Background:

Thyroxine sulfate is a thyroid hormone metabolite.

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[1].

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[1]. Thyroxine undergoes significant sulfation in rats, and biliary excretion of T4S is enhanced if its type I deiodination is inhibited[2]. 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[3].

[1]. Wu SY, et al. Identification of thyroxine-sulfate (T4S) in human serum and amniotic fluid by a novel T4S radioimmunoassay. Thyroid. 1992 Summer;2(2):101-5. [2]. Rutgers M, et al. Effects of propylthiouracil on the biliary clearance of thyroxine (T4) in rats: decreased excretion of 3,5,3’-triiodothyronine glucuronide and increased excretion of 3,3’,5’-triiodothyronine glucuronide and T4 sulfate. Endocrinology. 1989 Oct;125(4):2175-86. [3]. Peeters RP, et al. Increased thyroxine sulfate levels in critically ill patients as a result of a decreased hepatic type Ideiodinase activity. J Clin Endocrinol Metab. 2005 Dec;90(12):6460-5.