Predictive factors for ovarian recovery include younger age at first chemotherapy administration and absence of concomitant radiotherapy (91)

Predictive factors for ovarian recovery include younger age at first chemotherapy administration and absence of concomitant radiotherapy (91)

Ovarian or egg cryopreservation and transplantation of the thawed tissue are not yet clinically established; however there is no contraindication for cryopreservation combined with GnRH agonist administration (101).

Some studies have reported the spontaneous return of ovarian function after several years in women with chemotherapy- or radiotherapy-induced ovarian failure (106, 107). The exact mechanism is unknown; however, it is theoretically possible that the constant stimulation of ovaries by postmenopausal levels of gonadotropins ent. Successful pregnancies have been reported among women who had return of ovarian function. There is an increase in miscarriage, small for gestational age offspring, and reduction in live births in women treated with chemotherapy (108).

Although no prospective studies of ovarian function and gonadotropin levels before and after pelvic-adnexal surgeries have been done, these procedures have the potential to damage the ovary by affecting its blood supply or causing inflammation in the pelvic area (109,110). Recovery after interventions that compromise ovarian blood supply would seem to be possible if sufficient collateral circulation develops and the resting follicles resume their cycles.

Uterine artery embolization has a potential to result in POF by compromising the vascular supply to the ovary (109, 111). It is unknown whether polyvinyl alcohol particles used for embolization have a direct toxic effect on the ovary.

Infectious causes

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Mumps oophoritis has been considered to be a cause of POF. True incidence of post-oophritis ovarian failure is unknown. In the vast majority of affected women, return of ovarian function occurs following recovery (1, 15).

There are also anecdotal reports of viral and microbial infection, such as tuberculosis, varicella, cytomegalovirus, malaria, and shigella being followed by POF (12).

Environmental toxins

Smoking is the most widely studied toxin that alters ovarian function, and on average, the female smokers experience menopause earlier than nonsmokers suggesting a possible detrimental effect of cigarette smoking on ovarian function (112). Chang et al. (113) reported an increased risk of idiopathic POF with cigarette smoking. An increased risk of developing POF has also been reported in the women with epilepsy (114).


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POF is defined by the association of amenorrhea, sex steroid deficiency and menopausal levels of serum gonadotropins before the age of 40 years. Intermittent and unpredictable ovarian function, and even spontaneous pregnancy have been reported in young women with spontaneous POF subsequent to diagnosis (4, 7). Premature ovarian dysfunction” or ”premature ovarian insufficiency” may be a more accurate phrase to reflect the reversible nature of this condition.

Although most cases of POF are idiopathic (13), diverse etiologies are associated with POF ( Table 1 ). The observation of familial cases with POF indicates the role of genetic aberrations in its pathogenesis (14). Genetic defects mostly involve the X chromosome. X chromosome abnormalities range from a numerical defects like complete deletion of one X chromosome to partial defects in the form of deletions, isochromosomes and balanced X autosome translocations (16). Association between 48XXXX, Trisomy X, X chromosome deletions, X-autosomal translocations, mosaic conditions such as 45X/46XX, 46XX/47XXX, and POF have been extensively reported in literature (15, 16, 24, 26, 27).

Adolescent girls with Turner’s syndrome or other chromosomal abnormalities who still have follicles in their ovaries could be candidates for oocyte or/ and ovarian tissue cryopreservation, to save their ovaries for future fertilization (31, 32).

Fragile X syndrome is an X-linked dominant condition with incomplete penetration, (33). It is the most common hereditary cause of mental retardation and developmental delay (34). Premutation alleles are at risk of expansion into a full mutation in the next generation (35, 36). A recent study showed that a number of CGG repeats between 30 and 40 might be used to predict premature ovarian aging and POF in infertile patients (37). The women who carry the FMR1 premutation develop premature ovarian failure (42), tremor-ataxia syndrome (43), and mild neuro-cognitive dysfunction (36).