Because of the increase in sex hormone–binding globulin (SHBG) with aging, total testosterone level is a less sensitive indicator of hypogonadism after age 50. Some syndromes of hypogonadism (eg, cryptorchidism, some systemic disorders) affect sperm production more than testosterone levels. When primary hypogonadism affects testosterone production, testosterone is insufficient to inhibit production of FSH and LH; hence, FSH and LH levels are elevated. It may result from a disorder of the testes (primary hypogonadism) or of the hypothalamic-pituitary axis (secondary hypogonadism). Endocrinologists diagnose the condition using hormone tests and imaging and treat it with testosterone therapy, lifestyle changes, and fertility-preserving methods. Treatment aims to bring testosterone back to normal levels, reduce symptoms, and improve overall quality of life.
Primary hypogonadism requires no further investigation into the cause, although some clinicians do a karyotype to definitively diagnose or exclude Klinefelter syndrome. Klinefelter syndrome should be considered in adolescent males in whom puberty is delayed, young men with hypogonadism, and all adult men with very small testes and/or azoospermia (absent sperm in semen). Adult-onset testosterone deficiency has varied manifestations depending on the degree and duration of the deficiency. As adults, affected patients have poor muscle development, a high-pitched voice, a small scrotum, decreased phallic and testicular growth, sparse pubic and axillary hair, and an absence of body hair. Childhood-onset testosterone deficiency (see Male Hypogonadism in Children) is unrecognized until puberty is delayed. Second- or third-trimester onset of testosterone deficiency results in microphallus and undescended testes. Congenital hypogonadism of first-trimester onset results in inadequate male sexual differentiation (see also Sexual Differentiation, Adrenarche, and Puberty).
Further improvement in these symptoms may be seen after longer term use (9,29,32,67). Oral testosterone undecanoate, however, bypasses first-pass metabolism through its preferential absorption into the lymphatic system. The modified testosterone 17α-methyl testosterone, however, has delayed metabolism in the liver. The testosterone pellets are usually implanted under the skin of the lower abdomen using a trochar and cannula or are inserted into the gluteus muscle.
Prostate volume does, however, increase during testosterone therapy usually in the first 6 months, but this is usually to the normal volume seen in eugonadal men. At 3 months and 1 year after starting therapy, the clinical response of testosterone should be evaluated by documenting serum testosterone levels, monitoring serum PSA levels, and performing a DRE. As a result of the concerns about prostate cancer it is important to monitor PSA levels and perform a DRE regularly during the course of treatment. Once testosterone replacement therapy has started, patients need to be carefully monitored. Although it is an effective oral androgen formulation, it is not recommended as a testosterone therapy for hypogonadism because of its hepatotoxic side effects and its association with long-term development of liver tumours.
There is a high prevalence of hypogonadism in the older adult male population and the proportion of older men in the population is projected to rise in the future.
Primary hypogonadism involves failure of the testes to respond to follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Treatment varies with etiology but typically includes gonadotropin-releasing hormone, gonadotropin, or testosterone replacement. A tailored treatment plan helps improve symptoms and overall quality of life. Secondary hypogonadism happens when the brain fails to signal the testes to make enough testosterone.

Gender: Female

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