Introduction
If an ovary of a woman fails before the age 40, she has an early onset of Premature Ovarian Failure (POF). Early premature ovarian failure affects approximately 1% of women. Some women develop premature ovarian failure in adolescence. In the event of such an event, these women will never have normal ovarian function. Ovarian function involves the production of ovules and estrogen and progesterone hormones. Unlike menopause, premature ovarian failure may occur in most women alternately [1, 2]. Perhaps the term "early ovarian inefficiency" should be used for this disorder. Many women have symptoms that are naturally associated with menopause. These symptoms include hot flashes, vaginal dryness, itching, night sweats and drowsiness. Menstruation may be discontinuous or completely stopped. Also, some women may never experience the onset of menstrual periods, they may not enter the normal period of puberty or have no symptoms, and will notice ovarian inefficiency during infertility tests. The onset of these symptoms is due to low levels of estrogen due to ovarian failure or poor performance and it does not have clear cause in many people.
Premature ovarian failure is very common in some families. Perhaps this disease is associated with autoimmune diseases that affect adrenal glands and thyroid glands. Other causes of premature ovarian failure can be genetic (Turner syndrome and chromosome X fragility syndrome) [1, 2]. It may also be caused by radiation therapy or chemotherapy. In addition to the aforementioned symptoms, low estrogen levels can cause osteoporosis or premature cardiac disease. Women with premature ovarian failure are susceptible to depression. If premature ovarian failure is caused by genetic factors, there is a long-term risk for the patient and their children. Therefore, genetic counseling is recommended [3, 4]. Approximately 10% of women with premature ovarian failure get pregnant using their ossytes with or without supportive methods, however, the overall fertility rate is difficult to predict. Blood tests include hormonal tests (estrogen levels and follicular stimulating hormones) and chromosomal analysis and chromosomal X fragmentation syndrome mutations (FMR1) to investigate genetic factors [1, 5]. The bone density test can also be appropriate.

Patients and methods
Between May 2007 and July 2012, 13 women with premature ovarian failure who referred to Sarem Hospital were were cytogenetically studied. Entrance criteria included early amenorrhea or secondary amenorrhea for at least 4 months, age below 40 years, and serum FSH less than 40 international units per ml in two separate test with one month interval, as well as stigmata Turner patients [3,6]. Using family tree pedigree, if one of the relatives of grade one or two had premature ovarian failure or early menopause (menopause before age 54) was considered positive.
Cytogenetic analysis: Karyotype analyzes were performed on metaphase chromosomes prepared by G-bonding staining technique, derived from blood lymphocyte cultures and based on standard methods of clarity in the range of 400 to 450. For each patient, at least 50 metaphases were examined. The only tissue studied was routine blood. Therefore, the study was limited to blood analysis.
These 13 had the mean age of 29.1 ± 1. 0. Among the subjects, in one person, relatives of grade one or two had early premature ovary failure or early menopause.
Chromosomal abnormalities were diagnosed in 2 of 13 patients (15.38%) with premature ovarian failure. A patient with chromosomal mosaic was 45, X [8] / 46, XX [42]. The second patient had a transition between chromosome X and chromosome azosam 9 as 46, XX, t (X 9) (q22.1; q22.1) (Table 1).

 

Discussion
In connection with the transfer of chromosome X and chromosome 9, various studies on patients with premature ovarian failure have been performed precisely at this fracture point in different populations [7, 8].
Despite the decrease in the mean age of the menarche during the twentieth century, it seems that the average age of menopause varies with time and race, and occurs almost at age 50. Premature ovarian failure is defined as secondary amenorrhoea with increased gonadotropin, before the age of 40, and ovarian emptying and lack of oocyte release are commonly seen. However, an ovarian that is no longer sensitive to gonadotrophin can be considered as a true ovarian failure [ 9, 10]. Premature ovarian failure is usually idiopathic (unknown), but may occasionally be a genetic condition that is associated with rapid onset of follicles, such as Turner syndrome [11], or formation of small numbers of follicles, such as galactose [12]. The destruction of sex cells before and after puberty can be related to viral infections, drugs, cigarette smoking, anti-tumor drugs, or radiation therapy. Autoimmune is also the basis for premature ovarian failure in patients with anti-ovarian antibodies, Addison and Myasthenia gravis disease. The role of family factors was introduced by de Moraes-Ruehsen [2] and Smith [13]. Mattison et al. [5] suggested that premature ovarian failure could be a Mendelian disease inherited from father or mother, and it can be observed as an autosomal or X dominant attribute. In this study, the frequency of chromosomal anomalies was about 15.38% in patients, which is roughly the same as in previous studies in different populations [14-19] (Table 2).

Table 2) Summary of the frequency of chromosomal abnormalities reported in patients with premature ovarian failure in different populations

*CA: chromosomal abnormalities

Determining the cytogenetic details of new patients with premature ovarian failure phenotype will play an important role in obtaining more information and identifying all the genetic factors involved in the disease.

Conclusion
This study confirms the importance of cytogenetic studies in premature ovarian failure. Many genes are essential for the development or function of the ovary. these genes are on the long arm of the chromosome X. The chromosomal X deactivation center is turned off in the Xq13 region in chromosomal rearrangements. X and autosomal rearrangements may not interfere with the genes involved in ovarian function, but rearrangements may alter the expression of genes due to spatial effects. By determining the genes involved in the evolution of the ovary in the area around the fracture, the spatial hypothesis is introduced as one of the important mechanisms involved in the phenotype of the premature ovarian failure.

Acknowledgments: The case was not found by the authors.
Ethical permissions: The case was not found by the authors.
Conflict of Interest: The case was not found by the authors.
Financial support: This study was supported by Sarem Fertility and Infertility Research Center.
Contribution of authors: Fatemeh Hadipour (First author), author of the article/methodology/main author/author of discussion (%20); Zahra Hadipour (Second author), author of the article/methodology/main author/author of discussion (%20); Fahimeh Mousavi (Third author), author of the article/methodology/main author/author of discussion (%10); Iman Bagherizadeh (Fourth author), author of the article/methodology/main author/statistical analyst (%10); Yousef Shafeghati (Fifth author), author of the article/main author/statistical analyst (%20); Farkhondeh Behjati (Sixth author), author of the article/main author/statistical analyst (%20).