Premature ovarian failure
Premature ovarian failure (POF), also known as premature menopause, or early menopause, is a condition characterized by amenorrhea, hypoestrogenism, and elevated serum gonadotropin levels in women less than 40 years. Although often used synonymously, POF is not menopause. Some women with POF have intermittent ovarian function and pregnancies may occur.
Women exposed to various forms of cancer therapy (high-dose chemotherapy and/or gonadal irradiation) have increased risk of developing premature ovarian failure. The risk is high if the treatment occurs after the onset of puberty (relative risk [RR] 2.32), in survivors of Hodgkin lymphoma (RR 3.25), and in patients treated with combined chemotherapy and radiation therapy below the diaphragm (RR 8.56-9.6). After a bone marrow transplant using busulfan, almost 100% of women develop ovarian failure.
The mechanism of premature ovarian failure includes damage to the proliferating ovarian granulosa cells and/or to the oocytes by chemotherapy or radiation as noted above. Subsequently, follicular depletion and premature ovarian failure develop. Exposure to solvents (2-bromopropane) also can result in oocyte depletion and premature ovarian failure.
Finally, bilateral oophorectomy can be regarded as a form of induced POF. In the case of chemotherapy or radiation the POF can be temporary in some cases ovarian function may return spontaneously. Some women continue to have regular menstrual cycles despite elevated serum FSH levels and reduced fertility (ovarian insufficiency, diminished ovarian reserve). If a woman does not cycle after such therapies and she has low estrogen levels treatments are provided to protect her bones.
While chemotherapy, radiation and surgical removal of the ovaries are understood causes of premature ovarian failure, the cause of spontaneous premature ovarian failure in most cases is unknown. Two mechanisms are presumed to play a role in spontaneous ovarian failure - follicle depletion and follicle dysfunction. Follicle depletion can occur due to: pure gonadal dysgenesis, thymic aplasia/hypoplasia syndrome, autosomal recessive disorders (ataxia-telangiectasia mental retardation), X chromosome related disorders (Turner syndrome, X chromosome deletions and translocations), galactosemia, fragile X mental retardation 1 (FMR1) gene permutation, viral oophoritis, autoimmunity, environmental toxins, steroidogenic enzyme defects (17-alpha-hydroxylase, 17-20-desmolase, and aromatase enzyme deficiencies), lymphocytic oophoritis with positive adrenal antibodies, signal defects (gonadotropin receptor and G-protein signals) and in the blepharophimosis-epicanthus-ptosis syndrome.
Your reproductive endocrinologist will assess the situation and recommend appropriate follow-up and therapies. The diagnosis does not necessarily preclude reproduction and may even include spontaneous reproduction with a woman’s own eggs.
