Although factitious thyrotoxicosis involves all situations in which usage of (excessive doses) thyroid hormone leads to symptoms of thyrotoxicosis, the term "factitious" is usually associated with surreptitious ingestion of thyroid hormone in supraphysiological doses. Patients usually deny taking thyroid hormones in excess. This primarily psychiatric disorder may lead to wrong diagnosis and treatment if physicians are not aware of the phenomenon. Patients are clinically thyrotoxic, however they do not show eyesigns as seen in Graves' disease, except for those related to sympathetic overactivity (lid retraction). Deliberate intake of high doses of thyroid hormone leads to TSH suppression and shrinkage of the thyroid, so that no thyroid tissue is palpated. Serum TSH and the uptake of 123-I or TcO4- are all suppressed. Color flow Doppler sonography shows absent thyroidal vascularity and low-normal peak systolic velocity, while with this technique these signs are increased in Graves' disease. (49a) Thus, factitious thyrotoxicosis is not difficult to differentiate from thyrotoxic Graves' disease, toxic adenoma or toxic multinodular goiter. In subacute (De Quervain's) thyroiditis symptoms are typical in that, apart from thyrotoxicosis, patients may have fever in the initial phase of the disease and the thyroid is very tender. Silent thyroiditis however, is not so easily distinguished from thyrotoxicosis factitia. In both situations the uptake of radioactive iodine is suppressed and patients lack eyesigns. However, in patients with silent thyroiditis a palpable firm painless thyroid gland is present. Furthermore patients with silent thyroiditis show high levels of thyroglobulin. In thyrotoxicosis factitia excessive intake of thyroid hormone leads to suppression of TSH and therefore also to suppression of thyroglobulin leakage from the thyroid gland. Mariotti et al. (50) performed thyroglobulin measurements in 6 women with thyrotoxicosis factitia. They used a very sensitive thyroglobulin assay and excluded the presence of thyroglobulin antibodies that can interfere with the assay. In all 6 women thyroglobulin was undetectable in the serum (lower detection limit 1.25 ng/ml) (Table 13-5).

The possibility of this syndrome should be considered especially when thyrotoxicosis appears to be resistant to treatment or where laboratory data are contradictory. Patients may be very persistent in denying the deliberate intake of thyroid hormone and persist in this attitude even after factitious thyrotoxicosis has been unequivocally confirmed. Consultation with a psychiatrist is urgently needed in such patients.

Suppressed radioactive uptake of the thyroid gland in combination with thyrotoxicosis may also exist in patients with hyperfunctioning metastases of follicular thyroid carcinoma. However, in these extremely rare patients, thyroglobulin levels are almost invariably elevated and radioactive iodine uptake will be detected in metastases by using whole body scanning.

It should be noted that the profile of serum thyroid hormones in thyrotoxicosis factitia is determined by the composition of the preparation ingested. Both T4 and T3 are elevated in overdose of L-thyroxine and desiccated thyroid, whereas only T3 is elevated and T4 is low or non-detectable when preparations containing only T3 are being taken. Treatment of thyrotoxicosis factitia is not difficult with regard to thyrotoxic symptoms, as discontinuation of thyroid hormone ingestion is usually sufficient. In more severe cases treatment with propranolol may be helpful. However, treatment of the psychiatric disorder is more challenging and may fail in the long run.

Thyrotoxicosis induced by excessive thyroid hormone intake, not based on deliberate choice of the patient, has been observed in the "hamburger thyrotoxicosis" patients. Two epidemics of thyrotoxicosis in the United States were caused by inclusion of bovine thyroid in hamburger (51,52). Inclusion of the thyroid in neck muscle trimmings is now prohibited by US Department of Agriculture regulations.

Prescription of supranormal amounts of thyroid hormone to suppress serum TSH for medical reasons can be designated as iatrogenic (usually subclinical) thyrotoxicosis. TSH suppression is usually given in patients after thyroidectomy for thyroid carcinoma and also to suppress benign thyroid growth in goiter patients. It is discussed further in the relevant chapters. Long-term use of suppressive amounts of thyroid hormone has been reported to enhance osteoporosis and also cause cardiac abnormalities including arrhythmias and function disturbances (53,54), but other studies have not confirmed these findings (55-56)