Remind you fellow members that PCOS without excess androgen
comprises one of the least severe phenotypes .
Who is more responsible for prime disorder of PCO? Is it primary androgen excess
or Hyperinsulinaemia ??
Quick recapitulation of criteria of defining PCO:: The
Androgen Excess and PCOS (AE-PCOS) Society concluded that PCOS should be first
considered as a disorder of
androgen excess or hyperandrogenism. The key message of AE-PCOS Society
task force, therefore boils down to the fact that PCOS should be defined by the presence of hyperandrogenism (clinical and/or biochemical .
However looking back:- The
recommended NIH-NICHD diagnostic criteria were 1) clinical or biochemical
evidence of hyperandrogenism and 2) chronic anovulation. Most gynacologists thereafter
considered and still feel that sonographic evidence of PCOM should
be an element in PCOS diagnosis.
As we know , that in 2003, new guidelines for diagnosing
PCOS were suggested at a joint meeting of the European Society for Human
Reproduction and the American Society of Reproductive Medicine. Redefining PCOS
to incorporate an appropriate definition of a polycystic ovary was then strongly
felt.
A diagnosis of PCOS can now be reached when at least two findings
among 1) HA(hyperandrogenism) 2) Oligo-An,
(oligo-anovulation ) and 3) PCOM are present and after the exclusion of causes
of any androgen excess disorders .
The Rotterdam 2003 criteria have expanded rather than replaced the 1990
NIH criteria, having added the following two
PCOM phenotypes: PCOM with HA(hyperandrogenism)
but without Oligo-An(oligo-amenorrhoea) , and PCOM with Oligo-An and without HA Few women with a)
PCOS had PCOS without HA,
and nearly equal number exhibit PCOS without Oligo-An (oligo-amenorrhoea) .However, the patient
populations with the newly extended phenotypes had less severe ovulatory
dysfunction and less androgen excess than patients diagnosed using the 1990 NIH
criteria which were very strict and included few population only .
The prevalence of abnormal
sonographic features (PCOM) has been suggested to be higher than 20% in both
Asian and Western women. Follow up of
about 1000 cases and keeping records for such women since2009 till date my personal
observation is that PCOM (ovarian morphology) is the most common component
AS m=many as 85% of patients in my personal series diagnosed
with Rotterdam criteria had abnormal USG
findings .Regarding clinical presentation, excess androgen has been suggested
to have a principal role in diagnostic criteria. Analytical results have
demonstrated that PCOS without excess androgen comprises one of the least
severe phenotypes
In some far East countries , it has been observed that PCOS without HA is a common phenotype and
these are the women who are less likely
to have metabolic dysfunction, insulin resistance, or elevated blood pressure.
Most previous reports support the proposal that excess androgen is the
condition directly responsible for the signs and symptoms that are recognized
as PCOS and not hyperinsulinaemia .More recently, clinical data have
demonstrated that hyperandrogenism is the key component of PCOS, and the
Androgen Excess and PCOS (AE-PCOS) Society concluded that PCOS should be first
considered as a disorder of androgen excess or hyperandrogenism.
The AE-PCOS Society task force recommended that PCOS should be defined by the
presence of hyperandrogenism (clinical and/or biochemical), ovarian dysfunction
(oligo-anovulation and/or polycystic ovaries), and the exclusion of related
disorders .
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