahn RS. Graves’ ophthalmopathy. N Engl J Med. 2010;362(8):726-738. 3. Bothun ED, Scheurer RA, Harrison AR, Lee MS. Update on thyroid eye disease and management. Clin Ophthalmol. 2009;3:543-551. 4. Bhatti MT, Dutton JJ. Thyroid eye disease: therapy in the active phase. J Neuroophthalmol. 2014;34(2):186-197. 5. Smith TJ, Hegedüs L. Graves’ disease. N Engl J Med. 2016;375(16):1552-1565. 6. Dickinson AJ, Hintschich C. Clinical manifestations. In: Wiersinga WM, Kahaly GJ, eds. Graves’ Orbitopathy: A Multidisciplinary Approach—Questions and Answers. 3rd ed. Basel, Switzerland: Karger;2017:1-25. 7. Barrio-Barrio J, Sabater AL, Bonet-Farriol E, Velázquez- Villoria Á, Galofré JC. Graves’ ophthalmopathy: VISA versus EUGOGO classification, assessment, and management. J Ophthalmol. 2015. doi:10.1155/2015/249125. 8. Rootman DB, Golan S, Pavlovich P, Rootman J. Postoperative changes in strabismus, ductions, exophthalmometry, and eyelid retraction after orbital decompression for thyroid orbitopathy. Ophthalmic Plast Reconstr Surg. 2017;33(4):289-293. 9. Huang Y, Fang S, Li D, Zhou H, Li B, Fan X. The involvement of T cell pathogenesis in thyroid-associated ophthalmopathy. Eye (Lond). 2019;33(2):176-182. 10. Naik MN, Nair AG, Gupta A, Kamal S. Minimally invasive surgery for thyroid eye disease. Indian J Ophthalmol. 2015;63(11):847-853. 11. Shan SJ, Douglas RS. The pathophysiology of thyroid eye disease. J Neuroophthalmol. 2014;34(2):177-185. 12. Ponto KA, Merkesdal S, Hommel G, Pitz S, Pfeiffer N, Kahaly GJ. Public health relevance of Graves’ orbitopathy. J Clin Endocrinol Metab. 2013;98(1):145-152. 13. Bartley GB, Fatourechi V, Kadrmas EF, et al. Clinical features of Graves’ ophthalmopathy in an incidence cohort. Am J Ophthalmol. 1996;121(3):284-290. 14. Terwee C, Wakelkamp I, Tan S, Dekker F, Prummel MF, Wiersinga W. Long-term effects of Graves’ ophthalmopathy on health-related quality of life. Eur J Endocrinol. 2002;146(6):751-757. 15. Bartley GB. The epidemiologic characteristics and clinical course of ophthalmopathy associated with autoimmune thyroid disease in Olmsted County, Minnesota. Trans Am Ophthalmol Soc. 1994;92(1):477-588. 16. Neigel JM, Rootman J, Belkin RI, et al. Dysthyroid optic neuropathy. The crowded orbital apex syndrome. Ophthalmology. 1988;95(11):1515-1521. 17. McAlinden C. An overview of thyroid disease. Eye Vis (Lond). 2014;1:9. doi:10.1186/s40662-014-0009-8. 18. Kahaly GJ, Petrak F, Hardt J, Pitz S, Egle UT. Psychosocial morbidity of Graves’ orbitopathy. Clin Endocrinol (Oxf). 2005;63(4):395-402. 19. 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(1):75-78. 20. 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(17):283-289. 21. Stan MN, Garrity JA, Bahn RS. The evaluation and treatment of Graves ophthalmopathy. Med Clin North Am. 2012;96(2):311-328. 22. Bartalena L, Tanda ML. Graves’ ophthalmopathy. N Engl J Med. 2009;360(10):994-1001.