PCOS is a complex endocrine disorder with various presentations and diagnostic challenges. It is characterized by oligo/amenorrhea, clinical or biochemical signs of hyperandrogenism, and polycystic ovaries. Insulin resistance appears to play a central role in the pathogenesis of PCOS through its effects on androgen production and metabolism. Diagnosis involves assessing menstrual history, hirsutism, acne, obesity, biochemical markers of hyperandrogenism and insulin resistance, and ultrasound of the ovaries. Treatment focuses on symptoms management and addressing underlying insulin resistance. Asymptomatic PCOS and ovulatory PCOS may still involve luteal phase defects impacting fertility. PCOS often begins in adolescence but may not be diagnosed

1. •DR. RABI NARAYAN SATAPATHY
•ASST.PROFESSOR
•DEPT. OF OBST.& GYNAECOLOGY
•SCB MEDICAL COLLEGE, CUTTACK
•MOB-09861281510
•EMAIL-drrabisatpathy@gmail.com

2. PCOS-PRACTICAL APPROACH TO
DIAGNOSIS
• Dr. V.K.PODDAR
DGO, FICOG, MD (Gold Medalist)
• CHAIRMAN, REPRODUCTIVE ENDOCRINOLOGY
COMMITTEE, FOGSI
• CHAIRMAN, IMA-AMS(NORTH-WEST),
KOLKATA
• SENIOR VICE PRESIDENT, BOGS , KOLKATA
• CONSULTANT- OBSTETRICIAN AND
GYNAECOLOGIST, ADVANCED MEDICAL
RESEARCH INSTITUTE, KOLKATA.

3. Presentation
• Patients with PCOS present with various symptoms
including the following:
• *Amenorrhea
• *Oligomenorrhea
• *Infertility
• *Hirsutism
• *Obesity
• *Acne Vulgaris
• *Asymptomatic

4. Physical Signs
• *Hirsutism
• Patients may have excess body
hair in male distribution pattern
and acne.
• *Obesity: approximately 50%
of patients are obese
• *Acanthosis Nigricans
• This is thought to be the result
of insulin resistance in these
patients

5. Clinical features of 1557 patients with
PCOS
Acanthosis nigricans 3.1%
Hirsutism 13.9%
Acne 31.1%
Infertility 24.8%
Menstrual cycle status
Regular 25.0%
Oligo. 51.5%
Amen. 23.0%
Balen et al. Hum Report 1995

6. Diagnosis
• In the past (before 2003) Necessary Lab
Tests or sonar
• Recently ( after 2003)…clinically.

7. • PCOS could be defined when at least two
of the following three features are present,
after exclusion of other etiologies :
(i) Oligomenorrhea and or Anovulation
(ii) Clinical and/or biochemical
Hyperandrogenism.
(iii) Polycystic ovaries (sonar).
Rotterdam, MayRotterdam, May
2003 Definition2003 Definition

8. Pitfalls Rotterdam Definition
1. doubts still exist regarding borderline
groups of patients ,such as hirsute ovulatory
Normoandrogenic women with PCO???.
2. Neglected the role of IR
• Chronic anovulation & hyperandrogenism in
absence of other endocrine disorders
• January issue of Fertility & Sterility J, 2004
•3

9. • Polycystic ovaries
(PCO), observed on
ultrasound are a sign
of PCOS and not by
themselves diagnostic
of the syndrome.
PCO & PCOS

10. Ultrasonic Criteria of PCOUltrasonic Criteria of PCO
• At least one of the following:
12 or more follicles measuring 2–9 mm in diameter,
increased ovarian volume (>10 cm3
).
• If there is a follicle >10 mm in diameter, the scan
should be repeated at a time of ovarian quiescence
in order to calculate volume and area.
• The presence of a single PCO is sufficient to
provide the diagnosis.
• The distribution of follicles and a description of the
stroma are not required for diagnosis.

12. Imaging studies
• However, there is significant intra-observer
and inter-observer variability and
ultrasonography alone may not be a reliable
method of diagnosis or excluding PCOS

13. What is The significance ofWhat is The significance of
polycystic-appearing ovaries versuspolycystic-appearing ovaries versus
normal appearing ovaries in patientsnormal appearing ovaries in patients
with PCOS??with PCOS??
The presence of polycystic-appearing
ovaries correlates with the presence of
insulin resistance (Richard J 2002).

14. USG- Only Evidence of PCO
PREDICTS
• *Fertility outcome with specific regime .
*The risk of OHSS.
The presence of many antral follicles may assist to
decide collection of immature oocytes for in vitro
maturation.
*PCO with increased vol.& more than12-15
follicles(>2-9mm) are less likely to respond to CC
singly.
They may require gonadotrophin ,ovarian drilling
or IVF.

15. Prevalence• About 20% of reproductive age women demonstrate
the ultrasound picture of polycystic ovaries.
Oligomenorrhia-4-21% AND
oligomenorrhia+hyperandrogenism-3.5-9%
• About 5- 10 % have clinical or biochemical signs of
anovulation and androgen excess (dunaif 1995 , Norman
etal 2002)
• Estimation of 'true' prevalence PCOS must be made
with caution since there is no overall consensus on
the diagnostic criteria that must be satisfied to make a
diagnosis (Ledger and Clark 2003).

16. Laboratory studies
• Increased androgen levels in blood (testosterone
and androstendione)
• Increased LH, exaggerated surge
• Increased fasting insulin
• Increased prolactin
• Increased estradiol and estrone levels
• Decreased SHBG levels

18. •LH levels are elevated in 10%
women with PCOS.
LH/FSH ratios can be elevated in up
to 95% of women with PCOS if
women with recent ovulation are
excluded.
•LH levels are not necessary for
clinical diagnosis of PCOS.

19. 1.The clinical implications of this
abnormality are unclear. Although some
research has suggested lower fertility rates
and higher miscarriage rates for women
with high LH levels, other studies have
contradicted this data.
2. LH levels or the administration of
exogenous LH do not affect much in the
chances of ovulation or pregnancy rates
using CC or HMG.

20. Clinical
Biochemical

21. Hirsutism is the best
clinical marker of
hyperandrogenism.
Acne is a more variable
marker of
hyperandrogenism.

22. Hirsutism
• Defined as the growth of pigmented coarse hair in androgen-
dependent areas such as the face, chest, back, and lower
abdomen
• The most common manifestations of hyperandrogenism &
PCOS
The Ferriman- Gallway (FG) scale
• To assess the degree of hirsutism in 11 areas of the body
• Ranges from 0 – 44 & higher the score, more severe hirsutism
• A typical score for someone with hirsutism is between 8 and 29
• Though subjective, it allows the physician to monitor the
improvement in hair growth.

23. •The best biochemical markers of
hyperandrogenism are
free testosterone levels or
free testosterone index.
However, not all patients with PCOS have
elevated circulating androgen levels.
•Routine measurement of androstenedione
cannot be recommended.
•DHEAS is raised in small fraction of
patient with PCOS .

24. DHEAS
• Assessment ascertains Adernal Androgen.
In elevated DHEAS treatment with Insulin
sensitizing agent more rewarding than
Dexamathsone. As this Androgen is due to
Hyperinsulinemia & Long contiued use of
Dexamathasone causes adverse side effects.

25. • Women with regular cycles
but with hyperandrogenism &
PCO may have the PCOS.
•Women without
hyperandrogenism, but with PCO
& ovarian dysfunction may have
PCOS.

26. •PCOS should be excluded from other
disorders in which hirsutism and menstrual
irregularities are prominent, such as
Congenital adrenal hyperplasia,
Cushing's syndrome, and
Androgen-secreting tumors.
•In oilgo/anovulation: E2 & FSH to
exclude hypogonadotrophic
hypogonadism (central origin of
ovarian dysfunction)

27. • Late onset congenital adrenal hyperplasia
DHEAS > 18mmol/l
17 OH Prog > 1 mmol/l
• Ovarian + adrenal androgen secreting tumours
V. high testosterone > 1mmol/l
• Cushings Syndrome
- Dexamethsone suppression test
- 24 hours urinary cortisol
- DHEAS > 13 mmol/l
Anovulation & HyperandrogenismAnovulation & Hyperandrogenism
What is DDWhat is DD??

28. •In hyperandrogenic females:
prolactin to exclude
hyperprolactinaemia.
•Thyroid disorders in PCOS
patients are not more common
than in other young women-
TSH

30. Studies indicate that insulin
resistance may be an important
marker of a poor outcome and of
patients at high risk for ovarian
hyperstimulation.

31. How IR Can Be Assessed ??
• OGTT ( the best ).
• Fasting glucose (mmol/ L) to fasting
insulin (mul/L) ( Hyperinsulinemic –
euglycemic).Normal Value -< 4.5
• Clamp technique ( Gold standard) , too
expensive time consuming

32. Insulin resistance: decreased
insulin-mediated glucose utilization.
occur in up to 50% of patients with
PCOS,
so the consensus group recommends
it for PCOS patients.
1. Evaluation for metabolic
syndrome
2. Oral glucose tolerance tests

33. Metabolic syndrome
3 of 5 of the following
1. Waist circumference >88cm
2. Triglycerides >150 mg/dl
3. HDL <50 mg/dl
4. Blood pressure > 130/85
5. Fasting Blood glucose 110-121 &/or 2-h
glucose 140-199 mg/dl.

34. 2) PCOS Without IR:
What are characteristics?
• Lean.
• Euinsulinemic/ Euglycemic
• Enhanced Ovarian Sensitivity
to insulin (although no
Hyperinsulinemia).

35. • PCOS + IR ( 50-70 % ).
• PCOS without IR (Legro etal 2004).
Phenotypes
According to IR

36. 1) IR Phenotype of PCOS:
What are the characteristics ?
 Obese ( may be lean)
 Acanthosis Nigerians.
 Hirsutism.
 Resistance to CC,

37. • The central paradox regarding the
role of insulin in PCOS:
– Is the high ovarian response to insulin,
as opposed by the the whole body
resistance.
The Central Player ( InsulinThe Central Player ( Insulin
Resistance )Resistance )

38. Obesity plays a central role in the
development of PCOS leading to
hyperinsulinemia in susceptible individuals.
This hyperinsulinemia may alter
androgen metabolism via a variety of
mechanisms, the net result of which is
hyperandrogenism.

39. Elevated DHEASElevated DHEAS Elevated AndrogensElevated Androgens
PancreasPancreasPancreasPancreas
Insulin Receptor Dysfunction
Hyperinsulinaemia
LHRH
HypothalamusHypothalamusHypothalamusHypothalamus
PituitaryPituitaryPituitaryPituitary
AdrenalAdrenalAdrenalAdrenal StromaStromaStromaStroma FollicleFollicleFollicleFollicle
↑ LH FSH
LiverLiverLiverLiver
Reduced SHBGReduced SHBG
 Free androgens Free androgens
Hyperinsulinaemia & Hyperandrogenaemia

40. • Patients with anovulatory PCOS and
normal menses seemed to be leaner
and have lower insulin and
gonadotropin levels than those with
irregular menses (Carmina 2000).
Anovulation + PCO +
Normoandrogenemia
What is The difference bet.
Regular and irregular menst ?

41. IR
• Treatment of PCOS should be
directed towards causative rather
than symptomatic especially if IR is
proved as the central player !!!!
•IR

42. 1) Symptomatic PCOS :
What is the most important
parameter ?• Increased BMI is associated with
increased severity of the PCOS.
• No differences in basic , clinical and
biochemical parameters between
eumenorrhoic and oligomenorrhoic
PCOS (Vanky etal 2004).

43. 2) Asymptomatic PCOS
• Very lean
• Athletic women
• May be underweight.
• This may mask the
PCOS.
The less symptoms, the
better response to
medication and treatment.

44. Asymptomatic PCO (Ovulatory +
Normoandrogenic )
• There is significantly lower levels of
progesterone in the early Luteal phase.
• This may contribute to the delay in
conception in these patients.
• May be the starting cascade of Pcos!!!!!!!!!

45. Is Fertility Normal in patientsIs Fertility Normal in patients
With Ovulatory PCOS?With Ovulatory PCOS?
• These patients should be
regarded as fertile but many
studies have shown that women
with ovulatory PCOS have
luteal phase defect (Joseph H
etal 2002).

46. PCOS, starts in adolescence.
But
Unfortunately, not always
diagnosed at that age.

47. At The
End
We Can Say That
PCOS is A never –
ended story.