ABSTRACT
The polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders, although its aetiology remains unknown.1 This heterogeneous disorder may present, at one end of the spectrum, with the single finding of polycystic ovarian morphology as detected by
pelvic ultrasonography. At the other end of the spectrum symptoms such as obesity, hyperandrogenism, menstrual cycle disturbance and infertility may occur either singly or in combination (Table 3.1). Metabolic disturbances such as elevated serum concentrations
of luteinizing hormone (LH), testosterone, insulin and prolactin are common and may have profound implications on the long-term health of women with PCOS. The syndrome is a familial condition and a number of candidate genes have been implicated (see Chapter 4). The syndrome appears to have its origins during adolescence and is thought to be associated with increased weight gain during puberty.2 However, the polycystic ovary gene or genes have not yet been identified and the effect of environmental influences such as weight changes and circulating hormone concentrations, and the age at which these occur, is unknown.
