Hyperestrogenism

Hyperestrogenism
Specialty	Endocrinology

Hyperestrogenism, hyperestrogenic state, or estrogen excess, is a medical condition characterized by an excessive amount of estrogenic activity in the body.[1]

Signs and symptoms

Signs of hyperestrogenism may include heightened levels of one or more of the estrogen sex hormones (usually estradiol and/or estrone), lowered levels of follicle-stimulating hormone and/or luteinizing hormone (due to suppression of the hypothalamic–pituitary–gonadal axis by estrogen), and lowered levels of androgens such as testosterone (generally only relevant to males).[1] Symptoms of the condition in women may consist of menstrual irregularities, amenorrhea, abnormal vaginal bleeding, and enlargement of the uterus and breasts.[1][2] It may also present as isosexual precocity in children[1][2] and as hypogonadism, gynecomastia, feminization, impotence, and loss of libido in males.[3] If left untreated, hyperestrogenism may increase the risk of estrogen-sensitive cancers such as breast cancer later in life.

Causes

Hyperestrogenism can be caused by ovarian tumors,[2] genetic conditions such as aromatase excess syndrome (also known as familial hyperestrogenism), or overconsumption of exogenous sources of estrogen, including medications used in hormone replacement therapy and hormonal contraception.[3] Liver cirrhosis is another cause, though through lowered metabolism of estrogen, not oversecretion or overconsumption like the aforementioned. It's necessary to know that exists two kind of hyperestrogenism: Absolute (more concentration than usual of estrogen) and relative (we can have a normal concentration of estrogen, but it's higher with respect to progesterone). An example of absolute hyperestrogenism could be: persistent follicles that later undergo atresia without ovulating; and the example of relative hyperestrogenism: luteal insufficiency.

Diagnosis

Treatments

Treatment may consist of surgery in the case of tumors,[1] lower doses of estrogen in the case of exogenously-mediated estrogen excess, and estrogen-suppressing medications like gonadotropin-releasing hormone analogues and progestogens. In addition, androgens may be supplemented in the case of males.

References

Norman Lavin (1 April 2009). Manual of Endocrinology and Metabolism. Lippincott Williams & Wilkins. p. 274. ISBN 978-0-7817-6886-3. Retrieved 5 June 2012.
Ricardo V. Lloyd (14 January 2010). Endocrine Pathology:: Differential Diagnosis and Molecular Advances. Springer. p. 316. ISBN 978-1-4419-1068-4. Retrieved 5 June 2012.
Lewis R. Goldfrank; Neal Flomenbaum (24 March 2006). Goldfrank's Toxicologic Emergencies. McGraw-Hill Professional. p. 443. ISBN 978-0-07-147914-1. Retrieved 5 June 2012.

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[Lavin2009-1] Norman Lavin (1 April 2009). Manual of Endocrinology and Metabolism. Lippincott Williams & Wilkins. p. 274. ISBN 978-0-7817-6886-3. Retrieved 5 June 2012.

[Lloyd2010-2] Ricardo V. Lloyd (14 January 2010). Endocrine Pathology:: Differential Diagnosis and Molecular Advances. Springer. p. 316. ISBN 978-1-4419-1068-4. Retrieved 5 June 2012.

[GoldfrankFlomenbaum2006-3] Lewis R. Goldfrank; Neal Flomenbaum (24 March 2006). Goldfrank's Toxicologic Emergencies. McGraw-Hill Professional. p. 443. ISBN 978-0-07-147914-1. Retrieved 5 June 2012.