Thyroxine Binding Globulin LabCorp

Distinguish between high T(4) 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 T(4), high T(3) (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 T(4) and decreased T(3) uptake.[2] Structural variants of TBG are inherited as X-chromosome linked traits, most inherited structural abnormalities in TBG cause decreased affinity for thyroid hormone.[3]