Mechanisms of Central Hypogonadism

Reproductive function depends upon an operational hypothalamo–pituitary–gonadal (HPG) axis. Due to its role in determining survival versus reproductive strategies, the HPG axis is vulnerable a diverse plethora of signals that ultimately manifest with Central Hypogonadism (CH) all many guises. Acquired CH can result from any pituitary or hypothalamic lesion, including treatment (such as surgical resection and/or radiotherapy). The particularly sensitive suppressive effects hyperprolactinaemia occur for reasons, prolactinomas, and side effect certain drug therapies. Physiologically, prolactin (combined autonomic neural suckling) plays key suppressing gonadal establishing temporary during lactation. Leptin further endocrine regulator During starvation, hypoleptinaemia (from diminished fat stores) results activation agouti-related peptide neurons have dual purpose enhance appetite (important survival) concomitantly suppresses GnRH via on kisspeptin release. Obesity associated hyperleptinaemia leptin resistance may also suppress suppressibility leaves it external include morphine, anabolic-androgenic steroids, physical trauma stress, which are relatively common causes CH. Finally, susceptible congenital malformations, reports mutations within >50 genes CH, Kallmann Syndrome hyposmia anosmia (reduction loss sense smell due closely migration olfactory embryogenesis). Analogous itself, patients often vulnerable, their clinical management requires both sensitivity empathy.