Hashimoto’s thyroiditis is an autoimmune disorder where the body’s immune system mistakenly attacks the thyroid gland. This chronic attack causes inflammation and progressive damage, which ultimately impairs the gland’s ability to produce sufficient thyroid hormones, resulting in hypothyroidism. Hypothyroidism, or an underactive thyroid, slows down the body’s metabolism. The question of whether this specific autoimmune process extends its damage to the eyes is complex, touching on shared biological pathways and the distinction between the effects of low hormone levels and direct autoimmune attack.
Clarifying the Autoimmune Link to Eye Disease
The most severe form of thyroid-related eye problem is Thyroid Eye Disease (TED), also known as Graves’ Orbitopathy, which involves inflammation and swelling of the tissues and muscles behind the eye. This condition is overwhelmingly associated with Graves’ disease, the opposite autoimmune disorder causing hyperthyroidism. Graves’ disease is driven by stimulating TSH receptor antibodies (TSAb) that activate the thyroid gland and also target the TSH receptors present in the fat and muscle tissue within the eye socket.
Hashimoto’s thyroiditis rarely causes severe TED, but the possibility exists because of the shared underlying autoimmune mechanism. Both conditions are autoimmune thyroid diseases, and some individuals with Hashimoto’s may also produce low levels of the TSAb that typically characterize Graves’ disease. This overlap means that up to six percent of people with Hashimoto’s may develop clinically apparent TED, though it is usually milder and less common than in Graves’ patients. When TED does occur, the autoimmune attack involves the orbital fibroblasts being targeted by the stimulating antibodies, leading to muscle enlargement and fat expansion, which pushes the eyeball forward (proptosis).
Eye Symptoms Related to Low Thyroid Function
Separate from the direct autoimmune attack that causes TED, the state of hypothyroidism itself can lead to milder, more common eye complaints. The body’s overall slowed metabolism and altered fluid regulation affect the delicate tissues around the eyes. These symptoms are generally related to the lack of thyroid hormone and are distinct from the structural damage seen in TED.
One of the most frequent complaints is dry eye syndrome, which is thought to be linked to the thyroid hormone’s role in the function of the tear ducts and the overall health of the eye’s surface. Reduced tear production or a change in tear quality can lead to a gritty or foreign body sensation, irritation, and redness.
Another common manifestation of poorly controlled hypothyroidism is periorbital edema, a noticeable puffiness or swelling around the eyes. This swelling occurs due to the systemic effect of low thyroid hormone levels causing the accumulation of a substance called mucin and water retention in the surrounding tissues. Unlike the inflammation of TED, this puffiness is metabolic in origin and typically reversible when thyroid hormone levels are returned to a healthy range with medication. These less severe eye symptoms are a direct consequence of the hypothyroid state and often resolve completely once thyroid-stimulating hormone (TSH) levels are normalized.
Clinical Evaluation and Treatment Approaches
The clinical evaluation of eye problems in a patient with Hashimoto’s thyroiditis begins with a comprehensive eye examination and specific blood tests. Measuring thyroid hormone levels, specifically TSH and free T4, determines the patient’s current thyroid status and helps differentiate between symptoms caused by low hormone levels and those caused by autoimmunity. Crucially, the presence of specific antibodies, such as TSH receptor antibodies (TRAb) or thyroid-stimulating immunoglobulins (TSI), is checked to confirm if the more severe autoimmune-driven TED is present.
If the eye complaints are mild, such as dryness or puffiness, and the TRAb test is negative, the management focus is on thyroid hormone optimization and supportive care. The endocrinologist will adjust the levothyroxine dosage to bring the TSH level into the target range, which often resolves the periorbital edema. The ophthalmologist may recommend lubricating eye drops or ointments to manage dry eye symptoms.
If the evaluation suggests TED, perhaps due to eye bulging (proptosis) or double vision, the patient is referred to specialists for more intensive management. Imaging tests like magnetic resonance imaging (MRI) or computed tomography (CT) scans may be ordered to visualize the enlarged eye muscles and orbital fat. Active, inflammatory TED is often treated with high-dose steroids or newer medications like teprotumumab, which targets the insulin-like growth factor 1 receptor (IGF-1R) pathway involved in the orbital autoimmune process.
For chronic or inactive TED that results in permanent changes, treatment may involve surgical procedures to correct the structural issues. Orbital decompression surgery can create more space in the eye socket to relieve pressure and reduce proptosis. Eye muscle surgery (strabismus surgery) may be necessary to correct double vision caused by scarred or shortened eye muscles.