Evaluation of thyroid status in patients with thyrotoxicosis

Abstract

Abstract The generic term thyrotoxicosis defines the clinical syndrome of hypermetabolism associated with excess amounts of circulating free thyroxine (T4) and (or) triiodothyronine (T3) concentrations, irrespective of the source of the excess hormones. The term hyperthyroidism is reserved for those patients with thyrotoxicosis caused by increased synthesis and secretion of thyroid hormones from the gland due either to thyroid stimulators in the blood or to autonomously functioning thyroid nodules and is almost always associated with an increased radioactive iodine uptake (RAIU) by the thyroid. Another major cause of thyrotoxicosis is increased release of thyroid hormone from the gland, not associated with increased synthesis, caused by inflammatory changes, and always associated with a low thyroid RAIU. The most common miscellaneous cause of thyrotoxicosis is the exogenous ingestion of excess thyroid hormone, associated with a low thyroid RAIU. The serum concentration of thyrotropin (TSH) is low in all causes of thyrotoxicosis, except for TSH-secreting pituitary tumors and selective pituitary resistance to thyroid hormones. Anti-thyroglobulin and anti-thyroid peroxidase antibodies are present in patients with autoimmune thyroid disease, and serum thyroglobulin is increased in all patients with thyrotoxicosis except those with thyrotoxicosis facticia. A decreased serum TSH and normal concentrations of serum free T4 and T3 define the syndrome of subclinical thyrotoxicosis.