Abstract
Testis was considered unresponsive to thyroid hormone for a long time. However, like in animals, the presence of thyroid hormone receptors in different testicular cell types was demonstrated also in humans. Accordingly, thyrotoxicosis and hypothyroidism have remarkable effects on testicular function and more extensively on fertility. Thyrotoxicosis and hypothyroidism are associated with changes affecting the endocrine, sexual, or reproductive functions. Particularly, compared with controls, hyperthyroid patients have higher serum SHBG and lower free and bioavailable testosterone concentrations, a higher rate of astheno-zoospermia, oligo-zoospermia, and terato-zoospermia, and a higher prevalence of sexual disturbances, such as premature ejaculation. In hypothyroid patients, hormonal changes are in the opposite direction compared with hyperthyroid patients. Thyroid hormone regulates a number of functions in the testis, such as proliferation and differentiations of non-germ cells, steroidogenesis, and sperm motility. Furthermore, thyroid hormone regulates testicular redox status. Consequently, thyroid hormone excess or deficiency can affect testicular function at different levels. In view of the high prevalence of thyrotoxicosis and hypothyroidism, a considerable part of infertile patients may harbor overt or subclinical thyroid disease. Identification and management of thyrotoxicosis/hypothyroidism associated infertility needs the collaboration of andrologists, endocrinologists, gynecologists, and general practitioners.
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