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Primary ovarian insufficiency (POI), also called premature ovarian insufficiency and premature ovarian failure, is the partial or total loss of reproductive and hormonal function of the ovaries before age 40 because of follicular (egg producing area) dysfunction or early loss of eggs.
Iatrogenic, e.g., due to radiation, chemotherapy or surgery, such as laserization of the surface of the ovary to treat endometriosis. Excessive laparoscopic ovarian drilling has been reported to cause premature ovarian failure. [10] [11] (The primordial follicles are located in the thin outer one-millimeter layer of the ovary.) [12]
Primary ovarian insufficiency, also known as premature ovarian failure, can develop in women before the age of forty as a consequence of hypergonadotropic hypogonadism. [19] POI can present as amenorrhea and has similar symptoms to menopause, but measuring FSH levels is used for diagnosis. [21]
Fragile X-associated primary ovarian insufficiency (FXPOI) is the most common genetic cause of premature ovarian failure in women with a normal karyotype 46,XX. [1] The expansion of a CGG repeat in the 5' untranslated region of the FMR1 gene from the normal range of 5-45 repeats to the premutation range of 55-199 CGGs leads to risk of FXPOI for ovary-bearing individuals. [2]
In 2015 a research was done on the role of autoimmunity in premature ovarian failure. [11] In 2014 there was an ovarian autoimmune disease research that revealed at least two mechanisms that protect the ovary from an autoimmune attack. [12] Research showed that Theca cells were targeting the autoimmune deficiency within the ovary.
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Female infertility by chemotherapy appears to be secondary to premature ovarian failure by loss of primordial follicles. [20] This loss is not necessarily a direct effect of the chemotherapeutic agents, but could be due to an increased rate of growth initiation to replace damaged developing follicles. [ 20 ]
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