J Hyperthyroidism
Definition
Hyperthyroidism is defined as thyroid gland hyperactivity. Thyrotoxicosis is more specifically defined as a state of thyroid hormone excess. The most common cause of thyrotoxicosis in the United States is Graves’ disease. Graves’ disease is an autoimmune disease in which thyroid-stimulating hormone (TSH) receptor antibodies bind to and stimulate the thyroid gland, causing excessive production and secretion of thyroxine (T4) and triiodothyronine (T3). The immunoglobulin G (IgG) autoantibodies mimic the action of TSH, but their effects are longer, lasting up to 12 hours compared with 1 hour for normal TSH.
The aberrant immunologic response associated with Graves’ disease targets primarily the thyroid gland but also other tissues, including extraocular muscles and skin. There is a familial tendency and a higher incidence of other autoimmune disorders in patients with Graves’ disease. The disease occurs most often in women (prevalence, 1%–3% in women; 0.1% in men) and between 20 and 50 years of age. Graves’ disease has an unpredictable course marked by relapses and exacerbations.
Pathophysiology
Thyrotoxicosis can also be caused by benign follicular adenomas, which are not believed to have an autoimmune etiology. Exogenous iodine excess (radiocontrast agents or angiography dye) or the administration of thyroid hormones may induce iatrogenic thyrotoxicosis. The antiarrhythmic agent amiodarone is iodine rich and may cause either hypothyroidism or hyperthyroidism. Toxic multinodular goiter, subacute viral thyroiditis, postpartum thyroiditis, TSH-secreting pituitary tumors, and thyroid cancer are less common causes of thyrotoxicosis.
Clinical manifestations
Clinical manifestations associated with thyrotoxicosis reflect the widespread hypermetabolic effects of excess thyroid hormones. Physical signs include tachycardia, tremor, goiter, and muscle weakness. Sleep is often difficult. Weight loss despite increased food consumption, anxiety, fatigue, and heat intolerance are symptoms of thyrotoxicosis.
Signs of ophthalmopathy and dermopathy are associated with Graves’ disease. Thyroid-associated ophthalmopathy may cause proptosis, eye redness, and a gritty sensation in early stages, with diplopia, ocular pain, and (rarely) loss of visual acuity in more advanced stages. Graves’ ophthalmopathy results from cytokine-mediated inflammation and swelling of the periorbital connective tissue and extraocular muscles.
The blood volume increases slightly under the influence of excess thyroid hormone, a result of vasodilation. Mean arterial pressure usually remains unchanged, but the pulse pressure increases. The systolic blood pressure is typically elevated 10 to 15 mmHg, and the diastolic blood pressure is reduced. Blood flow to the skin increases because of the increased need for heat elimination.
The effects of thyrotoxicosis on the heart are pronounced. Palpitations, tachycardia, and cardiac dysrhythmias affect most patients. The cardiac output increases, sometimes to 60% or more above normal. About 10% of thyrotoxic patients have atrial fibrillation. Mitral valve prolapse is more common in patients with Graves’ disease than in the general population. With protracted high thyroid hormone levels, the heart muscle strength may become depressed as a result of protein catabolism. Diagnosis of thyrotoxicosis is more difficult in elderly adults because many of the hyperkinetic manifestations of hyperthyroidism are absent. Elderly patients may initially present with myocardial failure. Hyperthyroid patients may feel a constant fatigue from the exhausting effect of thyroid hormone on the musculature and on the central nervous system.
Diagnosis
The diagnosis of primary disease is biochemically established in most cases by the combined findings of an abnormally high total and unbound serum T3 and T4 assay and depressed TSH levels. With Graves’ disease, the diagnosis may be supported by the presence of stimulatory TSH receptor autoantibodies. An elevated uptake of radioactive iodine by the thyroid gland may be used to confirm gland hyperactivity. Serum alkaline phosphatase and calcium concentrations are mildly elevated in approximately 20% of patients with Graves’ disease.
Other autoimmune diseases such as myasthenia gravis, rheumatoid arthritis, systemic lupus erythematosus, and DM are more common in patients with Graves’ disease.
Treatment
A variety of treatment options are available for patients with Graves’ disease. The three primary treatment options for thyrotoxicosis are radioactive gland ablation, surgery, and antithyroid drug therapy.
Radioactive iodine
A common therapy for Graves’ disease is ablation of the thyroid gland with radioactive iodine. A total of 2 to 4 months is needed to reverse the effects of hyperthyroidism. Hypothyroidism is common after treatment, and it is contraindicated in pregnancy.
Subtotal thyroidectomy
Surgery for treatment of Graves’ disease is an option when antithyroid drugs are ineffective, if radioiodine treatment is refused, in children or pregnant women, or if the thyroid goiter is exceptionally large. Patients should be treated preoperatively with antithyroid medication and rendered euthyroid before surgery. Complications associated with thyroid surgery occur in less than 1% of cases and include damage to the recurrent laryngeal nerve, hypoparathyroidism, and neck hematoma.
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