Thyroid Eye Disease

Posted by Elaine Moore Apr 19, 2006

Thyroid eye disease or TED is technically known as Graves' opthalmopathy. About 80 percent of all patients with TED have the autoimmune hyperthyroid disorder known as Graves' disease. Another 10 percent of all cases are seen in patients with autoimmune hypothyroidism, either Hashimoto's thyroiditis Hashitoxicosis, or atrophic thyroiditis. In addition, another 10 percent of all cases are seen in people with normal thyroid function. When thyroid functionis normal, the eye conditon is referred to as euthyroid Graves' disease. Euthyroid is a term meaning that thyroid function tests are normal. Most people with euthyroid Graves' disease develop a thyroid disorder within eighteen months of the emergence of the eye disorder. But some people with euthryoid Graves' disease never develop thyroid dysfunction.

Similar to most autoimmune disorders, symptoms in TEDE tend to wax and wane and this condition can vary tremendously in terms of disease severity. The severity of symptoms and the particular predominant symptoms can also vary over time. Some people may notice mild eye dryness or grittiness. On the opposite end of the spectrum, some people will experience vision loss. Symptoms of TED include proptosis (exophthalmos or bulging), conjunctivitis (inflammation of the conjunctiva, the inner lining or rim of the eye), dryness, eyelid retraction, eyelid lag, twitching, redness, itching, double vision (diplopia), retrobulbar pain, painful oppressive feeling on or behind the globe of the eye, chemosis (edema or swelling of the bulbar conjunctiva), swelling, blurriness, eye muscle paralysis, corneal irritation resulting in ulcertion or corneal inflammation (keratitis), eye motility problems, foreign body sensation, fibrosis or scar tissue formation, lacrimation (tearing), photophobia or light sensitivity, ptosis (upper eyelid drooping), staring, and visual impairment. Symptoms of concern include blurriness and loss of color vision, with red being the first color affected, with tones becoming grayish or subdued.

There are two major subtypes of TED: a milder form related to abnormal thyroid hormone levels, and an autoimmune congestive disorder that is usually more clinically significant. The first type of TED is the most common TED subtype seen, and with sensitive imaging tests, its seen in nearly all patients with autoimmune hyperthyroidism and in a smaller number of patients with hypothyroidism.

In hyperthyroidism, eye symptoms are usually spastic and include staring, dryness, and eyelid retraction. In hypothyroidism, periorbital edema or swelling all around the eye socket occurs. Both of these forms of TED are related to thyroid hormone imbalance, either excess hormone acting on the nerves that supply the eye or deficient hormone causing venous congestion, impaired circulation and fluid stagnation.l

This form of TED resolves within a few weeks after thyroid hormone levels are corrected and brought back into the normal range. Note, by thyroid hormone levels I mean FT4 and FT3 levels. The pituitary hormone TSH can stay low or suppressed for many months during the course of treatment for hyperthyroidism and doesn't mean that the patient is still hyperthyroid. TSH also lags at least 6 weeks behind thyroid hormone levels and often remains elevated longer in people who have been hypothyroid. Relying on the TSH level can be misleading, and in treating TED, hypothyroidism must be avoided for reasons described in the next paragraph.

The congestive autoimmune form of TED is caused by both stimulating and blocking TSH receptor antibodies (TRAb) and also immune system chemicals known as cytokines. Stimulating TRAb are also known as TSI. These thyroid antibodies are primarily seen in patients with Graves' disease although most people with autoimmune thyroid disease have a combination of different thyroid antibodies. Blocking TRAb are seen in Hashimoto's thyroiditis and atrophic thyroiditis where they contribute to hypothyroidism. They're also seen along with TSI in Hashitoxicosis. In people with euthyroid Graves' disease, equal amounts of both blocking and stimulating TRAb are present. In hypothyroidism, including that resulting from treatment for hyperthyroidism, the cells of the thyroid gland including immune system cells try to correct the problem. In doing so they increase their activity. This includes increased thyroid antibody production, which can trigger or worsen existing cases of TED. For this reason, it's important to avoid becoming even temporarily hypothyroid due to inadequate or inappropriate treatment.

The congestive or autoimmune form of TED has three phases: an active phase, a plateau phase with reduced activity and a resolution phase, a time when symptoms usually regress and the eyes return to normal. In rare cases, especially in severe cases, cosmetic surgery or decompression surgery may be needed to assist with these changes. Surgery performed too soon, however, especially during the active phase, will prevent the normal healing process and lead to subsequent surgeries. Some patients who have TED as a result of radioiodine ablation for hyperthyroidism have had as many as 20 corrective surgeries as a result of having surgery too soon. Today, the autoimmune nature of TED is better understood and surgery is rarely performed.

The active phase of TED varies. In some patients symptoms resolve quickly although on average the active phase lasts about 12-18 months. In some cases, especially if TRAb levels are high, patients are smokers, nutrient deficiencies are present, or the patient continues to be exposed to environmental triggers such as excess dietary iodine, the active phase can last as long as 5 years.

Source: Elaine Moore, Thyroid Eye Disease, Understanding Graves' Opthalmopathy, Sara Health Press, 2003.