A 31-year-old lady with normal physical characteristics was found to have persistent high FSH and LH and was suspected possible premature ovarian failure after reported to have not normal menstrual cycle. Leucocytes were collected from patient’s fresh peripheral blood sample and Giemsa banding (G-banding) was done. All metaphases were captured and analysed using Cytovision software 4.5 and the final analysis show 47,XXX
Premature Ovarian Failure

Premature Ovarian Failure (POF) is associated with subfertility. Despite efforts to induce ovulation, success rates are low. We report a case of POF spontaneously conceiving twins while on hormone replacement therapy.
Ovarian Failure, Premature ; Spontaneous ; Twin Multiple Birth ; Pregnancy ; success

No abstract available.
Pregnancy* ; Primary Ovarian Insufficiency*

No abstract available.
Primary Ovarian Insufficiency*

No abstract available.
Antibodies* ; Female ; Humans ; Primary Ovarian Insufficiency*

Premature ovarian failure (POF) is menopause before the age of 40 years. The frequency of POF is about 1% of all women. Recently inhibin alpha gene (INHalpha) has been indicated as candidate in POF pathogenesis. Inhibin, a glycoprotein, is a gonadal hormone, which can inhibit the synthesis and secretion of pituitary follicle-stimulating hormone (FSH), which has an important role in the recruitment and development of ovarian follicles during the folliculogenesis. G769A variation of INH alpha, alanine, is highly conserved across species, and has an important role of its receptor binding. We screened a G769A transition in the INHalpha from the total population of the patients of 84 women with POF and 100 normal fertile women. We found no variation between the normal subjects and the POF patients. G769A variation of INHalpha is rare in Korea women with POF.
Adult ; Female ; Follicle Stimulating Hormone/metabolism ; Human ; Infertility, Female/genetics ; Inhibins/*genetics/metabolism ; Korea ; Ovarian Failure, Premature/*genetics/metabolism ; *Polymorphism, Restriction Fragment Length ; Support, Non-U.S. Gov't

This study was performed to determine whether the LHbeta -subunit gene missense mutation is present in Korean infertile patients with 46,XX POF women. The variants of LHbeta exon 2 (Trp 8Arg; TGG to CGG and Ile15Thr; ATC ti ACC) were studied in forty-four 46.XX idiopathic POF and 54 nonpregnant women. The LHbeta exon 2 variants were more frequent in POF patients (20.5%) than nonpregnant( 16.7%) women (p>0.05). POF patients with the variant was slightly higher than nonpregnant women with the variant.
Exons ; Female ; Humans ; Korea* ; Mutation, Missense ; Primary Ovarian Insufficiency*

OBJECTIVE: This study was performed to determine whether the FSH receptor mutation is present in infertile Korean patients with 46,XX premature ovarian failure (POF) women. METHODS: The variant of FSH receptor exon 10 in thirteen 46, XX idiopathic POF and 4 healthy fertile (control) women were studied. Missense mutation in Exon 10 was detected in POF patients and healthy fertile women by polymerase chain reaction-single stranded conformation polymorphism (PCR-SSCP). RESULTS: The variant types of FSH receptor exon 10 (Thr307Ala; A919G) were found in healthy fertile (control) and POF women. CONCLUSIONS: This mutation may not be specific in POF patients and further study is needed in fertile (control) and POF women.
Exons* ; Female ; Humans ; Mutation, Missense ; Primary Ovarian Insufficiency* ; Receptors, FSH*

Female ; Humans ; Consensus ; Menopause, Premature ; Primary Ovarian Insufficiency/therapy*

The ovarian reserve is necessary for female fertility and endocrine health. Commonly used cancer therapies diminish the ovarian reserve, thus, resulting in primary ovarian insufficiency, which clinically presents as infertility and endocrine dysfunction. Prepubertal children who have undergone cancer therapies often experience delayed puberty or cannot initiate puberty and require endocrine support to maintain a normal life. Thus, developing an effective intervention to prevent loss of the ovarian reserve is an unmet need for these cancer patients. The selection of adjuvant therapies to protect the ovarian reserve against cancer therapies underlies the mechanism of loss of primordial follicles (PFs). Several theories have been proposed to explain the loss of PFs. The “burn out” theory postulates that chemotherapeutic agents activate dormant PFs through an activation pathway. Another theory posits that chemotherapeutic agents destroy PFs through an “apoptotic pathway” due to high sensitivity to DNA damage. However, the mechanisms causing loss of the ovarian reserve remains largely speculative. Here, we review current literature in this area and consider the mechanisms of how gonadotoxic therapies deplete PFs in the ovarian reserve.
Adolescent ; Child ; DNA Damage ; Female ; Fertility ; Fertility Preservation ; Humans ; Infertility ; Ovarian Follicle ; Ovarian Reserve ; Primary Ovarian Insufficiency ; Puberty ; Puberty, Delayed