doiSerbia

Premature ovarian failure

Vujović Svetlana (Medicinski fakultet, Beograd + Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Ivović Miomira (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Tančić-Gajić Milina (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Marina Ljiljana (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Barać Marija (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Arizanović Zorana (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Nenezić Ana (Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)
Ivanišević Maja (Klinika za ginekologiju i akušerstvo, Klinički centar Srbije, Beograd)
Micić Jelena (Klinika za ginekologiju i akušerstvo, Klinički centar Srbije, Beograd)
Sajić Silvija (Medicinski fakultet, Beograd + Univerzitetska dečja klinika, Beograd)
Micić Dragan (Medicinski fakultet, Beograd + Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Klinički centar Srbije, Beograd)

Premature ovarian failure (POF) is the occurrence of hypergonadotropic hypoestrogenic amenorrhea in women under the age of forty years. It is idiopathic in 74-90% patients. Known cases can be divided into primary and secondary POF. In primary POF genetic aberrations can involve the X chromosome (monosomy, trisomy, translocations, deletions) or autosomes. Genetic mechanisms include reduced gene dosage and non-specific chromosome effects impairing meiosis, decreasing the pool of primordial follicles and increasing atresia due to apoptosis or failure of follicle maturation. Autoimmune ovarian damage is caused by alteration of T-cell subsets and T-cell mediated injury, increase of autoantibody producing B-cells, a low number of effector/cytotoxic lymphocyte, which decreases the number and activity of natural killer cells. Bilateral oophorectomy, chemotherapy, radiotherapy and infections cause the secondary POF. Symptoms of POF include irritability, nervousness, loss of libido, depression, lack of concentration, hot flushes, weight gaining, dry skin, vaginal dryness, frequent infections etc. The diagnosis is confirmed by the level of FSH of over 40 IU/L and estradiol below 50 pmol/L in women aged below 40 years. Biochemical and other hormonal analysis (free thyroxin, TSH, prolactin, testosterone), karyotype (<30 years of age), ultrasound of the breasts and pelvis are advisable. Optimal therapy is combined estrogen progestagen therapy given in a sequential rhythm, after excluding absolute contraindications. Testosterone can be added to adnexectomized women and those with a low libido. Sequential estrogen progestagen replacement therapy is the first line therapy for ovulation induction in those looking for pregnancy and after that oocyte donation will be advised. Appropriate estro-progestagen therapy improves the quality of life and prevents complications such as cardiovascular diseases, osteoporosis, stroke etc.

Keywords: premature ovarian failure, etiology, therapy