Polycystic ovary syndrome; causes, symptoms and treatment


The irregular cycle: polycystic ovary syndrome

Many women are troubled by an erratic or unpredictable menstrual cycle. In the ‘developed world’ the commonest cause is polycystic ovary syndrome (PCOS). Overall, PCOS is also the commonest endocrine disturbance affecting women. The classical symptoms of ‘Stein-Leventhal syndrome’ as it was eponymously referred to for many years—namely menstrual disturbance (amenorrhea or oligomenorrhea, hyperandrogenism and obesity)—are now known to describe the extreme end of the spectrum of what we believe to be a very heterogeneous condition, whose pathophysiology appears to be multifactorial and polygenic. The definition of the syndrome has been much debated. Key features include menstrual cycle disturbance, hyperandrogenism and obesity. There are many extra-ovarian aspects to the pathophysiology of PCOS yet ovarian dysfunction is central. At a recent joint American Society of Reproductive Medicine/European Society of Human Reproduction and Embryology (ASRM/ ESHRE) consensus meeting a refined definition of PCOS was agreed, namely the presence of two out of the following three criteria:

(1) Oligo- and/or anovulation;

(2) Hyperandrogenism (clinical and/or biochemical);

(3) Polycystic ovaries, with the exclusion of other etiologies.

The morphology of the polycystic ovary, which has been redefined as an ovary with 12 or more follicles measuring 2–9 mm in diameter and/or increased ovarian volume (>10cm3).


There is considerable heterogeneity of symptoms and signs amongst women with PCOS and for an individual these may change over time. PCOS is familial and various aspects of the syndrome may be differentially inherited. Polycystic ovaries can exist without clinical signs of the syndrome, which may then become expressed over time. There are a number of interlinking factors that affect expression of PCOS. A gain in weight is associated with a worsening of symptoms whilst weight loss will ameliorate the endocrine and metabolic profile and symptomatology.

Elevated serum concentrations of insulin are more common both in lean and obese women with PCOS when compared with weightmatched controls. Indeed it is hyperinsulinemia that appears to be the key to the pathogenesis of the syndrome as insulin stimulates androgen secretion by the ovarian stroma and appears to affect the normal development of ovarian follicles, both by the adverse effects of androgens on follicular growth and possibly also by suppressing apoptosis and permitting the survival of follicles otherwise destined to disappear


Polycystic ovaries are commonly detected by ultrasound or other forms of pelvic imaging, with an estimated 20–33% prevalence in the general population. However, not all women with polycystic ovaries demonstrate the clinical and biochemical features that define polycystic ovary syndrome. The biochemical disturbance includes elevated serum concentrations of luteinizing hormone (LH), testosterone, androstenedione, and insulin.

Defining the ‘syndrome’

While it is now clear that ultrasound provides an excellent technique for the detection of polycystic ovarian morphology, identification of polycystic ovaries by ultrasound does not automatically confer a diagnosis of PCOS. Controversy still exists over a precise definition of the ‘syndrome’ and whether or not the diagnosis requires confirmation of polycystic ovarian morphology. The generally accepted view in Europe is that a spectrum exists, ranging from women with polycystic ovarian morphology and no overt abnormality at one end, to those with polycystic ovaries associated with severe clinical and biochemical disorders at the other end. Using a combination of clinical, ultrasonographic, and biochemical criteria, the diagnosis of PCOS is usually reserved for those women who exhibit an ultrasound picture of polycystic ovaries, and who display one or more of the clinical symptoms (menstrual cycle disturbances, hirsutism, obesity, hyperandrogenism), and/or one or more of the recognized biochemical disturbances (elevated LH, testosterone, androstenedione, or insulin). A joint ASRM/ESHRE consensus meeting on PCOS was held in Rotterdam, in May 2003. At this meeting a refined definition of PCOS was agreed, which, for the first time, includes a description of the morphology of the polycystic ovary. The new definition requires the presence of two out of the following three criteria:

(1) Oligo- and/or anovulation;

(2) Hyperandrogenism (clinical and/or biochemical);

(3) Polycystic ovaries, with the exclusion of other etiologies

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