Lakhasly

Introduction
Spontaneous abortion is a common complication in human reproduction. An estimated 60% of spontane- ous abortions occur before or after implantation (termed preclinical losses), while 10–15% are confirmed by ultra- sound or histological evidence (termed clinical miscar- riage) . Most clinical miscarriages occur during the first trimester, and the leading cause of miscar- riage is embryonal chromosomal abnormalities .Although parental chromosomal structure abnormalities are the main genetic factor leading to recurrent miscar- riages, the prevalence of chromosomal abnormalities in the affected couples is relatively low (2.78–4.1%) . Few studies have investigated the parental karyotype of sporadic miscarriage [3]. The frequency of balanced rearrangements in the general population is very low (0.4%) [1, 2, 8].
Apart from inheritable factors, a variety of maternal factors have been found to be related to spontaneous abortion or embryonic chromosomal aberrations, includ- ing age, reproductive history, and immune or endocrine dysfunction [1–3, 9]. In addition, elevated maternal serum level of homocysteine was shown to increase the risk of fetal loss and stillbirth [10]. Supplementation of folic acid can decrease the concentration of homocyst- eine and reduce the risk of pregnancy loss [11, 12]. Poly- morphisms in folate metabolizing genes are associated with chromosome breaks and fetal chromosomal ane- uploidy [13, 14].
Apart from maternal factors, embryonic chromosomal abnormalities may be attributable to abnormal game- togenesis in father. Sperm DNA fragmentation index tends to increase with paternal age [15, 16]. Patients with high levels of sperm DNA damage showed a significantly higher miscarriage rate [17]. Therefore, advanced pater- nal age may be associated with miscarriage, infertility, and birth defects [18].
Other non-hereditary factors implicated in embryonic chromosomal aberrations may include environmen- tal factors. Prenatal exposure to environmental factors, such as drugs and pesticides, may increase the risk of birth defects or embryonic DNA damage [19, 20]. While several causes of teratogenesis have been identified, the etiopathogenetic mechanisms are not well characterized [20–22]. There is a paucity of epidemiological evidence pertaining to the risk factors for embryonic chromo- somal aberrations in cases of spontaneous abortion. Mis- carriage is a distressing event for the affected women and their families. Therefore, exploring the etiopathogenesis of spontaneous abortion may help inform interventions to protect the developing embryo and prevent miscar- riage. The aim of this study was to assess the risk factors for spontaneous abortions with and without embryonic chromosomal aberrations by investigating the clinical and demographic characteristics of these cases.