Chapter 236: Graves Disease and Goiter

PATIENT STORY

A 32-year-old woman presents with fatigue and "eye strain" (Figure 236-1). 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 thyroxine (T₄) level 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 236-2). The patient chose radioactive iodine (RAI) as her treatment and her symptoms resolved. One year later she required levothyroxine treatment.

INTRODUCTION

GD is an autoimmune thyroid disorder characterized by circulating antibodies that stimulate the TSH receptor, resulting in hyperthyroidism.¹ GD is caused by a combination of environmental and genetic factors. Risk factors include stress, smoking, and sudden increases in iodine uptake.¹ Goiter is an enlargement of the thyroid gland.

SYNONYMS

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

EPIDEMIOLOGY

• GD is a common disorder affecting about 2% to 3% of women and 0.5% of men in their lifetime.^1,2 Peak onset is between ages 20 and 50 years.¹

• The annual incidence of GD is 20 to 50 cases per 100,000 persons.³

• Among patients with hyperthyroidism (1.2% of the U.S. population), 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.¹

• Graves ophthalmopathy (GO; see "Clinical Features" below) occurs in about 75% of patients within 1 year before or after diagnosis of GD.¹

• Goiter is typically present; the thyroid gland is diffusely enlarged to two to three times its normal size with a firm consistency.¹

• Untreated hyperthyroidism can lead to osteoporosis, atrial fibrillation, cardiomyopathy, and congestive heart failure; mortality rate prior to satisfactory treatment was 10% to 30%.¹

ETIOLOGY AND PATHOPHYSIOLOGY

• The hyperthyroidism of GD results from circulating immunoglobulin (Ig) G antibodies directed against the thyrotropin receptor that mimic the action of thyrotropin and stimulate thyroid hormone production.³ These antibodies are synthesized in the ...