from PART II - INFERTILITY EVALUATION AND TREATMENT
Published online by Cambridge University Press: 04 August 2010
INTRODUCTION
Polycystic ovarian syndrome (PCOS) is a common and illunderstood endocrine disorder with multisystem sequelae. Clinical presentation is variable. It is characterized clinically by oligoamenorrhoea, signs of androgen excess such as hirsutism, acne, alopecia, obesity, and infertility, biochemically by elevation of serum androgens, luteinizing hormone (LH), and LH/follicular-stimulating hormone (FSH) ratio and not infrequently by insulin resistance (1). Morphologically, the ovaries are enlarged and have thick shiny capsules with peripherally placed multiple intermediate sized (2–8 mm in diameter) follicles. However, not all patients with clinically or endocrinologically defined PCOS demonstrate polycystic ovaries, nor do all women with polycystic ovaries have PCOS. Among 257 “normal volunteers,” 23 percent were found to have polycystic ovaries, and of the patients with polycystic ovaries, only about 50 percent had PCOS (2). Alternatively, of those women with PCOS, approximately, 70 percent have polycystic ovaries on ultrasonographic examination (3).
The diagnostic criteria of PCOS have been recently revised after a joint meeting of the European Society for Human Reproduction (ESHRE) and American Society for Reproductive Medicine (ASRM) in Rotterdam in May 2003 (4). It was agreed that the diagnosis of PCOS required the presence of at least two of the following three criteria: 1) oligo- and/or anovulation, 2) hyperandrogenism (clinical and/or biochemical), and 3) ultrasonographic appearance of polycystic ovaries, after the exclusion of other etiological factors (4).
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