Thyroxine sulfate (T4S) is a normal component of human serum and amniotic fluid, and it is mostly derived from thyroxine peripherally and accumulates when type I 5-monodeiodinating activity is low in fetuses or inhibited by drugs, such as ipodate.

Significant amounts of thyroxine sulfate (T4S) in fetal sheep serum, meconium, bile, and amniotic and allantoic fluids are observed. T4S concentration in amniotic fluid from women at 18-19 weeks of gestation (25.5 ng/dL) is higher than that at 14-15 weeks of gestation (14.3 ng/dL). A significant rise in serum T4S is detected in hyperthyroid patients 1 day after ingestion of 1 g of ipodate. Thyroxine undergoes significant sulfation in rats, and biliary excretion of T4S is enhanced if its type I deiodination is inhibited. Serum T4S levels are clearly elevated compared with healthy references, and the decreased deiodination by liver D1 during critical illness appears to play a role in this increase in serum T4S levels.