Subclinical hypothyroidism, defined as an elevated TSH level and normal thyroid hormone levels, occurs in 4–10% of the general population and increases to 20% in women older than age 50. Levothyroxine should be individualized based on the risks and benefits of treatment. The consensus of expert thyroid organizations concluded that thyroid hormone therapy should be considered for patients with TSH levels greater than 10 mIU/L while close TSH monitoring is appropriate for those with lower TSH elevations.
E. Drug-Induced Hypothyroidism
Drug-induced hypothyroidism (Table 38–3) can be satisfactorily managed with levothyroxine therapy if the offending agent cannot be stopped. In the case of amiodarone-induced hypothyroidism, levothyroxine therapy may be necessary even after discontinuance because of amiodarone’s very long half-life.
Hyperthyroidism (thyrotoxicosis) is the clinical syndrome that results when tissues are exposed to high levels of thyroid hormone (Table 38–4).
The most common form of hyperthyroidism is Graves’ disease, or diffuse toxic goiter. The presenting signs and symptoms of Graves’ disease are set forth in Table 38–4.
Graves’ disease is considered to be an autoimmune disorder in which a defect in suppressor T lymphocytes stimulates B lymphocytes to synthesize antibodies (TSH-R Ab [stim]) to thyroidal antigens. The TSH-R Ab [stim] is directed against the TSH receptor in the thyroid cell membrane and stimulates growth and biosynthetic activity of the thyroid cell. Genetics, the postpartum state, cigarette smoking, and physical and emotional stress increase TSH-R Ab [stim] development. A genetic predisposition is shown by a high frequency of HLA-B8 and HLA-DR3 in Caucasians, HLA-Bw46 and HLA-B5 in Chinese, and HLA-B17 in African Americans. Spontaneous remission occurs but some patients require years of antithyroid therapy.
In most patients with hyperthyroidism, T3, T4, FT4, and FT3 are elevated and TSH is suppressed (Table 38–2). Radioiodine uptake is usually markedly elevated as well. Antithyroglobulin, thyroid peroxidase, and TSH-R Ab [stim] antibodies are usually present.
Management of Graves’ Disease
The three primary methods for controlling hyperthyroidism are antithyroid drug therapy, destruction of the gland with radioactive iodine, and surgical thyroidectomy. None of these methods alters the underlying pathogenesis of the disease.
A. Antithyroid Drug Therapy
Drug therapy is most useful in young patients with small glands and mild disease. Methimazole (preferred) or propylthiouracil is administered until the disease undergoes spontaneous remission. This is the only therapy that leaves an intact thyroid gland, but it does require a long period of treatment and observation (12–18 months), and there is a 50–60% incidence of relapse.