Hypergonadotropic hypogonadism

Hypergonadotropic hypogonadism (HH), also known as primary or peripheral/gonadal hypogonadism, is a condition which is characterized by hypogonadism due to an impaired response of the gonads to the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), and in turn a lack of sex steroid production and elevated gonadotropin levels (as an attempt of compensation by the body). HH may present as either congenital or acquired, but the majority of cases are of the former nature.[1][2]

Causes

There are a multitude of different etiologies of HH. Congenital causes include the following:[1][3][4]

Acquired causes (due to damage to or dysfunction of the gonads) include ovarian torsion, vanishing/anorchia, orchitis, premature ovarian failure, ovarian resistance syndrome, trauma, surgery, autoimmunity, chemotherapy, radiation, infections (e.g., sexually-transmitted diseases), toxins (e.g., endocrine disruptors), and drugs (e.g., antiandrogens, opioids, alcohol).[1][3][4]

Symptoms

See also: hypogonadism

Examples of symptoms of hypogonadism include delayed, reduced, or absent puberty, low libido, and infertility.

Treatment

Treatment of HH is usually with hormone replacement therapy, consisting of androgen and estrogen administration in males and females, respectively.[3]

See also

References

  1. 1 2 3 John P. Mulhall (22 April 2011). Cancer and Sexual Health. Springer. pp. 207–208. ISBN 978-1-60761-915-4. Retrieved 10 June 2012.
  2. Ramón Piñón (1 January 2002). Biology of Human Reproduction. University Science Books. p. 363. ISBN 978-1-891389-12-2. Retrieved 10 June 2012.
  3. 1 2 3 Marschall Stevens Runge; Cam Patterson (20 June 2006). Principles of Molecular Medicine. Humana Press. p. 463. ISBN 978-1-58829-202-5. Retrieved 10 June 2012.
  4. 1 2 J. Larry Jameson (1998). Principles of Molecular Medicine. Humana Press. p. 601. ISBN 978-0-89603-529-4. Retrieved 10 June 2012.


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