Premature ovarian failure from current perspective

Abstract

Premature ovarian failure (POF) is a syndrome characterised by amenorrhoea, hypoestrogenism and hypergonadotropinism before the age of 40. It is a disorder affecting approximately 1% of women <40 years, 1/1,000 women by the age of 30 and 1/10,000 women by the age of 20. POF is not merely an early menopause. Up to 50% of the patients with POF will have intermittent and unpredictable ovarian function which may persist for some years. Heterogeneity of POF is also reflected by the variety of possible causes, including autoimmunity, toxics, drugs, radiation, infectious as well as genetic defects. HRT remains the cornerstone of treatment and the only proven method of achieving pregnancy in these patients is by ovum donation.

Ovarian-Cell-Like Cells from Skin Stem Cells Restored Estradiol Production and Estrus Cycling in Ovariectomized Mice

“…This may cause a significantly higher risk for osteoporosis and cardiovascular disease [40]. Therapies for the relief of symptoms and for decreasing the associated disease risks are currently based on hormone replacement, particularly estradiol [41]. A WHO study published in 2002, however, showed an increased risk of breast cancer, stroke, and heart disease associated with the use of estradiol-based hormone therapy and this has led many women to discontinue or choose not to receive treatment, although hormone-based therapy is still the most effective therapy available to date [42].…”

Insight into the Genomics of Premature Ovarian Failure

“…About 25% of POF cases are iatrogenic, being related to postsurgical ovarian failure and cancer treatments (radiotherapy and chemotherapy) [21][22][23]. It has been also hypothesized that POF may be induced by environmental factors, such as cigarette smoking, heavy metals, solvents, pesticides, plastics, industrial chemicals [21].…”

“…It has been also hypothesized that POF may be induced by environmental factors, such as cigarette smoking, heavy metals, solvents, pesticides, plastics, industrial chemicals [21]. Moreover, there is evidence that POF can be secondary to infections (mumps, herpes zoster, cytomegalovirus), autoimmune (i.e., systemic lupus erythematosus, Hashimoto's thyroiditis, Addison's disease, rheumatoid arthritis, autoimmune poly-endocrinopathy-candidiasis-ectodermal dystrophy) and metabolic diseases (galactosemia) [21,24,25]. Some cases of POF are syndromic, i.e., in Turner syndrome, carbohydratedeficient glycoprotein syndromes, pseudohypoparathyroidism type 1a, progressive external ophthalmoplegia, autoimmune polyglandular syndrome type I, and ovarian leukodystrophy [21].…”

“…Page 2 of 7 the ovarian reserve are: i) decreased pool of primordial follicles, due to alteration in mechanism regulating germ cell migration, proliferation of oogonia and meiosis occurring before birth; ii) accelerated rate of follicle atresia by deregulation of those factors that control the rate of apoptosis (i.e., gonadotropins, estrogens, androgens, growth factors, cytokines, reorganisation of the actin cytoskeleton, nitric oxide, tumour necrosis factor-a, Fas ligand and activated peripheral T cells); iii) dysfunction in follicular recruitment or maturation [21].…”

“…About 25% of POF cases are iatrogenic, being related to postsurgical ovarian failure and cancer treatments (radiotherapy and chemotherapy) [21][22][23]. It has been also hypothesized that POF may be induced by environmental factors, such as cigarette smoking, heavy metals, solvents, pesticides, plastics, industrial chemicals [21]. Moreover, there is evidence that POF can be secondary to infections (mumps, herpes zoster, cytomegalovirus), autoimmune (i.e., systemic lupus erythematosus, Hashimoto's thyroiditis, Addison's disease, rheumatoid arthritis, autoimmune poly-endocrinopathy-candidiasis-ectodermal dystrophy) and metabolic diseases (galactosemia) [21,24,25].…”