Metabolic Syndrome Clinical Trial
Official title:
Prevalence of Metabolic Syndrome Amongst Malay Women With PCOS
The abnormalities that characterize the Metabolic Syndrome (MetS) confer an increased risk of
cardiovascular and other diseases. Women with Polycystic Ovary Syndrome (PCOS), the commonest
endocrine disease among women of childbearing age, have an increased risk of developing MetS.
2) The prevalence of MetS in PCOS patients varies among different ethnic groups. Malaysia is
a unique country with a multiethnic population. The 3 largest ethnic groups are the Malays,
Chinese and Indians. Previous studies in India and China have been able to determine the
incidence of PCOS amongst those ethnic groups, but as yet, there is no published data on the
prevalence of this disorder amongst women of Malay ethnicity. In this study, I intend to
discover the prevalence of MetS amongst Malay women with established PCOS.
Metabolic syndrome (MetS) is a well-known collection of interrelated metabolic conditions
that identify patients at increased risk of developing cardiovascular disease. These
conditions include diabetes mellitus (DM), high blood pressure, obesity and dyslipidaemia.1
Though the exact pathogenesis of MetS still remains elusive, central obesity and insulin
resistance are generally acknowledged as important causative factors. The most recent
International Diabetes Federation (IDF) consensus has developed a definition emphasizing the
importance of central obesity with modifications according to ethnic groups.2 Polycystic
Ovarian Syndrome (PCOS) is the commonest endocrine disorder in women of reproductive age.3
Around 6-7% of women in the reproductive age group are estimated afflicted with this
disorder, which accounts for more than 75% of anovulatory infertility.4 PCOS is characterized
by both reproductive and metabolic dysfunctions such as hyperandrogenism, infertility, and
increased long term risks of type 2 diabetes, dyslipidaemia, hypertension, visceral obesity,
and endometrial cancer. Women with PCOS have been noted to have high incidences of age
group-specific prevalence of type 2 DM, myocardial infarct and angina (Mani H 2012). The
criteria developed in Rotterdam in 2003 remains the most widely accepted for the diagnosis of
PCOS.7 For a diagnosis of PCOS to be made, a minimum of 2 features from oligo/anovulation,
hyperandrogenaemia and ultrasound demonstration of polycystic ovaries need to be present.
Other causes of polycystic ovaries such as adrenal hyperplasia, androgen-secreting tumours
and Cushing's syndrome have to be excluded, of course.
Insulin resistance, which is an established feature of PCOS, leads to compensatory
hyperinsulinaemia and affects both the theca and granulosa of the ovary (Franks S 1999,
Franks S 2008). Insulin increases serum androgen levels through its function as an ovarian
growth hormone (leading to increased theca cell androgen synthesis) and its action on adrenal
steroidogenesis (Barbieri RL 1986, Moghetti P 1996). The consequent hyperandrogenaemia
interferes with normal folliculogenesis and ovulation. The concerted effects of the elevated
serum insulin and androgen levels account for many of the features of PCOS and the metabolic
syndrome (Barber TM 2012). It is apparent that insulin resistance, androgen excess,
anovulation, metabolic abnormalities and PCOS are all related to each other and form a
tangled web. PCOS is now viewed as a clinical phenotype of MetS.5,6
.
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