Abstract

Graves’ disease (GD) is the most frequent cause of hyperthyroidism, where iodine levels are abundant.

One of the extrathyroidal symptoms is Graves’ ophthalmopathy (GO) which presents with ophthalmic symptoms that can range from minor (e.g., dry eye) to sight-threatening (e.g., corneal ulceration and compressive optic neuropathy) features.

About 79% of Graves’ disease cases can be attributed to genetic predispositions, while the remaining 21% are due to environmental factors. Acute stress, active or passive smoking, and past radioactive iodine therapy have all been linked to the development or aggravation of thyroid eye disease (TED).

The devastating effects of GO or TED might include diplopia, ocular hypertension, optic nerve degeneration, and glaucoma.

A low basal serum Thyroid Stimulating hormone (TSH) level has the highest sensitivity and specificity for diagnosing hyperthyroidism. Moreover, the appearance of Thyroid Stimulating hormone receptors (TSHR) autoantibodies (TRAbs) is presumed to be highly specific for the diagnosis of Graves’ disease.

Imaging studies of the orbit that use ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI), for example, can confirm the diagnosis of TED.

In order to treat Graves’s eye disease optimally, a multidisciplinary approach must be applied involving primary care physicians, ophthalmologists, internists and endocrinologists. Therefore, it is essential to restore the euthyroid state and this can be obtained by either antithyroid medications, radioactive iodine or surgical thyroidectomy.

Treatment of GO ranges from supportive treatment (lubricants and moisturizer drops), to medical intervention, preferably corticosteroid, and variable surgical interventions.

Key words: Graves’ disease, Medical and surgical management