Hyperthyroid Disorders

Lesson 8: Accompanying Conditions and Complications

Thyroid Eye Disease

Thyroid eye disease or TED is an eye disorder that can accompany thyroid disease. TED is also known as Graves’ ophthalmopathy. Eighty percent of clinically significant cases occur in patients with hyperthyroidism. Ten percent of cases occur in patients who are euthyroid, and another ten percent occurs in patients with Hashimoto’s thyroiditis. In euthyroid patients, the condition is called euthyroid Graves’ disease. More than 60 percent of these patients develop Graves’ disease within five years after the eye condition emerges.

There are two types of thyroid eye disease. The most common type is related to excess thyroid hormone levels. In this condition, excess thyroid hormone causes spastic signs such as eye tremor, dryness, a staring appearance and eyelid retraction. These symptoms resolve when thyroid hormone levels are corrected.

A more serious congestive form of TED is related to autoimmunity. Immune system chemicals known as cytokines and both stimulating and blocking TSH receptor antibodies contribute to disease development. Clinically significant congestive TED is most likely to occur in patients who have high levels of both stimulating and blocking TSH receptor antibodies who do not have TPO antibodies.

Congestive TED occurs when TSH receptor antibodies react with the TSH receptor protein found on orbital cells. The cells are stimulated to produce of a sticky chemical known as glycosaminoglycan or GAG. In congestive TED the eye muscles enlarge because deposits lodge between eye muscle fibers. These deposits include clusters of white blood cells, GAG and cellular debris, which also crowd the orbital cavity that houses the eyeball. This pushes the eyeball forward in its socket causing a protrusion known as proptosis or exophthalmos. If severe, this congestion can cause pressure on the optic nerve, threatening vision.

Signs and Symptoms
Other symptoms in TED include diplopia or double vision which results when compression restricts the movement of eye muscles, eyelid retraction, light sensitivity, a staring appearance, chemosis, which causes edema in the conjunctiva, conjunctival exposure, corneal compromise, exposure keratitis, eye motility problems, fibrosis or scarring, grittiness, foreign body sensation, dryness, tearing, lid lag, periorbital edema, redness, ptosis, which causes eyelid drooping, swelling, pain, and visual impairment.

The signs of TED include changes related to eye muscle enlargement and orbital crowding. Signs include upper eyelid lag when gazing downward, incomplete and infrequent blinking, upper eyelid retraction in which the lid can’t completely close, eye muscle paralysis, spasms in the levator muscle with upper eyelid retraction, uneven, jerky motion of upper eyelid, difficulty in fixing gaze, absent creases in the forehead on superior gaze, lower lid lag on upward gaze, and eyelid puffiness or tremor.

Contributing Factors
Congestive TED is autoimmune in nature and directly affected by things that injure the immune system including stress, radioiodine therapy, diets rich in saturated fats, sugar or iodine, nutrient deficiencies, cigarette smoke and other toxins.

Disease Course
Like Graves’ hyperthyroidism, congestive TED runs its own individual course. An active or hot phase of one to five years is followed by a plateau phase in which symptoms remain stable, and finally a resolution phase in which symptoms can improve spontaneously.

Similar to Graves’ disease, cigarette smoke, iodine and other environmental triggers prolong the disease course. Corticosteroids can be used to slow down the immune system, but symptoms return when the medication is stopped. Hypothyroidism should be avoided because it encourages thyroid antibody production as the gland speeds up its activity trying to fix the problem.

Treatment
When vision is threatened corticosteroids or orbital radiotherapy, a form of external beam radiation, is used to destroy white blood cells in the area or reduce their activity. These treatments are only effective during the hot or active phase. If the active phase is prolonged and scar tissue develops, muscle changes and deviations in normal alignment will be permanent. If this occurs, surgery is available to correct the problems. Surgery should not be performed until the hot phase has ended since its effects can interfere with the normal healing process.

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