Test Directory

Distinguish between high T₄ levels due to hyperthyroidism and due to increased binding by TBG in euthyroid individuals who have normal levels of free hormones; document cases of hereditary deficiency or increase of TBG; work-up of thyroid disease. In patients with low T₄, high T₃ (uptake) or the reverse, who clinically seem eumetabolic and have normal FTI, measurement of TBG is only occasionally needed. Some such patients may have hereditary anomalies of TBG. TBG is increased by estrogens, tamoxifen, pregnancy, perphenazine, and in some cases of liver disease, including hepatitis. Decreased TBG is found with some instances of chronic liver disease, nephrosis and systemic disease, and with large amounts of glucocorticoids, androgens/anabolic steroids, and acromegaly. Although alterations of TBG are usually resolved by the thyroid profile, TBG must occasionally be directly measured.

Kindreds are described with elevated TBG and hyperthyroxinemia as a harmless genetic abnormality. They have normal levels of TSH and free T₄ and decreased T₃ uptake. Structural variants of TBG are inherited as X-chromosome-linked traits, most inherited structural abnormalities in TBG cause decreased affinity for thyroid hormone.

Specimen Type: Serum

Collection Container: Gold Top, Serum Separator

Alternate Collection Container: Red Top, Plain

Desired Specimen Volume: 0.8 mL

1. Collect specimen in gold top, serum separator tube via venipuncture.

1. Separate serum from cells
2. Transfer 0.8 mL of serum to a clear aliquot tube

Transport to the laboratory refridgerated. 

• Gross hemolysis

See patient report.

TBG is normal in familial dysalbuminemic hyperthyroxinemia, an entity which can be incorrectly identified as thyrotoxicosis. Triiodothyronine uptake was described as having produced information equivalent to TBG in a study of 372 subjects.