Thyroid Research and Practice

CASE REPORT
Year
: 2013  |  Volume : 10  |  Issue : 1  |  Page : 32--34

Euthyroid ophthalmopathy


Subodh Banzal1, Abhishek Singhai2, Pragya Jain3,  
1 Department of Endocrinology, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India
2 Department of Medicine, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India
3 Department of Ophthalmology, Sri Aurobindo Medical College, Indore, Madhya Pradesh, India

Correspondence Address:
Abhishek Singhai
Department of Medicine, Sri Aurobindo Medical College, Sanwer Road, Indore, Madhya Pradesh
India

Abstract

Thyroid-associated ophthalmopathy usually occurs in a close temporal relationship with hyperthyroidism. It is rare in patients with normal thyroid function (euthyroid ophthalmopathy) and in patients with hypothyroid forms of thyroid autoimmune disease (hypothyroid ophthalmopathy). Here we report wide spectrum of euthyroid ophthalmopathy ranging from mild proptosis, unilateral proptosis to severe keratopathy with blindness.



How to cite this article:
Banzal S, Singhai A, Jain P. Euthyroid ophthalmopathy.Thyroid Res Pract 2013;10:32-34


How to cite this URL:
Banzal S, Singhai A, Jain P. Euthyroid ophthalmopathy. Thyroid Res Pract [serial online] 2013 [cited 2019 Dec 15 ];10:32-34
Available from: http://www.thetrp.net/text.asp?2013/10/1/32/105846


Full Text

 Introduction



Thyroid-associated ophthalmopathy (TAO), frequently termed Graves ophthalmopathy, is part of an autoimmune process that can affect the orbital and periorbital tissue, the thyroid gland, and, rarely, the pretibial skin or digits (thyroid acropachy). [1],[2],[3] TAO may precede, coincide, or follow the systemic complications of dysthyroidism. The ocular manifestations of TAO include eyelid retraction, proptosis, chemosis, periorbital edema, and altered ocular motility with significant functional, social, and cosmetic consequences. Of those patients affected, 20% indicate the ocular morbidity of this condition is more troublesome than the systemic complications of dysthyroidism. Although most cases of TAO can be managed medically and without visual loss, it may result in vision-threatening exposure keratopathy, troublesome diplopia, and compressive optic neuropathy. The prevalence of TAO in primarily euthyroid and primarily hypothyroid patients ranges between 1.6% and 8.6%. [4],[5],[6],[7]

 Case Report



A 55-year-old gentleman developed mild redness and watering from eyes since last 1 month. He also felt that his eyes are little prominent since last 10 months [Figure 1]. With these complaints he presented to ophthalmologist who examined him and noticed that proptosis, chemosis, and lid edema bilaterally. Fundus examination and eye movements were normal. Routine investigations including hemogram, liver function tests, and renal function tests were normal. Computerised tomography (CT) scan orbit showed prominent extraocular muscles and soft tissue edema [Figure 2]. There was no space occupying lesion bilaterally. In view of these findings, he was referred to endocrinologist. On examination, patient was obese with body mass index (BMI) 32, pulse 80/min, blood pressure (BP) 110/78 mmHg, and no thyromegaly. Free T3, Free T4 and thyroid-stimulating hormone (TSH) were normal. His thyroid peroxidase (TPO) antibodies were strongly positive (330, reference value <9 IU/ml). With these findings euthyroid ophthalmopathy diagnosed. He was advised methylcellulose eye drops and kept under regular follow-up.{Figure 1}{Figure 2}

Second case was that of a 45-year-old lady presented to ophthalmologist with loss of vision in both eyes gradually since last 2 years. Initially, patient noticed prominence of both eyes, followed by redness of both eyes and gradual loss of vision. On examination, she was found to have bilateral corneal opacity with phthisis bulbi [Figure 3]. CT scan orbit showed prominent extraocular muscles, soft tissue edema and phthisis bulbi [Figure 4]. She was referred for endocrine opinion. On examination, patient was thin built with BMI 22, no thyromegaly, pulse 80/min, BP 124/80 mmHg. Free T3, Free T4 and TSH were within normal limits. Antibodies to TPO were strongly positive (500, reference value <9 IU/ml).{Figure 3}{Figure 4}

Third case was a young lady of 26-year-old presented with prominence of left eye, gradually increasing in size [Figure 5]. She had gritty sensation in same eye. On examination, pulse was 86/min, BP 120/80 mmHg and thyroid gland was just palpable. She had mild proptosis. Fundus examination and eye movements were normal. Free T3, Free T4, TSH were consistently normal. Anti TPO antibodies were positive (150, reference value <9 IU/ml). Patient is under regular follow-up without any worsening symptoms.{Figure 5}

 Discussion



The annual incidence rate of TAO has been estimated at 16 cases per 100,000 women and 2.9 cases per 100,000 men. [8] There appears to be a female preponderance in which women are affected 2.5-6 times more frequently than men; however, severe cases occur more often in men than in women. In addition, most patients are aged 30-50 years, with severe cases appearing to be more frequent in those older than 50 years. Although most cases of TAO do not result in visual loss, this condition can cause vision-threatening exposure keratopathy, troublesome diplopia, and compressive optic neuropathy. Therefore, although the prognosis is generally favorable for patients with this condition, and most patients do not require surgical intervention, [9],[10] all clinicians should be able to recognize TAO.

The thyroid gland itself does not cause TAO, and regulation of thyroid function does not abort this condition. Rather, the thyroid gland, eye muscles, and pretibial skin are especially subject to the autoimmune attack. Many patients with TAO are hyperthyroid, but euthyroidism, Hashimoto thyroiditis, thyroid carcinoma, and neck irradiation are also associated with TAO. TAO is associated strongly with smoking; [11],[12] the more severe the eye disease, the stronger the association. Autoimmune diseases such as myasthenia gravis, Addison disease, vitiligo, and pernicious anemia have been described with TAO. In simplest terms, the underlying pathophysiology of TAO is thought to be an antibody-mediated reaction against the TSH receptor with orbital fibroblast modulation of T-cell lymphocytes. T-cell lymphocytes are believed to react against thyroid follicular cells with shared antigenic epitopes in the retro-orbital space. An active phase of inflammation is initially present.

Lymphocytic infiltration of the orbital tissue causes a release of cytokines (e.g., tumor necrosis factor [TNF], interleukin-1 [IL-1]) from CD4+ T-cells stimulating the orbital fibroblasts to produce mucopolysaccharides, which, by hyperosmotic shift, cause tissue edema in the extraocular muscles. In screening for thyroid disease, the combination of free T4 (thyroxine) and TSH or serum TSH (thyrotropin) are highly sensitive and specific. Assays that measure the binding of TSH to a solubilized receptor are thyroid receptor antibody (TRAb), TSH receptor binding immunoglobulins (TBII), and long-acting thyroid stimulator assays. TPO antibodies (antimicrosomal antibodies) and antibodies to thyroglobulin may be useful when trying to associate eye findings with a thyroid abnormality, such as euthyroid Graves's disease.

Most patients with TAO can be observed; the follow-up interval depends on disease activity. Monitor for visual loss from corneal exposure and optic neuropathy and for strabismus development. If a patient has dry eye symptoms, consider having them use artificial tears during the day, lubricating ointment at night, and punctual plugs. In addition, encourage patients to stop smoking to decrease the risk of congestive ophthalmopathy. Sleeping with the head of the bed elevated may decrease morning lid edema. Systemic steroids are usually reserved for patients with severe inflammation or compressive optic neuropathy in TAO. Adjunctive cyclosporine, octreotide, and intravenous immunoglobulin are less common modalities of medical treatment for optic nerve compression. Orbital irradiation is sometimes is prescribed for moderate to severe inflammatory symptoms, diplopia, and visual loss in patients with TAO. Approximately, 5% of patients with TAO may require surgical intervention. Unless compressive optic neuropathy or severe corneal exposure is present, surgery is generally delayed during the active inflammatory phase of TAO. Surgery is usually performed during the quiescent cicatricial phase of the disease.

 Conclusion



Thyroid ophthalmopathy can be a devastating illness for thousands of patients who develop this condition each year. Clinicians should consider workup for euthyroid ophthalmopathy in patients with normal thyroid functions. Early diagnosis and appropriate monitoring of TAO may decrease corneal exposure and compressive optic neuropathy.

 Acknowledgment



The author would like to thank the patients for providing consent to use their photograph in this article.

References

1Ing E, Abuhaleeqa K. Graves' ophthalmopathy (thyroid-associated ophthalmopathy). Clin Surg Ophthalmol 2007;25:386-92.
2Yeatts RP. Quality of life in patients with Graves ophthalmopathy. Trans Am Ophthalmol Soc 2005;103:368-411.
3Bartalena L, Baldeschi L, Dickinson A, Eckstein A, Kendall-Taylor P, Marcocci C, et al. Consensus statement of the European group on Graves' orbitopathy (EUGOGO) on management of GO. Eur J Endocrinol 2008;158:273-85.
4Bartley GB, Fatourechi V, Kadrmas EF, Jacobsen SJ, Ilstrup DM, Garrity JA, et al. Clinical features of Graves' ophthalmopathy in an incidence cohort. Am J Ophthalmol 1996;121:284-90.
5Khoo DH, Eng PH, Ho SC, Tai ES, Morgenthaler NG, Seah LL, et al. Graves' ophthalmopathy in the absence of elevated free thyroxine and triiodothyronine levels: Prevalence, natural history, and thyrotropin receptor antibody levels. Thyroid 2000;10:1093-100.
6Marcocci C, Bartalena L, Bogazzi F, Panicucci M, Pinchera A. Studies on the occurrence of ophthalmopathy in Graves' disease. Acta Endocrinol (Copenh) 1989;120:473-8.
7Paunkovic J, Paunkovic N. Does autoantibody-negative Graves' disease exist? A second evaluation of the clinical diagnosis. Horm Metab Res 2006;38:53-6.
8Bartley GB, Fatourechi V, Kadrmas EF, Jacobsen SJ, Ilstrup DM, Garrity JA, et al. The incidence of Graves' ophthalmopathy in Olmsted County, Minnesota. Am J Ophthalmol 1995;120:511-7.
9Nassar MM, Dickinson AJ, Neoh C, Powell C, Buck D, Galal E, et al. Parameters predicting outcomes of strabismus surgery in the management of Graves' ophthalmopathy. J AAPOS 2009;13:236-40.
10Ujhelyi B, Erdei A, Galuska L, Varga J, Szabados L, Balazs E, et al. Retrobulbar 99mTc-diethylenetriamine-pentaacetic-acid uptake may predict the effectiveness of immunosuppressive therapy in Graves' ophthalmopathy. Thyroid 2009;19:375-80.
11Prummel MF, Wiersinga WM. Smoking and risk of Graves' disease. JAMA 1993;269:479-82.
12Bertelsen JB, Hegedüs L. Cigarette smoking and the thyroid. Thyroid Fall 1994;4:327-31.