Abstract
Human chorionic gonadotropin (HCG) is a member of the glycoproteins family synthesized by the placenta, which consists of 2 noncovalently joined subunits (alpha(α) and beta(β)). The α- and β-subunits have a structural homology with the α- and β-subunits of TSH and LH. The thyrotropic action of HCG results from its structural similarity to TSH, so β-HCG can bind to the TSH receptor in the thyroid gland. A high level of HCG accompanied by an increased thyroid hormone level, can be observed in gestational trophoblastic disease (GTD), such as a hydatidiform mole or a choriocarcinoma, but the clinical symptoms of hyperthyroidism are rarely observed. We experienced a case of Hashimoto's thyroiditis, where the patient was diagnosed with T3-thyrotoxicosis, which had initially been induced by excess β-HCG due to an H-mole; after evacuation of the H-mole, the condition was diagnosed as hypothyroidism.
It has been speculated that a patient with Hashimoto's thyroiditis could have hyperthyroidism, induced by β-HCG, due to an H-mole.
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