Thyroid – Related Eye Disease

Eye disease

Thyroid-associated ophthalmopathy is one of the most typical symptoms of Graves’ disease. It is known by a variety of terms, the most common being Graves’ ophthalmopathy. Thyroid eye disease is an inflammatory condition, which affects the orbital contents including the extraocular muscles and orbital fat. It is almost always associated with Graves’ disease but may rarely be seen in Hashimoto’s thyroiditis, primary hypothyroidism, or thyroid cancer.

The ocular manifestations that are relatively specific to Grave’s disease include soft tissue inflammation, proptosis (protrusion of one or both globes of the eyes), corneal exposure, and optic nerve compression. Also seen, if the patient is hyperthyroid, (i.e., has too much thryoid hormone) are more general manifestations, which are due to hyperthyroidism itself and which may be seen in any conditions that cause hyperthyroidism (such as toxic multinodular goiter or even thyroid poisoning). These more general symptoms include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid, during downward gaze.

It is believed that fibroblasts in the orbital tissues may express the Thyroid Stimulating Hormone receptor (TSHr). This may explain why one autoantibody to the TSHr can cause disease in both the thyroid and the eyes

Grave’s Ophthalmolopathy is the most common caused of unilateral or bilateral proptosis in adults.

It commonly occurs between the ages of 25-50, although it may also present in adolescents.

Diagnosis is made based on clinical findings including proptosis, eyelid retraction, restrictive myopathy and possibly compressive optic neuropathy. It is often grouped into two independent manifestations of this syndrome:

a non-pitting edema (pretibial myxedema), with thickening of the skin usually found on the lower extremities

fatigue, weight loss with increased appetite, and other symptoms of hyperthyroidism

The two signs that are truly ‘diagnostic’ of Graves’ disease (i.e., not seen in other hyperthyroid conditions) are exophthalmos and non-pitting edema (pretibial myxedema). Goiter is an enlarged thyroid gland and is of the diffuse type (i.e., spread throughout the gland). Diffuse goiter may be seen with other causes of hyperthyroidism, although Graves’ disease is the most common cause of diffuse goiter. A large goiter will be visible to the naked eye, but a smaller goiter (very mild enlargement of the gland) may be detectable only by physical exam. Occasionally, goiter is not clinically detectable but may be seen only with CT or ultrasound examination of the thyroid.

Another sign of Graves’ disease is hyperthyroidism, i.e., overproduction of the thyroid hormones T3 and T4. Normothyroidism is also seen, and occasionally also hypothyroidism, which may assist in causing goiter (though it is not the cause of the Graves disease). Hyperthyroidism in Graves’ disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4.

Other useful laboratory measurements in Graves’ disease include thyroid-stimulating hormone (TSH, usually low in Graves’ disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Thyroid-stimulating antibodies may also be detected serologically.

Biopsy to obtain histiological testing is not normally required but may be obtained if thyroidectomy is performed.

Differentiating two common forms of hyperthyroidism such as Graves’ disease and Toxic multinodular goiter is important to determine proper treatment. Measuring TSH-receptor antibodies with the h-TBII assay has been proven efficient and was the most practical approach found in one study.