Yes, you can have Thyroid Eye Disease (TED) even without Graves’ hyperthyroidism. TED is an autoimmune condition where the immune system attacks the tissues surrounding the eyes, causing inflammation and swelling. Graves’ Disease is an autoimmune disorder that typically causes the thyroid gland to become overactive, leading to hyperthyroidism. While the two conditions frequently occur together, TED can manifest independently of thyroid hormone imbalance, which can make diagnosis more challenging.
Understanding Thyroid Eye Disease
Thyroid Eye Disease, also known as Graves’ ophthalmopathy, is an inflammatory process that specifically targets the tissues and muscles located behind the eye. This inflammation results in the buildup of specific molecules, mainly glycosaminoglycans, within the orbital space, causing the affected tissues to swell and expand. Because the bony orbit surrounding the eye is a confined space, this expansion pushes the eyeballs forward, a defining sign called proptosis, or eye bulging.
Symptoms include a gritty or dry sensation in the eyes, excessive tearing, and noticeable redness or irritation of the conjunctiva. The swelling can also cause the eyelids to pull back (eyelid retraction), which contributes to the dry, exposed surface of the eye.
The extraocular muscles, which control eye movement, can become thickened and restricted by the inflammation. This restriction prevents the eyes from moving together correctly, commonly resulting in double vision (diplopia). In rare, severe cases, the swelling and pressure within the orbit can compress the optic nerve, potentially leading to vision loss.
The Typical Autoimmune Connection: Graves’ Disease
Graves’ Disease is the most common cause of hyperthyroidism and the context in which TED is most often diagnosed. It is characterized by the immune system mistakenly producing antibodies that target the thyroid-stimulating hormone (TSH) receptor on the thyroid gland. These autoantibodies act like a continuous “on” switch, causing the thyroid to produce excessive amounts of hormone.
TED and Graves’ Disease are closely related due to the shared target of the immune system attack. The same TSH receptors present on the thyroid gland are also found on the fibroblasts in the fatty and connective tissue behind the eyes. When the autoantibodies circulate, they bind to the receptors in the orbital tissues, triggering the inflammation and swelling characteristic of TED.
It is estimated that 30 to 50 percent of people diagnosed with Graves’ Disease will develop some degree of TED. Approximately 90 percent of all TED cases are found in individuals who have a current or previous diagnosis of Graves’ Disease. This strong statistical link is why TED is often mistakenly believed to be dependent on an active thyroid hormone imbalance.
The Exception: TED Without Hyperthyroidism
It is possible to develop Thyroid Eye Disease without experiencing hyperthyroidism, a condition often referred to as Euthyroid Graves’ Disease (EGD). In these cases, the patient’s blood work shows normal levels of thyroid hormones, meaning they are “euthyroid.” However, the autoimmune process remains active, targeting the eye tissues.
The TSH receptor autoantibodies are the mechanism driving the eye disease, not the resulting thyroid hormone level. In EGD, these antibodies are present and sufficient to trigger the inflammatory response in the orbital tissues. They may be too low in concentration or not potent enough to cause the thyroid gland to become overactive.
This variant accounts for about 10 percent of all individuals with TED. Diagnosis can be delayed because the absence of classic hyperthyroidism symptoms, like a rapid heart rate or unintentional weight loss, often leads doctors to look for other causes of eye inflammation. TED can also rarely occur in people with Hashimoto’s thyroiditis, an autoimmune condition that causes an underactive thyroid, demonstrating that the eye disease is fundamentally an orbital autoimmune disorder.