ABS1073 Sigma-AldrichAnti-Dio3 Antibody

Type 3 iodothyronine deiodinase (D3) is the major physiologic inactivator of thyroid hormone. This selenoenzyme, previously identified in human placenta and brain, catalyzes the inner-ring deiodination of T(4) to reverse T(3) and T(3) to 3, 3'-diiodothyronine, both of which are biologically inactive. We analyzed D3 expression in several human adult and fetal tissues by immunohistochemistry and correlated the results with D3 activity assays where possible. High D3 expression was present in the placental syncytiotrophoblasts and cytotrophoblasts, endothelium of fetal vessels, and maternal decidua. D3 was also present at other sites of maternal-fetal interface, including the umbilical arteries and vein and the fetal respiratory, digestive, and urinary tract epithelium. Surprisingly, D3 was also present in the endometrial glands of nonpregnant human uteri, and endometrial activity approximated that of term placenta. The presence of D3 at maternal-fetal interfaces is consistent with its role in modulating the thyroid status of the human fetus and its expression in endometrium suggests that local regulation of thyroid status is important in implantation.

We present a 21-yr-old female with a large hepatic vascular tumor and subclinical hypothyroidism. A high level of the thyroid hormone inactivating enzyme type 3 iodothyronine deiodinase (D3) was detected in her tumor, and the TSH of 26.2 mU/liter returned to normal after surgical resection of the mass. This indicates that the vascular tumor caused this adult's hypothyroidism as has now been documented in nine infants with this syndrome. This first example of consumptive hypothyroidism in an adult indicates that the inactivation rate of thyroid hormone by D3 in a vascular tumor can stress the secretory capacity even of the TSH-stimulated normal adult thyroid gland.