dry eye dx and tx
Thyroid Disease and Ocular Dryness, Part 1
BY WILLIAM TOWNSEND, OD, FAAO
The ocular manifestations of thyroid disease are well established. An eyecare practitioner may be the initial health provider to elicit a history and identify signs that suggest thyroid disease in a given individual. Ocular complications of thyroid disease include proptosis, lid abnormalities, enlargement and inflammation of extraocular muscles, diplopia, compressive optic neuropathy, and ocular surface changes including dryness. The thyroid gland is an important endocrine organ whose hormones affect virtually every cell in the body. Thyroid disease is not rare; altered thyroid hormone secretion affects about 5 percent of women and 0.5 percent of men.
Examining the Thyroid Gland
To adequately understand the mechanisms through which thyroid disease exerts changes in the eye, we should understand the basic anatomy, physiology and pathology of the thyroid gland.
The name thyroid derives from "thyreos," the Greek word for shield, which probably refers to its shape. The thyroid is morphologically composed of two vertically shaped lobes connected by an isthmus. It's located anterior to the esophagus, just beneath the larynx. It is highly vascularized, an important characteristic because the thyroid captures iodide from circulation and thyroid hormones are dispatched to the rest of the body once they bind to circulating blood proteins.
Thyroid tissue is composed of spherical follicles, each of which consists of cuboidal follicle cells surrounding a central core of clear, viscous colloid containing thyroglobulin. The follicle cells actively transport iodide from fenestrated surface capillaries into the cell cytoplasm. Uptake of iodide is crucial for hormone synthesis and is regulated by the pituitary gland, which releases thyroid stimulating hormone (TSH). The concentration of iodide in thyroid tissue is 30 to 50 times that of the circulation.
Once inside the follicular cell, iodide is oxidized to active iodine by hydrogen peroxide. It then crosses the cell membrane into the colloid and couples with thyroglobulin to form tri-iodothyronine (T3) and tetra-iodothyronine or thyroxine (T4). Follicle cells then transport these hormones into the capillaries and eventually to the rest of the body via the circulatory system.
Once they reach the bloodstream, T3 and T4 mostly bind to circulating proteins; only the unbound fraction is active. The free portion of hormone is small: 0.04 percent of T4 is unbound, and 0.5 percent of T3 is unbound.
Some of the important effects of T3 and T4 include increased fat and carbohydrate metabolism, increased oxygen consumption in most body tissues (generating heat), rapid mentation, irritability, restlessness and reduced cholesterol levels. These powerful responses are normally limited by a negative feedback loop; as T3 and T4 levels increase, TSH levels decline, thus maintaining thyroid hormone at optimum levels.
A Critical Balance
Any condition that alters the critical balance in thyroid hormone levels can dramatically affect overall physical health and function. Excessively high thyroid levels can result in "thyroid storm," manifested as fever, excess sweating, nausea, diarrhea, hypertension and tachycardia. This condition can be fatal if untreated. Moreover, it has the potential to induce ocular changes including dryness. In part 2 of this series we will address thyroid gland abnormalities and their potential adverse affects on systemic and ocular tissue. CLS
For references, please visit www.clspectrum.com/references.asp and click on document #148.
Dr. Townsend practices in Canyon, Texas and is an adjunct faculty member at UHCO. E-mail him at firstname.lastname@example.org.