الفهرس 
Introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Although polycystic ovaries were described as early as the 19thcentury, it was not until 1935 that a syndrome was identified and named subsequently for Stein and Leventhal, who first associated amenorrhea, infertility, obesity, and hirsutism with polycystic ovaries. If the idea was adherent strictly to the criteria for diagnosis amenorrhea, obesity, and hirsutism-a large number of cases would go undetected. Consequently during the past few years, the term ”Stein and Leventhal syndrome” has fallen into disuse and polycystic ovarian disease (PCOD) has been adopted as the generic description for a broad spectrum of abnormalities in women with endocrine dysfunction, especially abnormal androgen metabolism,1Ild production. There is no definition of PCOD for which there isuniforll1 worldwide agreement. Incidence of polycystic ovarian disease depends upon the ”index of suspicion”. The etiology of PCOD suggesting possibility of local factors in the ovary itself, brain (either cerebral cortex, hypothalall1us or anterior pituitary gland), thyroid disorders, adrenalglands dysfunction or abnormal androgen and prolactin metabolism. It has been proved that women with PCOD have metabolicdisturbance such as hyperinsulinemia, increased insulin resistance and hypertriglyceridemia. Also there is low level of insulin like growth factor binding protein-l (IGFBPI) which leads to greater free insulin-like growth factor-l (IGFI) which stimulate the ovary resulting in excessive follicular stimulation with overproduction of androgen and subsequent follicular atresia. In recent years, many authors have suggested that PCOD is genetically determined but the responsible genes remain elusive.