Maternal hyperthyroidism and neonatal testicular dysfunction.

What is it about?

The functions of hypothalamic-pituitary-thyroid axis (HPTA) are warranted for the developing newborns, specifically the developing testes (spermatogenesis, sperm mobility and eventually fertility). During the different developmental periods, the 3,5,3'-triiodothyronine (T3) and its receptors and transporters can regulate the proliferation of the Sertoli and Leydig cells, steroidogenesis, and testicular development and maturation. There are association between the hyperthyroidism and disorders in the testes. In men, hyperthyroidism caused oligospermia, delayed the mobility of the spermatozoa, and decreased the total sperm counts, libido, and semen quality. Also, Grave’s disease damaged the sexual maturation, and caused hypospermia, teratospermia, asthenospermia, necrospermia and oligospermia. In addition, precocious ejaculation, erectile dysfunction, and sexual disorders were noticed during the hyperthyroidism. The volume and function of the prepubertal testicular were decreased due to the harmful effects of the hyperthyroidism. On the other hand, the treatment of thyrotoxicosis might improve the density and motility of the sperm, but no change was observed in the morphology of the sperm or the erectile complaints. Thus, the maternal hyperthyroidism may directly or indirectly delay the morphogenesis and functional development of the neonatal testis. This may perturb the structure of the sperm, decrease the quality, and amount of the semen, and cause infertility. Thus, the management of the maternal hyperthyroidism can be necessary to prevent these syndromes. This would afford improvement in maximizing the fertility consequence. However, it remains to be shown whether the severity of the hyperthyroidism during the gestation may cause more persistent perturbations in the neonatal testes. The molecular, biochemical and developmental mechanisms are required to explore these abnormal conditions.

Featured Image

Why is it important?

The maternal hyperthyroidism may directly or indirectly delay the morphogenesis and functional development of the neonatal testis. This may perturb the structure of the sperm, decrease the quality, and amount of the semen, and cause infertility. Thus, the management of the maternal hyperthyroidism can be necessary to prevent these syndromes. This would afford improvement in maximizing the fertility consequence.

Perspectives