Thyroid Dysfunction _________________________________________________________________________
Thyroid Eye Disease Thyroid eye disease (TED) is caused by inflammation of the muscles and connective tissue in the eye socket, which pushes the eyeball forward (i.e., proptosis). It most commonly occurs in patients with Graves disease [28]. Because more of the eye is exposed to the air, dryness and discomfort are common problems. Some interventions that may relieve the discomfort of mild-to-moderate TED include [7; 28]: • Do not smoke and avoid secondhand smoke • Use artificial tears to maintain eye moisture • Avoid strong sunlight • Apply cool compresses to the eyes • Wear wrap-around sunglasses when outdoors (when the eyes protrude, they are more vulnerable to ultraviolet rays) • Consume fluids in adequate amounts • Avoid ceiling fans • Do not use contact lenses In 2020, the U.S. Food and Drug Administration approved teprotumumab, the first medication for the treatment of thyroid eye disease [29]. This monoclonal antibody therapy is administered as IV infusions every three weeks. A small 2020 randomized, placebo-controlled, phase 3 trial found that proptosis was significantly reduced in the treatment vs. placebo group (78% response vs. 7% response) [30]. Proptosis was reduced by nearly 3 mm with teprotumumab, and qual- ity of life scores were greatly improved; several adverse events occurred but were mild or moderate. Standard treatment for individuals with moderate-to-severe TED is a course of pulse doses of IV methylprednisolone. Proptosis is typically reduced to manageable levels within four weeks to six months of steroid treatment and within one to two years of initiation of anti-thyroid medication. Some patients whose condition does not improve with medication may require orbital decompression surgery. Thyroidectomy will resolve TED within one year; many patients prefer this option over orbital decompression surgery. Radioactive iodine therapy is known to exasperate TED and should be avoided in patients with moderate-to-severe eye disease [22; 28] . Thyrotoxicosis Thyrotoxicosis, or “thyroid storm,” is a serious and potentially fatal complication of hyperthyroidism. It is characterized by high body temperature, vomiting, severe tachycardia, irritabil- ity, delirium, dehydration, and an increase in clotting factor VIII. Once more common than it is today, thyrotoxicosis can be caused by serious infection, surgery, trauma, labor and delivery, pulmonary embolus, myocardial infarction, or critical metabolic problems in a patient with undiagnosed or untreated hyperthyroidism. Treatment involves addressing the precipitating condition and administering medication to treat the severe hyperthyroid state [22; 24] .
Drug Therapy Two main types of medications are used to treat patients with hyperthyroidism—thyroid-suppressors and beta-blockers. Thyroid-suppressing drugs act by interfering with thyroid syn- thesis, preventing iodine from combining with thyroglobulin. The most frequently prescribed medications used to treat hyperthyroidism are methimazole and propylthiouracil [16; 22]. The U.S. Food and Drug Administration added a boxed warning to the labeling for propylthiouracil due to reports of severe liver injury and acute liver failure, some cases of which have been fatal. It is recommended that the drug be reserved for patients who cannot tolerate other treatments (e.g., methima- zole, radioactive iodine, surgery) [16; 22]. Neither methimazole nor propylthiouracil are considered to be a cure, and many patients report relapses despite continual use. Beta-blockers do not modulate the disease itself; instead, they are used to treat various symptoms of hyperthyroidism, includ- ing anxiety, heat intolerance, palpitations, tachycardia, and tremors [26]. The use of beta-blockers is recommended in the ATA treatment guideline as first-line therapy for all patients with symptomatic thyrotoxicosis, but especially for those with comorbid cardiovascular disease, a resting heart rate greater than 90 beats per minute, and elderly patients [22]. Atenolol, metoprolol, nadolol, and propanolol are a few of the ATA recommended beta-blockers, and the guideline notes that while these medications have not been specifically approved for hyperthyroidism, they are approved for the treatment of car- diovascular disease. Beta-blocking agents are contraindicated in individuals with bronchospastic asthma. Patients treated with thyroid-suppressors and beta-blockers have been shown to have less fatigue and shortness of breath, lower heart rates, and better self-reported overall functioning compared with patients taking thyroid-suppressors alone [22; 26] . Surgery Surgical removal of a portion or the entire thyroid is indicated for patients who cannot or do not wish to undergo radiation therapy and who have difficulty tolerating the antithyroid medications. Preoperative care includes administration of antithyroid medication, stable (i.e., cold) iodine treatment (to decrease gland vascularity), and beta-blocker therapy. After the thyroid gland is removed, the patient will permanently require supplementary T 4 medication [22] . CONDITIONS ASSOCIATED WITH HYPERTHYROIDISM Graves Disease The most common form of hyperthyroidism is Graves disease, so named for the Irish physician, Robert Graves, who first recognized the condition in 1834 [7; 27]. Graves disease occurs more frequently in women than in men and in individuals 30 years of age and older, although it can develop at any time of life. Because Graves disease tends to be seen in families, it was first believed to have a genetic etiology; however, it is now thought that a genetic susceptibility is triggered by an infectious cause (e.g., viral infection) [7; 27] .
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