Pitfalls to Avoid While Interpreting Thyroid Function Tests: Five Illustrative Cases

Michael J. Fowler, MD, Aaron F. Pannone, BA, Lewis S. Blevins, Jr., MD


South Med J. 2002;95(5) 

In This Article

Case 4

A 24-year-old woman was referred for evaluation of a discrepancy in thyroid function tests. She complained of fatigue, weight gain, heavy frequent menses, and cold intolerance. Physical examination had been remarkable for diastolic hypertension, a goiter, dry skin, and delayed relaxation of the deep tendon reflexes. Laboratory values were serum TSH 150 µU/mL, a free T4 of 0.5 ng/mL, and a total T3 of 65 ng/dL (normal, 80 to 160 ng/dL). Thyroid antibodies were positive. An I-123 scan showed a heterogeneous pattern of radiotracer distribution throughout the thyroid, and the 6-hour uptake was elevated at 58% (normal, 10% to 25%), which was thought to be consistent with Graves' disease. Based on the scan findings, the treating physician suspected a diagnosis of TSH-mediated hyperthyroidism.


This case illustrates the confusion that can result when thyroid function tests and thyroid scans are not interpreted in conjunction with one another. Clearly, based on the levels of TSH, free T4, and total T3, and the thyroid antibody test results, this patient has hypothyroidism due to autoimmune thyroid disease.

Hyperthyroid states caused by TSH (eg, TSH-secreting pituitary adenomas and central or pituitary thyroid-hormone resistance) are associated with clinical findings of hyperthyroidism and elevated T4 and T3 levels.[22] Levels of TSH are either inappropriately normal or elevated in these disorders, since hypersecretion of TSH is the result of abnormalities in thyrotroph function. In the patient presented, TSH levels are elevated due to thyrotroph secretion of TSH in response to thyroid failure, as evidenced by low T4 and T3 levels.

Provided that the thyroid mechanisms of uptake of iodide and other similarly sized molecules (eg, pertechnetate) are conserved in a disease state, any cause of hypersecretion of TSH will be associated with increased uptake of radiotracer during a thyroid scan.[23,24] In this patient, despite the autoimmune thyroid disease, iodide uptake and trapping were obviously preserved. These events are regulated by TSH and other stimulators of thyroid function (thyroid stimulating immunoglobulins in Graves' disease and human chorionic gonadotropin in pregnancy and choriocarcinoma).[25] It stands to reason that increases in these thyroid stimulators will lead to increases in radioiodine (or pertechnetate) uptake when the mechanisms of iodide incorporation have been preserved. Disorders characterized by areas of thyroid autonomy and excessive secretion of T4 and T3 (eg, toxic multinodular goiter, toxic adenoma), where iodide uptake is increased independent of TSH, which is usually suppressed, may also be associated with elevated radioiodine uptake. Subacute, postpartum, and chronic lymphocytic thyroiditis are associated with sufficient thyroidal inflammation and destruction and, when these patients are hyperthyroid, low TSH levels.[26] As a result, these disorders are typically associated with low radioiodine uptake.