Dry Eye Dx and Tx

Thyroid Disease and Ocular Dryness, Part 2

dry eye dx and tx

Thyroid Disease and Ocular Dryness, Part 2


In my last column we reviewed the normal physiology of the thyroid gland, an endocrine gland that affects virtually every cell in the body. It's interesting that both inadequate and excessive thyroid function can seriously impact tear physiology.


In 1912, Hashimoto first described chronic lymphocytic thyroiditis (CLT), or Hashimoto's disease. This most common cause of hypothyroidism results from inflammation and infiltration, primarily by CD3 T lymphocytes. CLT is about eight times more common in females and typically presents after age 40. Patients with CLT can be asymptomatic or may report reduced tolerance to cold; constipation; pale, dry skin; weight gain; and muscle or joint stiffness and pain.

Enlargement of the thyroid (goiter) is a common feature of CLT. Evaluation of patients after goiter excision showed decreased Schirmer's and TBUT values, increased rose bengal staining scores and decreased goblet cell density. Twenty-seven percent of patients with CLT showed signs of subclinical Sjögren's syndrome (SS). Patients who have CLT have a 69-fold higher incidence of SS than is found in the general population, suggesting a strong relationship between these two autoimmune diseases.


In genetically predisposed individuals, B-cells release auto-antibodies that bind to TSH receptors in thyroid tissue and stimulate the release of thyroid hormones. Rising levels of thyroid hormones have no inhibitory effect on the production of these auto-antibodies. The unrelenting release of hormones leads to fatigue, weakness, heat intolerance, weight loss, tachycardia, tremor and enlargement of the thyroid gland. Patients often present with a variety of ocular complications.

Graves' disease is the most common form of hyperthyroidism. Twenty-five percent to fifty percent of patients who have Graves' disease have some degree of ophthalmopathy. Advanced stages may include proptosis, exophthalmos, ophthalmoplegia, neuropathy, venous stasis and periorbital edema. A combination of these factors also leads to increased palpebral fissure width.

Ocular dryness is common in Graves' disease. Gilbard and Ferris (1983) demonstrated that increased fissure width was associated with ocular surface staining and elevated tear film osmolarity. Eckstein et al (2004) demonstrated altered tear film proteins and decreased Schirmer test values in individuals with Graves' disease. Their study also confirmed elevated ocular surface staining. Finally, they demonstrated TSH monoclonal antibody staining of lacrimal gland secretory cells. This suggests an inflammatory etiology for at least part of the ocular dryness associated with hyperthyroidism.

Management Strategies

In CLT, inflammatory T-cells dominate. Patients who have this condition may benefit from an immunomodulator such as Restasis (Allergan). Adjunctive therapy with a long-lasting artificial tear product such as Systane (Alcon) is also often beneficial. Patients need to understand the chronic nature of their disease and the need for ongoing therapy.

Graves' disease presents additional management challenges. Educate such patients about the potential for surface changes, proptosis, ophthalmoplegia and compressive neuropathy. Because lid lag and proptosis cause increased ocular surface area, frequent use of artificial tears and maximizing meibomian gland function to reduce evaporation are critical. CLS

For references, please visit and click on document #150.

Dr. Townsend practices in Canyon, Texas and is an adjunct faculty member at UHCO. E-mail him at