Thyroid Eye Disease

Table of Contents

  1. Overview
  2. Epidemiology
  3. Pathophysiology
  4. Risk Factors
  5. Clinical Presentation
  6. Dysthyroid Optic Neuropathy
  7. Diagnosis
  8. Treatment — Active Phase
  9. Treatment — Surgical Rehabilitation
  10. Complications
  11. Prognosis
  12. Prevention and Risk Reduction
  13. Recent Research
  14. Key Research Papers
  15. Connections
  16. Featured Videos

1. Overview

Thyroid Eye Disease (TED), also called Graves' orbitopathy or Graves' ophthalmopathy, is an autoimmune inflammatory condition of the orbit that most commonly accompanies Graves' hyperthyroidism. Stimulating autoantibodies against the TSH receptor (TRAb) cross-react with orbital fibroblasts, triggering a cascade of glycosaminoglycan (GAG) accumulation and adipogenesis that expands orbital volume beyond what the rigid bony walls can accommodate. The resulting proptosis, restrictive myopathy of the extraocular muscles, and exposure of the ocular surface cause the hallmark signs of TED: bulging eyes, eyelid retraction, diplopia, and — in its most severe form — compressive optic neuropathy that threatens permanent vision loss.

TED follows a biphasic course. The active inflammatory phase lasts 6 months to 2 years, during which orbital inflammation, edema, and tissue expansion are ongoing and potentially reversible with immunosuppressive treatment. It is followed by the chronic fibrotic phase, in which inflammation has resolved but structural damage — proptosis, muscle fibrosis, eyelid retraction — persists and requires surgical correction. The European Group on Graves' Orbitopathy (EUGOGO) severity classification (mild / moderate-to-severe / sight-threatening) and the Clinical Activity Score (CAS) are used to guide treatment decisions. A 2020 meta-analysis of 57 studies (26,804 patients) found a pooled TED prevalence of 40% among people with Graves' disease, ranging from 27% in North American studies to 58% in studies from Oceania (PubMed PMID: 32691849).

2. Epidemiology

TED is widely described as the most common cause of proptosis in adults. A population-based study of Olmsted County, Minnesota (1976–1990) found an age-adjusted annual incidence of 16.0 per 100,000 women and 2.9 per 100,000 men, reflecting the strong female predominance of the underlying autoimmune thyroid disease. Incidence peaked at ages 40–44 and 60–64 in women and at 45–49 and 65–69 in men (PubMed PMID: 7573310), though TED can occur at any age including childhood.

In the same Olmsted County cohort of 120 patients, 90% had Graves' hyperthyroidism, 3% had Hashimoto's thyroiditis, 1% had primary hypothyroidism and 6% were euthyroid (PubMed PMID: 8597271); in the euthyroid group orbital autoimmunity proceeds without clinically apparent thyroid dysfunction. Epidemiological studies consistently identify smoking as the strongest modifiable environmental risk factor: in a 1993 case-control study smoking was associated with an odds ratio of 7.7 for Graves' ophthalmopathy (versus 1.9 for Graves' hyperthyroidism without eye disease), and smokers had more severe eye disease (PubMed PMID: 8419666). The 2020 meta-analysis found a higher pooled prevalence of TED in study regions with predominantly Asian populations (45%) than in predominantly Caucasian ones (37%) (PubMed PMID: 32691849).

3. Pathophysiology

The central event in TED pathogenesis is activation of orbital fibroblasts by autoantibodies directed against a shared antigen on both thyroid follicular cells and orbital fibroblasts. The TSH receptor (TSHR) and the IGF-1 receptor (IGF-1R) co-immunoprecipitate on the surface of orbital fibroblasts, forming a functional signaling complex. TRAb and IGF-1R-stimulating antibodies act in concert to activate this complex, triggering downstream signaling via PI3K/Akt and Erk/MAPK pathways.

GAG Accumulation and Adipogenesis

Activated fibroblasts respond by synthesizing and secreting vast quantities of hyaluronate and other glycosaminoglycans. These highly hydrophilic molecules trap water within the orbital soft tissues, creating the edema, chemosis, and conjunctival injection characteristic of active TED. Simultaneously, a subpopulation of orbital fibroblasts — CD34-positive fibrocytes that traffic from bone marrow into the orbit via the bloodstream — differentiate into adipocytes under the influence of peroxisome proliferator-activated receptor gamma (PPAR-γ) signaling. This fat expansion compounds the volumetric increase caused by GAG accumulation, and together these processes generate enough pressure to push the globe forward (proptosis) and compress the optic nerve at the orbital apex.

Inflammatory Phases and Cytokine Profile

Studies of orbital tissue describe a sequence in which, during the active inflammatory phase, the orbital milieu is dominated by T-helper 1 cytokines — interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) — which promote fibroblast activation, GAG synthesis, and recruitment of inflammatory mononuclear cells. As the disease transitions into the fibrotic phase, the cytokine environment shifts toward a T-helper 2 profile dominated by IL-4 and IL-10, which drive collagen deposition and fibrosis within the extraocular muscles and orbital fat, locking in structural changes. This proposed cytokine shift is one explanation offered for why immunosuppressive treatments work best early in the active phase and much less once fibrosis is established.

4. Risk Factors

5. Clinical Presentation

TED has a characteristic constellation of orbital signs measurable at the bedside. The severity of each sign is captured by the VISA classification (Vision / Inflammation / Strabismus / Appearance) and by the internationally validated Clinical Activity Score (CAS).

Proptosis (Exophthalmos)

Forward displacement of the globe is measured by Hertel exophthalmometry. Values exceeding 21 mm (in Caucasian populations) or asymmetry greater than 2 mm between eyes are considered clinically significant, though population norms vary by race. Proptosis stretches the optic nerve and increases exposure of the ocular surface. Severe proptosis may prevent complete eyelid closure (lagophthalmos), risking corneal exposure keratopathy.

Eyelid Signs

Upper eyelid retraction — the most common TED sign, present at some point in 90% of patients in a population-based cohort (PubMed PMID: 8597271) — occurs because sympathetic over-stimulation of Muller's muscle (from hyperthyroidism) and inflammatory tethering of the levator muscle both pull the upper lid abnormally upward, exposing the sclera above the limbus (Dalrymple sign). Lid lag (von Graefe sign) — failure of the upper lid to descend smoothly as the eye looks downward — results from the same levator fibrosis. Periorbital and eyelid edema is also common in active disease.

Restrictive Myopathy and Diplopia

Inflammatory infiltration and subsequent fibrosis of the extraocular muscles create a restrictive pattern of strabismus. The inferior rectus is most commonly and most severely affected, restricting upgaze and producing vertical diplopia. The medial rectus is the second most commonly involved muscle, restricting abduction. Importantly, the muscle tendons are characteristically spared in TED (unlike idiopathic orbital myositis where tendons are involved), and CT imaging demonstrating fusiform muscle belly enlargement with tendon sparing is highly characteristic of TED.

Clinical Activity Score (CAS)

The 7-item CAS assigns one point each to: spontaneous retrobulbar pain; pain on eye movement; eyelid erythema; conjunctival injection; chemosis; swelling of the caruncle or plica; and eyelid edema. A CAS of 3 or more out of 7 is the threshold commonly used to classify disease as active. Mourits and colleagues introduced the activity score in 1989 (in its original form ranging from 0 to 10 points over two consecutive examinations); in that retrospective study, patients with a score of 3 or more at the start of therapy responded well to anti-inflammatory drugs, while those with a lower score mostly did not (PubMed PMID: 2765444). In their 1997 prospective study of 43 patients, a CAS of 4 or more predicted response to oral prednisone or retrobulbar irradiation with 86% specificity and 55% sensitivity (PubMed PMID: 9302365). The CAS remains the most widely used clinical activity tool in TED.

6. Dysthyroid Optic Neuropathy

Dysthyroid optic neuropathy (DON) is the most vision-threatening complication of TED; optic nerve dysfunction occurred in 6% of patients in the Olmsted County cohort (PubMed PMID: 8597271). It arises from compression of the optic nerve at the orbital apex, where the rigid bony canal and crowding of enlarged extraocular muscles leave no room for the nerve to escape increasing orbital pressure. DON can occur without marked proptosis, so the absence of proptosis does not exclude it.

Clinical Signs of DON

Management of DON

DON is treated as an ophthalmological emergency. The 2021 EUGOGO guideline describes treatment of sight-threatening disease with several high single doses of intravenous methylprednisolone per week and, if the disease does not respond, urgent orbital decompression surgery (PubMed PMID: 34297684). CT or MRI imaging demonstrating orbital apex crowding — with the optic nerve compressed between enlarged rectus muscles — supports the diagnosis and guides surgical planning.

7. Diagnosis

TED is primarily a clinical diagnosis, but laboratory testing and imaging are essential to confirm thyroid autoimmunity, assess disease activity, and plan treatment.

Clinical Examination

Laboratory Testing

TSH receptor antibodies (TRAb) are the single most diagnostically valuable laboratory test in TED. Third-generation competitive binding immunoassays and functional thyroid-stimulating immunoglobulin (TSI) assays have high sensitivity and specificity for Graves' disease and TED. Serial TRAb measurements track disease activity and predict prognosis — falling levels correlate with disease stabilization, while persistently elevated or rising levels predict continued orbital activity. Thyroid function tests (TSH, free T4, free T3) are essential for identifying and correcting thyroid dysfunction that worsens orbital disease.

Orbital Imaging

CT of the orbits (axial and coronal planes, without contrast for bony anatomy; with contrast to assess muscle enhancement in active disease) is the workhorse imaging modality for TED. The hallmark finding is fusiform enlargement of one or more extraocular muscle bellies with characteristic tendon sparing — a critical distinguishing feature from idiopathic orbital myositis, where tendon involvement is the rule. The inferior rectus and medial rectus are most commonly enlarged. CT also defines orbital apex anatomy, which is essential for planning decompression surgery. MRI of the orbits, with fat-suppressed T2-weighted sequences, detects active muscle edema and inflammatory signal in patients for whom radiation exposure is a particular concern (young patients, pregnant patients).

8. Treatment — Active Phase

Treatment during the active inflammatory phase aims to suppress orbital inflammation and prevent progression to irreversible fibrosis. The choice of treatment is guided by EUGOGO severity classification and CAS.

Intravenous Methylprednisolone (IVMP)

High-dose intravenous corticosteroids are the long-standing first-line treatment for moderate-to-severe active TED. The 2021 EUGOGO guideline recommends intravenous methylprednisolone combined with mycophenolate as first-line treatment, describes a cumulative 4.5 g of intravenous methylprednisolone in 12 weekly infusions as the optimal regimen, and allows higher cumulative doses not exceeding 8 g as monotherapy in the most severe cases (PubMed PMID: 34297684). In a 2005 randomized trial of 70 patients with active severe disease, weekly intravenous methylprednisolone (0.5 g, then 0.25 g, 6 weeks each) produced a treatment response at 3 months in 77% versus 51% with oral prednisolone, and was better tolerated (PubMed PMID: 15998777). Intravenous pulses have been associated with acute liver damage: in a cohort of 1,076 patients it occurred in 14 (1.3%), one of whom died, and risk rose with age and cumulative dose (PubMed PMID: 26090805); liver function tests are therefore monitored during the course. Contraindications include active hepatitis, uncontrolled diabetes, and recent severe cardiovascular events.

Teprotumumab

Teprotumumab, a fully human monoclonal antibody inhibitor of the IGF-1 receptor, was approved in the USA on 21 January 2020 (PubMed PMID: 33865501); the OPTIC report notes that no FDA-approved medical therapy for TED existed before it. The pivotal OPTIC trial randomized 83 patients with active TED (41 teprotumumab, 42 placebo) to infusions of teprotumumab (10 mg/kg first dose, 20 mg/kg thereafter) or placebo every 3 weeks for 21 weeks. The primary endpoint — a proptosis response (reduction of ≥2 mm) at week 24 — was achieved in 83% of teprotumumab patients versus 10% of placebo patients. Mean proptosis change was −2.82 mm with teprotumumab versus −0.54 mm with placebo, and all secondary outcomes were significantly better, including an overall response (CAS reduction of ≥2 points plus proptosis reduction of ≥2 mm) in 78% versus 7% and a diplopia response in 68% versus 29% (PubMed PMID: 31971679). In a pooled analysis of the two randomized trials (171 patients), the proptosis response was maintained 51 weeks after the final dose in 38 of 57 patients (67%) with follow-up data; muscle spasm (18%), hearing loss (10%) and hyperglycaemia (8%) were the adverse events with the greatest risk difference from placebo (PubMed PMID: 33865501). The hearing effects have been proposed to relate to IGF-1R inhibition in the cochlea. The 2021 EUGOGO guideline lists teprotumumab among second-line treatments, citing cost, availability and long-term effectiveness among the factors it weighed (PubMed PMID: 34297684).

Selenium Supplementation

For mild active TED, the 2021 EUGOGO guideline states that control of risk factors, local treatments and selenium (in selenium-deficient areas) are usually sufficient (PubMed PMID: 34297684). This rests largely on a 2011 randomized, double-blind trial of 159 patients with mild disease: selenium (100 μg twice daily for 6 months), but not pentoxifylline, improved quality of life, reduced eye involvement and slowed progression compared with placebo, and the Clinical Activity Score fell more with selenium; exploratory 12-month results were similar (PubMed PMID: 21591944). The proposed mechanism involves selenium's role as a cofactor in antioxidant selenoproteins (glutathione peroxidase, thioredoxin reductase) that counteract oxidative stress generated by infiltrating inflammatory cells in the orbit. No adverse events were evident with selenium in that trial, whereas pentoxifylline frequently caused gastrointestinal problems; the guideline limits its statement on selenium to selenium-deficient areas.

Orbital Radiation Therapy

External beam orbital irradiation (20 Gy delivered in 10 fractions over 2 weeks, targeting the retro-orbital soft tissues) reduces orbital fibroblast and lymphocyte activity through direct cytotoxic and anti-inflammatory effects. In a 1993 double-blind trial of 56 patients with moderately severe disease, retrobulbar irradiation (20 Gy) and a 3-month course of oral prednisone were similarly effective (13 and 14 responders), with side effects more frequent and severe during prednisone (PubMed PMID: 8105213). The 2021 EUGOGO guideline lists orbital radiotherapy combined with oral or intravenous glucocorticoids as a second-line option (PubMed PMID: 34297684). Orbital radiation carries a small risk of radiation retinopathy or cataract formation (especially in patients with diabetic retinopathy, for whom it is relatively contraindicated) and is generally not used in patients under 35 because of a theoretical risk of radiation-induced malignancy.

9. Treatment — Surgical Rehabilitation

Surgical correction of the structural consequences of TED is performed during the inactive fibrotic phase, after CAS has fallen below 3 and the disease has been stable for several months; the 2021 EUGOGO guideline lists orbital decompression, squint and eyelid surgery as rehabilitative surgery for inactive residual disease (PubMed PMID: 34297684). The cardinal rule of TED surgical rehabilitation is adherence to a strict sequential order: performing surgery out of sequence leads to suboptimal results and may require reoperation.

Sequence of Operations

  1. Step 1 — Orbital decompression: Removal of orbital bone walls (most commonly the medial wall and/or orbital floor, with fat decompression in combined procedures) increases the volume available for orbital contents, reducing intraorbital pressure and allowing the proptotic globe to recede. Decompression is also the definitive treatment for DON when corticosteroids have failed. Decompression predictably alters the strabismus pattern (by shifting extraocular muscle positions), so strabismus surgery is done after decompression.
  2. Step 2 — Strabismus surgery: Adjustable suture recession of the fibrosed inferior rectus muscle is the most common procedure, performed to restore single binocular vision in primary and reading gaze. Strabismus surgery follows decompression because decompression shifts the orbital anatomy and changes the muscle alignment. Adjustable sutures allow fine-tuning of alignment in the early postoperative period while the patient is awake, compensating for the difficulty of predicting the final alignment after operating on fibrotic muscles.
  3. Step 3 — Eyelid surgery: Upper eyelid retraction is corrected by recession of the levator muscle and/or Muller's muscle. Lower eyelid procedures address retraction and scleral show. Eyelid surgery comes last because both decompression and strabismus surgery alter eyelid position, and operating on the lids before these upstream corrections leads to under- or over-correction of lid retraction.

10. Complications

11. Prognosis

The natural history of TED follows the "Rundle curve" — a period of progressive worsening during the active inflammatory phase lasting 6 months to 2 years, followed by a plateau, and then a partial spontaneous improvement to a new stable baseline. In a 1995 study of 59 patients who received no immunosuppressive or surgical treatment for their eye disease, followed for a median of 12 months, 22% improved substantially, 42.4% improved slightly, 22% did not change and 13.5% deteriorated to the point that immunosuppressive treatment was considered necessary (PubMed PMID: 7889631). Moderate-to-severe disease often leaves residual structural changes that are corrected surgically.

In the OPTIC trial, teprotumumab improved proptosis, diplopia and quality of life compared with placebo (PubMed PMID: 31971679), and pooled long-term data show that the proptosis response was maintained 51 weeks after treatment in 67% of patients with follow-up (PubMed PMID: 33865501). A minority of patients develop sight-threatening disease; risk factors listed in the 2021 EUGOGO guideline include smoking, thyroid dysfunction, high serum TRAb levels, radioiodine treatment and hypercholesterolaemia (PubMed PMID: 34297684). Visual outcome after DON is generally described as better when decompression is not delayed.

12. Prevention and Risk Reduction

13. Recent Research

Teprotumumab (OPTIC trial and extensions): The OPTIC randomized controlled trial found a proptosis response in 83% of patients with teprotumumab versus 10% with placebo (PubMed PMID: 31971679). The trial compared teprotumumab with placebo, not with intravenous corticosteroids. A pooled analysis of the two randomized trials found proptosis and diplopia responses maintained in most responders 51 weeks after the final dose, and reported that studies of retreatment for non-responders and for patients who flare after a response were ongoing (PubMed PMID: 33865501).

Tocilizumab (IL-6 receptor inhibition) for steroid-refractory TED: Interleukin-6 is a pleiotropic proinflammatory cytokine that plays a key role in T-cell and B-cell activation and drives orbital fibroblast hyaluronate synthesis. Tocilizumab is a humanized monoclonal antibody blocking the IL-6 receptor. A 2014 prospective nonrandomized study by Pérez-Moreiras and colleagues of 18 patients resistant to intravenous steroids reported a mean CAS reduction of 5.89 points and proptosis reduction in 13 patients (PubMed PMID: 24503568). Their 2018 double-masked randomized trial of 32 patients with steroid-resistant moderate-to-severe disease found a CAS improvement of at least 2 points at week 16 in 93.3% with tocilizumab versus 58.8% with placebo, and an exophthalmos change of −1.5 mm versus 0.0 mm; the authors called for further studies (PubMed PMID: 30081019). The 2021 EUGOGO guideline lists tocilizumab among second-line options (PubMed PMID: 34297684).

Rituximab versus IV methylprednisolone: Rituximab (anti-CD20 B-cell depletion therapy) has been evaluated as an alternative to IVMP in active moderate-to-severe TED, based on the rationale that depleting autoreactive B cells should reduce TRAb production and orbital autoimmune activity. The randomized controlled trial by Salvi and colleagues (32 patients) compared rituximab directly with IVMP: CAS fell more after rituximab at weeks 16–24, all rituximab patients had improved at 24 weeks versus 69% after IVMP, disease reactivation occurred only after IVMP (five patients), and fewer rehabilitative operations followed rituximab (PubMed PMID: 25494967). A placebo-controlled trial published at the same time (25 patients) found no benefit of rituximab over placebo and more moderate or severe adverse events with rituximab (PubMed PMID: 25343233). The 2021 EUGOGO guideline lists rituximab among second-line options (PubMed PMID: 34297684).

Teprotumumab mechanism and IGF-1R biology: A 2019 perspective by Patel, Yang and Douglas summarizes evidence that IGF-1R is overexpressed in TED and acts as an autoantigen, and that in laboratory studies IGF-1R inhibition reduces cytokine and hyaluronan production and fibroblast differentiation — the rationale for blocking IGF-1R with teprotumumab (PubMed PMID: 31377284).

Key Research Papers

  1. Douglas RS, Kahaly GJ, Patel A, et al. (2020). Teprotumumab for the treatment of active thyroid eye disease (OPTIC trial). N Engl J Med. 382(4):341–352. — PubMed PMID: 31971679
  2. Kahaly GJ, Douglas RS, Holt RJ, Sile S, Smith TJ (2021). Teprotumumab for patients with active thyroid eye disease: a pooled data analysis, subgroup analyses, and off-treatment follow-up results from two randomised, double-masked, placebo-controlled, multicentre trials. Lancet Diabetes Endocrinol. 9(6):360–372. — PubMed PMID: 33865501
  3. Marcocci C, Kahaly GJ, Krassas GE, et al. (2011). Selenium and the course of mild Graves' orbitopathy (EUGOGO multicenter RCT). N Engl J Med. 364(20):1920–1931. — PubMed PMID: 21591944
  4. Bartalena L, Marcocci C, Bogazzi F, et al. (1998). Relation between therapy for hyperthyroidism and the course of Graves' ophthalmopathy. N Engl J Med. 338(2):73–78. — PubMed PMID: 9420337
  5. Mourits MP, Koornneef L, Wiersinga WM, et al. (1989). Clinical criteria for the assessment of disease activity in Graves' ophthalmopathy: a novel approach. Br J Ophthalmol. 73(8):639–644. — PubMed PMID: 2765444
  6. Bartalena L, Baldeschi L, Dickinson AJ, et al. (2008). Consensus statement of the European Group on Graves' Orbitopathy (EUGOGO) on management of Graves' orbitopathy. Thyroid. 18(3):333–346. — PubMed PMID: 18341379
  7. Bahn RS (2010). Graves' ophthalmopathy. N Engl J Med. 362(8):726–738. — PubMed PMID: 20181974
  8. Salvi M, Vannucchi G, Currò N, et al. (2015). Efficacy of B-cell targeted therapy with rituximab in patients with active moderate to severe Graves' orbitopathy: a randomized controlled study. J Clin Endocrinol Metab. 100(2):422–431. — PubMed PMID: 25494967
  9. Pérez-Moreiras JV, Alvarez-López A, Gómez EC (2014). Treatment of active corticosteroid-resistant Graves' orbitopathy. Ophthalmic Plast Reconstr Surg. 30(2):162–167. — PubMed PMID: 24503568
  10. Patel A, Yang H, Douglas RS (2019). A new era in the treatment of thyroid eye disease. Am J Ophthalmol. 208:281–288. — PubMed PMID: 31377284
  11. Prummel MF, Mourits MP, Blank L, et al. (1993). Randomized double-blind trial of prednisone versus radiotherapy in Graves' ophthalmopathy. Lancet. 342(8877):949–954. — PubMed PMID: 8105213
  12. Dickinson AJ, Perros P (2001). Controversies in the clinical evaluation of active thyroid-associated orbitopathy: use of a detailed protocol with comparative photographs for objective assessment. Clin Endocrinol (Oxf). 55(3):283–303. — PubMed PMID: 11589671
  13. Bartalena L, Kahaly GJ, Baldeschi L, et al. (2021). The 2021 European Group on Graves' orbitopathy (EUGOGO) clinical practice guidelines for the medical management of Graves' orbitopathy. Eur J Endocrinol. 185(4):G43–G67. — PubMed PMID: 34297684
  14. Kahaly GJ, Pitz S, Hommel G, Dittmar M (2005). Randomized, single blind trial of intravenous versus oral steroid monotherapy in Graves' orbitopathy. J Clin Endocrinol Metab. 90(9):5234–5240. — PubMed PMID: 15998777
  15. Sisti E, Coco B, Menconi F, et al. (2015). Age and dose are major risk factors for liver damage associated with intravenous glucocorticoid pulse therapy for Graves' orbitopathy. Thyroid. 25(7):846–850. — PubMed PMID: 26090805
  16. Perez-Moreiras JV, Gomez-Reino JJ, Maneiro JR, et al. (2018). Efficacy of tocilizumab in patients with moderate-to-severe corticosteroid-resistant Graves orbitopathy: a randomized clinical trial. Am J Ophthalmol. 195:181–190. — PubMed PMID: 30081019
  17. Stan MN, Garrity JA, Carranza Leon BG, et al. (2015). Randomized controlled trial of rituximab in patients with Graves' orbitopathy. J Clin Endocrinol Metab. 100(2):432–441. — PubMed PMID: 25343233
  18. Mourits MP, Prummel MF, Wiersinga WM, Koornneef L (1997). Clinical activity score as a guide in the management of patients with Graves' ophthalmopathy. Clin Endocrinol (Oxf). 47(1):9–14. — PubMed PMID: 9302365
  19. Bartley GB, Fatourechi V, Kadrmas EF, et al. (1995). The incidence of Graves' ophthalmopathy in Olmsted County, Minnesota. Am J Ophthalmol. 120(4):511–517. — PubMed PMID: 7573310
  20. Bartley GB, Fatourechi V, Kadrmas EF, et al. (1996). Clinical features of Graves' ophthalmopathy in an incidence cohort. Am J Ophthalmol. 121(3):284–290. — PubMed PMID: 8597271
  21. Perros P, Crombie AL, Kendall-Taylor P (1995). Natural history of thyroid associated ophthalmopathy. Clin Endocrinol (Oxf). 42(1):45–50. — PubMed PMID: 7889631
  22. Prummel MF, Wiersinga WM (1993). Smoking and risk of Graves' disease. JAMA. 269(4):479–482. — PubMed PMID: 8419666
  23. Chin YH, Ng CH, Lee MH, et al. (2020). Prevalence of thyroid eye disease in Graves' disease: a meta-analysis and systematic review. Clin Endocrinol (Oxf). 93(4):363–374. — PubMed PMID: 32691849

↑ Back to Table of Contents

Connections

↑ Back to Table of Contents