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A 32-year-old woman presents with fatigue and “eye strain” (Figure 227-1). She had been working as a secretary and noticed difficulty focusing her eyes. She said she was anxious and was having difficulty writing. She reported that her sister was taking medication for “thyroid trouble.” A low thyroid-stimulating hormone (TSH) and an elevated free thyroxin level (T4) were found on laboratory testing, and the patient was diagnosed with Graves disease (GD). Her thyroid scan showed an enlarged thyroid with increased uptake (Figure 227-2). The patient chose radioactive iodine (RAI) as her treatment and her symptoms resolved. One year later she required levothyroxine treatment.

Figure 227-1

This patient displays the following common findings of Graves disease: Lid retraction and mild proptosis (exophthalmus), particularly evident on the left eye, and goiter. (Courtesy of Dan Stulberg, MD.)

Figure 227-2

Nuclear scan of the thyroid in Graves disease showing increased uptake (61%). (Courtesy of Michael Freckleton, MD.)

GD is an autoimmune thyroid disorder characterized by circulating antibodies that stimulate the TSH receptor and resulting in hyperthyroidism.1

Thyrotoxicosis (clinical state resulting from inappropriately high thyroid hormone levels); hyperthyroidism (thyrotoxicosis caused by elevated synthesis and secretion of thyroid hormone).

  • GD is a common disorder affecting 0.5% to 1.2% of the population.
  • There is a female-to-male ratio of 5 to 10:1.
  • Among patients with hyperthyroidism, 60% to 80% have GD; younger patients (younger than age 64 years) with hyperthyroidism are more likely to have GD than are older patients with hyperthyroidism.
  • Graves ophthalmopathy (see “Clinical Features” below) occurs in more than 80% of patients within 18 months of diagnosis of GD. The ophthalmopathy is clinically apparent in 30% to 50% of patients.2
  • Goiter is present in 90% of patients younger than age 50 years (vs. 75% in older patients with GD).1
  • Untreated hyperthyroidism can lead to osteoporosis, atrial fibrillation, cardiomyopathy, and congestive heart failure; thyrotoxicosis (thyroid storm) has an associated mortality rate of 20% to 50%.3

  • The hyperthyroidism of GD results from circulating immunoglobulin (Ig) G antibodies that stimulate the TSH receptor.2 These antibodies are synthesized in the thyroid gland, bone marrow, and lymph nodes. Activation of the TSH receptor stimulates follicular hypertrophy and hyperplasia causing thyroid enlargement (goiter) and an increase in thyroid hormone production with an increased fraction of triiodothyronine (T3) relative to T4 (from approximately 20% to up to 30%).2
  • The etiology is seen as a combination of genetic (human leukocyte antigen-D related [HLA-DR] and cytotoxic T-lymphocyte antigen 4 [CTLA-4] polymorphisms) and environmental factors, including physical and emotional stress (e.g., infection, childbirth, life events).2 In addition, insulin-like growth factor-1 receptor (IGF-1R)-bearing fibroblasts and B-cells exhibiting the IGF-1R(+) phenotype may ...

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