Background: Human chorionic gonadotropin (hCG)-induced hyperthyroidism represents a rare paraneoplastic syndrome in hCG-secreting testicular cancer. In most cases, this hyperthyroidism remains subclinical. hCG belongs to the family of glycoprotein hormones with structural homology to thyroid- stimulating hormone (TSH). The thyrotropic potency and thereby the degree of cross reactivity of hCG is determined by several factors, such as content of sialic acid or lack of the C-terminal tail. In the absence of clinical signs of hyperthyroidism, treatment usually consists of specific antitumor therapy which will result in normalization of thyroid function if hCG declines. Where there are clinical signs of hyperthyroidism, overlapping thyreostatic treatment is recommended.
Case report: Here, we report of a young man presenting biochemical signs of hyperthyroidism without clinical signs at the time of diagnosis of non-seminomatous germ cell cancer. Beta-hCG initially exceeded 1,000,000 IU/ml and declined close to normal at the end of cancer treatment. Concomitantly, thyroid hormones returned to the normal range without any thyreostatic therapy. We observed a significant correlation of neta-hCG and thyroid hormones in linear regression analysis (r2 = 0.98, p< 0.05). A concise overview of potential mechanisms of hCG-induced hyperthyroidism in germ cell cancer but also in pregnancy is given and the case discussed according to the cited literature.