TBG excess production can be hereditary, which is X-linked dominant transmission, or it can be secondary to excess estrogens, as in pregnancy, use of oral contraceptives, hormone replacement, and medications like raloxifene or tamoxifen [4, 5]. The
more highly sialylated TBG is cleared
more slowly from plasma than the
more positively charged TBG, because sialylation inhibits the hepatic uptake of glycoproteins.