| 概要 |
Hyperthyroidism is a pathological disorder characterised by increased thyroid hormone synthesis and secretion from the thyroid gland. The term thyrotoxicosis is not synonymous with hyperthyroidism. Thyrotoxicosis is defined as the clinical syndrome of hypermetabolism resulting from increased thyroid hormone levels, irrespective of the source. The causes of hyperthyroidism include Graves' disease, toxic multinodular goiter, and solitary toxic adenoma. Less common causes of hyperthyroidism include thyrotropin-induced thyrotoxicosis and trophoblastic tumours. The causes of thyrotoxicosis without hyperthyroidism are less common and generally transient. In patients with silent thyroiditis, post-partum thyroiditis, or subacute painful thyroiditis, the destruction of thyrocytes leads to release of preformed hormones into the circulation. Drug-induced thyrotoxicosis has the same pathogenic mechanism as thyroiditis. Exogenous thyrotoxicosis develops after ingestion of excessive amounts of thyroid hormone, and is associated with low serum thyroglobulin concentrations. Patients of hyperthyroidism/thyrotoxicosis usually have fatigue, nervousness or anxiety, weight loss, palpitations, and heat sensitivity. Clinical findings almost always include tachycardia, warm moist skin, the presence of an enlarged thyroid, and a slight tremor. The three options for treating patients with hyperthyroidism are antithyroid drugs (ATDs), radioactive iodine ablation, and surgery. All three therapeutic options would be effective in the treatment of patients with Graves' disease, whereas patients with toxic adenoma or toxic multinodular goiter should have either radioactive iodine therapy or surgery, since these patients rarely go into remission. In patients with toxic nodular goiter, ATDs are generally used to restore euthyroidism before definitive treatment with surgery or radioactive iodine, and infrequently used as long-term treatment when the other two therapies are contraindicated or the patient has a short life expectancy.
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