Home » Health & Wellness » Graves' Disease » Graves' Ophthalmopathy

Graves' Ophthalmopathy

© Elaine Moore

Although Graves’ disease primarily affects the thyroid gland, causing hyperthyroidism, it may also affect the muscles, the skin and the eyes. The associated eye disorder is known as Graves’ ophthalmopathy (GO) or orbital dystrophy (OD) or thyroid eye disease (TED). When the eye disease occurs in the absence of thyroid disease, it's called euthyroid Graves' disease. About 20% of the cases of GO occur in patients with Hashimoto’s thyroiditis and other forms of autoimmune thyroid disease. GO occurs concomitantly with approximately 10% of cases of Hahimoto’s thyroiditis. GO has also occurred in patients on long-term lithium therapy (lithium decreases thyroid hormone synthesis and affects the autoimmune response).

The congestive or inflammatory form of Graves' ophthalmopathy has an autoimmune origin and runs its own course independent of the thyroid disorder. However, 33% to 50% of GO run parallel with the thyroid disturbances characteristic of GD. In most instances, the eye disorder emerges within 18 months of the initial thyroid disorder. Clinically evident GO occurs in 10% to 25% of GD patients if eyelid signs are excluded. If eyelid changes, such as eyelid retraction are considered, the disease affects 30% to 45% of all Graves’ disease patients. Fewer than 5% of GD patients experience severe ophthalmopathy. Men with GD who develop GO are usually more inclined to develop severe GO. This may be because men are less likely to be diagnosed early.

There are two separate forms of GO, a congestive infiltration caused by the autoimmune process and a spastic disorder caused by excess thyroid hormone. The congestive process is affected by the autoimmune process, particularly the effects of stimulating TSH receptor antibodies on thyroid receptors in the orbital muscles, whereas the symptoms caused by excess thyroid hormone abate as levels of excess thyroid hormone are reduced. Symptoms of the congestive form of GO generally begin to resolve after 6 months although TED may persist for as long as 3 to 5 years. The antithyroid drug Tapazole has a protective effect on GO which is probably due to the immune suppressing effect of the drug.

In the congestive form of GO, the extraocular eye muscles appear to be the primary target. The process is characterized by white blood cell infiltration of orbital fibroadipose and skeletal muscle tissue. Here, the white blood cells and a chemical known as glycosaminoglycan (GAG) form deposits which displace normal eye muscle. This infiltration, which causes inflammation, is often associated with edema (fluid retention) and may eventually progress to fibrosis (an increase of fibrous tissue similar to scar tissue).