iates this source of error and is the best test.
In the presence of typical symptoms, one measurement of suppressed TSH or elevated FT4 is sufficient to make a definite diagnosis, although it does not identify a cause. If the FT4 is normal, repetition is in order to rule out error, along with a second test such as serum FT3. A variety of methods for FT4 determination have become available, including commercial kits. Although these methods are usually reliable, assays using different kits do not always agree among themselves or with the determination of free T4 by dialysis. Usually T4 and T3 levels are both elevated in thyrotoxicosis, as is the FTI (Free Thyroxin Index), or an index constructed using the serum T3 and rT3U levels, and the newer measures of FT3.
|Table 3. Conditions Associated with Transient Elevations of the FT4 or FTI|
|Estrogen withdrawal||Rapid decrease in TBG level|
|Amphetamine abuse||Possibly induced TSH secretion(2)|
|Hyperemesis gravidarum||hCG, can cause thyrotoxicosis|
|Iodide administration||Thyroid autonomy|
|Beginning of T4 administration||Delayed T4 metabolism(3)|
|Severe illness (rarely)||Decreased T4 to T3 conversion (4)|
|Amiodarone treatment||Decreased T4 to T3 conversion, iodine load|
|Gallbladder contrast agents||Decreased T4 to T3 conversion, iodine load|
|Propranolol (large doses)||Inhibition of T4 to T3 conversion|
|Prednisone (rarely)||Inhibition of T4 to T3 conversion|
|High altitude exposure||Possibly hypothalamic activation|
|Selenium deficiency||Decreased T4 to T3 conversion|
T3 and FT3 ASSAY–
The serumT3 level determined by RIA is almost always elevated in thyrotoxicosis and is a useful but not commonly needed secondary test. Usually the serum T3 test is interpreted directly without use of a correction for protein binding, since alterations of TBG affect T3 to a lesser extent than T4. Any confusion caused by alterations in binding proteins can be avoided by use of a FT3 assay or T3 index calculated as for the FTI. Generally the FT3 assay is as diagnostically effective as the FT4. In patients with severe illness and thyrotoxicosis, especially those with liver disease or malnutrition or who are taking steroids or propranolol, the serum T3 level may not be elevated, since peripheral deiodination of T4 to T3 is suppressed (“T4 toxicosis”). A normal T3 level has also been observed in thyrotoxicosis combined with diabetic ketoacidosis. Whether or not these patients actually have tissue hypermetabolism at the time their serum T3 is normal is not entirely certain. In these patients the rT3 level may be elevated. If the complicating illness subsides, the normal pattern of elevated T4 , FTI, and T3 levels may return(5,6). Elevated T4 levels with normal serum T3 levels are also found in patients with thyrotoxicosis produced by iodine ingestion(7).
Since 1957, when the first patient with T3 thyrotoxicosis was identified, a number of patients have been detected who had clinical thyrotoxicosis, normal serum levels of T4 and TBG, and elevated concentrations of T3 and FT3. Hollander et al  found that approximately 4% of patients with thyrotoxicosis in the New York area fit this category. These patients often have mild disease but otherwise have been indistinguishable clinically from others with thyrotoxicosis. Some have had the diffuse thyroid hyperplasia of Graves’ disease, others toxic nodular goiter, and still others thyrotoxicosis with hyperfunctioning adenomas. Interestingly, in Chile, a country with generalized iodine deficiency, 12.5% of thyrotoxic subjects fulfilled the criteria for T3 thyrotoxicosis . Asymptomatic hypertriiodothyronemia is an occasional finding several months before the development of thyrotoxicosis with elevated T4 levels . Since T4 is normally metabolized to T3, and the latter hormone is predominantly the hormone bound to nuclear receptors, it makes sense that elevation of T3 alone can produce thyrotoxicosis.
Thyroid Isotope uptake
In patients with thyrotoxicosis the RAIU (Radioactive Iodine Uptake) at 24 hours is characteristically above normal. In the United State