Use
Measuring total T4 (thyroxine) levels in an outpatient setting is a valuable tool for assessing thyroid function and optimizing overall health and hormone balance. Total T4 reflects the amount of circulating thyroid hormone, which plays a crucial role in metabolism, energy production, and overall well-being. This test is particularly useful in detecting thyroid disorders such as hypothyroidism or hyperthyroidism, which can significantly impact mood, weight, and cardiovascular health. When interpreted alongside other thyroid markers like TSH and free T4, total T4 helps guide personalized treatment strategies, ensuring optimal hormonal balance and long-term health.
Decreased in hypothyroidism and in the third stage of (painful) subacute thyroiditis; increased with hyperthyroidism, with subacute thyroiditis in its first stage and with thyrotoxicosis due to Hashimoto disease. Used to diagnose T4 toxicosis.
T4 may be increased with excess intake of iodine or with surreptitious use of thyroxine. T4 levels may be abnormal in the presence of systemic nonthyroidal disease. Alterations in binding capacity or quantity of TBG may increase or decrease total thyroxine without causing symptoms. A common cause of elevated T4 in nonthyroidal disease is said to be liver disease. Serum thyroxine and free thyroxine index (FTI) are increased in familial dysalbuminemic hyperthyroxinemia, a euthyroid syndrome in which an abnormal binding site has affinity for thyroxine. The T3 is usually normal in this entity, as is T3 uptake (THBR). Thus, T3 uptake is commonly ordered with T4.
The combination of the serum T4 and T3 uptake (THBR) as an indirect assessment of TBG, helps to determine whether an abnormal T4 value is due to alterations in serum thyroxine-binding globulin or to changes of thyroid hormone levels. Deviations of both tests in the same direction usually indicate that an abnormal T4 is due to abnormalities in thyroid hormone. Deviations of the two tests in opposite directions provide evidence that an abnormal T4 may relate to alterations in TBG.
Causes of increased TBG binding include neonatal state, molar and conventional pregnancy, estrogens, oral contraceptives, heroin, methadone, 5-fluorouracil, clofibrate, infectious hepatitis, chronic active hepatitis, and primary biliary cirrhosis, acute intermittent porphyria, lymphoma, and hereditary TBG increase.
Amphetamines, iopanoic acid, ipodate, and amiodarone increase thyroxine. High dose propranolol may elevate T4 and FTI levels.
Causes of decreased TBG binding include abnormal protein states especially nephrotic syndrome, androgens, anabolic steroids, prednisone, acromegaly, liver or other systemic illness, severe stress or hereditary TBG deficiency. Salicylates and diphenylhydantoin may lower T4 significantly. Amiodarone may cause increased thyroxine levels and can cause hypothyroidism or hyperthyroidism.
Lithium carbonate may cause goiter with or without hypothyroidism.
Carbamazepine (Tegretol®) is reported to cause decreased values in thyroid function tests.
Preparation
Samples should not be collected during or soon after the administration of heparin. It is recommended to stop biotin consumption at least 72 hours prior to the collection of a sample.
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