The clinical presentation of<unk>  depend on the time of onset as well as the severity of the defect. Diagnostic tests to measure GnRH levels are difficult. This is because GnRH is confined within hypophyseal portal system and has a short half-life of 2–4 minutes. GnRH levels are thus checked indirectly via LH and FSH levels which will be totally or partially absent in<unk> . Exogenous GnRH can be used as a diagnostic tool. If the patient has hypothalamic GnRH deficiency, LH and FSH will gradually appear in response to the exogenous GnRH but in pituitary cases of<unk> , a minimal response will be generated. Typically, CHH is diagnosed in adolescence due to a lack of pubertal development, but it can be possible to diagnose in male neonates. Clinical presentations of CHH involve an absence of puberty by 18 years of age, poorly developed secondary sexual characteristics, or infertility. In men with CHH, serum levels of inhibin B are typically very low as inhibin B is a marker of Sertoli cell number. For females, CHH is most commonly revealed by primary amenorrhea. Breast development is variable and pubic hair may or may not be present. CHH can be diagnosed in the male neonate with cryptorchidism (maldescended testes) and a micropenis as signs of GnRH deficiency. There are no clear signs of CHH in female neonates. Another clinical sign of CHH, more specifically Kallmann syndrome, is a lack of a sense of smell due to the altered migration of GnRH neurons on the olfactory placode. Kallmann syndrome can also be shown through MRI imaging with irregular morphology or aplasia of the olfactory bulb and olfactory sulci. Anterior pituitary function must be normal for all other axes in CHH as it is an isolated disorder. Testing anterior pituitary function is helpful to identify if the<unk>  is due to hyperprolactinemia.
Hypogonadotropic hypogonadism
Hypergonadotropic hypogonadism
Late-onset hypogonadism
Isolated hypogonadotropic hypogonadism
Polyorchidism
Hypergonadotropic hypergonadism
Microorchidism
Dual-role transvestism