1. PANEL DISCUSSION
MANAGEMENT OF
PCOS
WOMB to TOMB
Dr. Sharda Jain

2. PANEL DISCUSSION
PCOS
MANAGEMENT OF
- WOMB to TOMB
HELD ON 10/10/2014
At Wood Apple
NEW DELHI
Dr. Sharda Jain
Organized by Delhi Gynaecologist Forum / Sheild H. Care

3. MANAGEMENT OF PCOS
WOMB to TOMB
MODERATOR : Sharda Jain
PANELISTS : Dr.Chitra setia
Dr Puneet Arora
Dr. Ila Gupta
Dr. Rupam Arora
Dr. Archana Sharma
Dr. Sangeeta Gupta
Dermatologists
Dr. V.K. Upadhyay
Dr. S. Kandhari

4. Stein1935Leventhol
ESHRE /ASRM

5. IMPORTANCE OF PCOS
Womb to Tomb
It is NOT A DISEASE, it is a syndrome with
varied presentations
PCOS has a CONTINUUM SPECTRUM
starting from the EARLY PREPUBERTAL
YEARS and continuing after Menopause
S/S peak through 2nd / 3rd decade of life
But Does not become quiescent till her death

6. Why has journey
From Womb To Tomb
• Above average (LFD) or
low birth weight for
gestational age.
• Premature Adrenarche,
• Atypical Sexual Precocity
Birth
Prepubertal
PCOS

7. PCOS
PCOS is condition which can effect
• women menstrual cycle,
• Fertility
• Her appearance (obesity, Acne, Hirsutism)
• Hormones / Depression
• Has long term health sequelae.
(Morbid Co-morbidities)

8. PCOS
Why has journey
From Womb To Tomb
INSULIN Resistance is the key …….finding
* Obesity * Dyslipidemia
*DM *Hypertension
• Acanthosis nigricans , skin Tags
• Fatty liver
• Sleep apnoea
4 Sibling
Endometrial Carcinoma

9. Q 1.
EPIDEMIOLOGY
Diagnosis & Incidence
Is the INCIDENCE of PCOS in
Adolescents Rising or
has the DIAGNOSIS Improved ?

10. EPIDEMIOLOGY
Yes, Both things are working
• There is a increase in incidence of PCOS in
adolescents
• Secondly because diagnosis has improved from
NIH-(1990) – TO ROTTERDOM(2004) – TO AES-PCOS
SOCIETY DIAG.CRITERIA (2009)
– many more cases are picked –up now

11. Improvement in
Diagnosis of PCOS over the years
NIH (1990)
1. Oligo ovulation
2. Hyperandrogenism and / or hyperandrogenemia
(with exclusion of related disorders)
ESHRE /ASRM (Rotterdam 2003)
To include TWO OUT OF THREE of the following:
1. Oligo – or anovulation
2. Clinical and / or biochemical signs of hyperandrogenism
3. Polycystic ovarian (with exclusion of related disorders)

12. Improvement in
Diagnosis of PCOS over the years
AES – PCOS (2009)
1. Hyperandrogenism : hirsutism and / or
hyperandrogenemia and
2. Ovarian dysfunction : oligo – anovulation and / or
polycystic ovaries and
3. Exclusion of other androgen excess or related
disorders

13. PCOS
Definition
1990 - 2009
Hyperandrogenism
(Clinical or
Biochemical )
Oligo- menorrhea
or
Oligo-Ovulation
Polycystic Ovaries
on USG
NIH (1990) yes yes no
Rotterdam
(2003)
yes Yes
2 of the 3 criteria
yes
AE-PCOS
Society
(2009)
yes Yes
1 of 2 criteria
yes
Diagnosis of Polycystic Ovarian Syndrome

14. Incidence of adolescent
PCOS
IF WE USE STRICTLY
NIH criteria = 6-8%
Rotterdam criteria = 15-25%
In Indian Asian Urban Community– this
number is more & seems to be rising
for reasons unknown ??

15. Prevalence of PCOD In India
30-36% Girls
Indian j pediatr.2012 jan;79suppl 1:s69-73
J pediatr adolesc gynecol.2011 Aug;24(4): 223-7

16. EXPERIENCE
DGF Survey of 2 schools 2004
Near 18-20% (1 in 5) girls going to private
schools in Delhi have PCOS (LPS)
OBESE – 50% (over weight , BMI>24 & obese >27)
MENSTRUAL PROBLEMS – 60%
Delayed Periods Most Common
Heavy Menstrual Bleeding – 20%
HIRSUTISM – 60-70%
ACNE – 30%

17. Q 2
What are the Conditions
That May Mimic PCOS ?
D/D

18. DIFFERENTIAL DIAGNOSIS
of PCOS
OLIGOMENORRHEA
•Pregnancy
•Hyperprolactinemia
•Thyroid Disease
•Ovarian Insufficiency
Hperanrogenism
Non – classic CAH
Cushing syndrome
Androgen – secreting tumors /
ovarian hyperthecosis
PCOM Non specific
incidental finding
has no meaning

19. What are the conditions
that may mimic PCOS ?
• Thyroid disorders
SSrr..TTSSHH,,SSrr..PPrrll
• Hyperprolactinemia
• Cushing’s syndrome
DDeexxaa ssuupprreessssiioonn tteesstt
• Late onset congenital adrenal hyperplasia (CAH)
• Basal morning 17-OHP
• Ovarian and adrenal tumors DHEAS
• WHO I &III –FSH,LH,E2
• Syndromes of severe insulin resistance(HAIRAN syn)

20. Q 3
Any Genetic or Familial Basis ?

21. Any Genetic or Familial Basis ?
• FAMILY Clustering is
known :
Risk of PCOS
• 40% - if her sister is having
PCOS
• 20% - if her mother suffered
from PCOS
• N = 5-10%
GENETIC ETIOLOGY NO LAST WORD AS YET

22. Genetic & PCOS
AUTOSOMAL DOMINANT pattern of
inheritance
Several genes namely
CYP 17
CYP11A
NO
CYP21,
SHBG
Insulin receptor
CONCLUSIVE
RESULT
TILL DATE

23. Q4(A)
DIAGNOSTICS – BLOOD TESTS
Which hormonal/blood tests are
done to confirm the diagnosis of
PCOS?

24. DIAGNOSTICS – BLOOD TESTS
 Testosterone level
 LH and FSH High LH & low FSH is seen in 60% cases
only
 TSH
 Prolactin level
 Fasting glucose level or 2 hr 75 gm OGTT
 Lipid profile, including total, LDL,HDL
 17-hydroxyprogesterone level*
*--(Fasting level to r/o CAH)

25. Q4B
DIAGNOSTICS – BLOOD TESTS
before METFORMIN
Which tests should be done before starting
insulin sensitizers – fasting / PP blood sugar,
insulin, Glycosylated Hb?

26. DIAGNOSTICS – BLOOD TESTS
• using fasting & 2 hrs blood sugar levels
following 75gm glucose load is all that is
needed
Category Fasting 2hrs PP
Normal <100 mg/dl <140 mg/dl
Impaired <100-126 mg/dl > 140 -199
NIDDM Over 126 Over 200
Insulin Levels are Really Not Needed for
diagnosis of PCOS

27. Q 4 C.
DIAGNOSTICS - USG
How is PCO and PCOM different
than PCOS?

28. UUSSGG CCRRIITTEERRIIAA ooff
PPOOLLYYCCYYSSTTIICC OOVVAARRIIAANN MMOORRPPHHOOLLOOGGYY
• PPrreesseennccee ooff 1122 oorr mmoorree ffoolllliicclleess iinn eeaacchh
oovvaarryy ,, 22 -- 99 mmmm iinn ddiiaammeetteerr aanndd oorr
iinnccrreeaasseedd oovvaarriiaann vvoolluummee >> 1100 mmll
OOrr 1100 ccmm33
• SSiinnggllee oovvaarryy iiss ssuuffffiicciieenntt
ttoo ddiiaaggnnoossee PPCCOOSS
• OOppttiimmaall ttiimmee ffoorr
uullttrraassoouunndd ((TTVVSS)) iiss DD33 –– DD55

29. Q5.
PCO, PCOM & PCOS
• It is a fact that PCOM ie POLYCYSTIC
OVARIAN MORPHOLOGY is present in
20 -35% girls with NORMAL menstrual
cycles &
• In Contrast there are patients of TYPICAL
PCOS who do not have PCOM on ultrasound.

30. Q 6.
What are the PHENOTYPES in
PCOS & what is there importance ?

31. Four Different Phenotypes of PCOS are
now identified
• TYPE A: hyperandrogenism, chronic anovulation and
<
polycystic ovaries.
• TYPE B: hyperandrogenism and chronic anovulation.
• TYPE C : hyperandrogenism and polycystic ovaries
• TYPE D : chronic anovulation and polycystic ovaries
Hyperandrogenemia is the
Hallmark of PCOS

32. Q7
SYMPTOMS
Which are the
COMMONEST SYMPTOMS
that women with PCOS present with?

33. Ans.
SYMPTOMS/ Management
current options
in Adolescents –Management Is Specific To Clinical
Symptoms
Three Commonest Presentation are
• MENSTRUAL DISORDERS when they consult
gynaecologists
•OBESITY when they consult endrocrinologists
•HISUITISM & ACNE when they consult dermatologist
Co-operations / Coordination
among specialists is needed

34. AAccnnee HHirirssuuttisismm OObbeessitityy
HAIR
LOSS
IRREGULAR
MENSES
AAccaanntthhoossisis Infertility &
Infertility &
pregnancy loss
pregnancy loss
HAIR
LOSS
IRREGULAR
MENSES
SPECTRUM
Clinical Manifestation of PCOD

35. Symptoms & There Frequency
in PCOS in Adolescents
Menstrual Cycle disturbance – 70%
- Oligomenorrhoea 50%
- Amenorrhoea 10%
- Abnormal heavy bleeding 10-15%
Hyperandrogenism 70%
Acne – 30 - 40%
Hirsutism 70%
Alopecia 10% as seen by Gynaecologits
Acanthosis Nigricans 1-3% lean & 20% obese
OBESITY 50- 60 %
NORMAL MENSTRUATION 20%
* INFERTILITY - 70% * EARLY PREGNANCY LOSS 50-60%

36. Q 8(A)
What is the Pattern of MENSTRUAL
IRREGULARITY in Adolescent PCOS
Q 8(B)
Why MENSTRUAL IRREGULARITY in
Adolescent PCOS needs treatment ?

37. Ans 8(A)
What is the Pattern of Menstrual
Irregularity in Adolescent PCOS
DELAYED PERIODS is most common
presentation
Other Presentations are:
• Withdrawal bleeding only
• Absent periods
• Heavy menstrual bleeding or
• Menometrorrhagia with Anemia
•20% PCOS have
• normal cycles
Obese
80%
Lean
30%

38. Ans 8(B)
Why MENSTRUAL IRREGULARITY in
Adolescent PCOS needs treatment ?
• Menstrual irregularity in adolescent
PCOS needs treatment because
chronic anovulation increases the risk
of developing Endometrial
Hyperplasia , which is associated with
Endometrial Carcinoma if not
monitored.
• In addition , anemia can result from
dysfunctional DUB or menorrhagia
Treatment IS Discussed LATER

39. • It is well accepted that If
menstrual
Irregularities persist for 2
years
After Menarche,
Then The Risk for PCOS is
Extremely High (70% of
Cases)

40. PCOS remains largely
UNDIAGNOSED as irregular
menses after menarche for 2
years & acne is commonly
seen in adolescents
• Transabdominal ultrasound
resolution has poor sensitivity
to diagnose PCOS
TVS is recommended

41. Q-9
COSMETIC CONCERNS
Question to Dermatologist
Dr. V. K. UPADHYAY / Dr. S
KANDHARI
WHAT ABOUT INCIDENCE OF
ALOPECIA & ACANTHOSIS
NIGRICANS IN ADOLESCENTS ?

42. COSMETIC CONCERNS
• Alopecia 10% as seen by Gynaecologists
(Dermatologist feel - Alopecia
is not all that uncommon & is
around 20%)
HAIR
LOSS
HAIR
LOSS
AAccaanntthhoossisis
Acanthosis Nigricans
1-3% lean & 20% obese

43. Q10(A).
COSMETIC CONCERNS
HIRSUTISM , ACNE, ALOPECIA
Is treatment for hirsutism based on
Ferring Gallway SCORING?

44. Ferring Gallway SCORING

45. Ferring Gallway Scale
This model quantities the extent of hair
growth in nine key anatomic sites: the
hair growth is graded using a scale from
0 (no terminal hair) to 4 (maximum
growth), for a maximum score of 36
A score of 8 or more indicates the
presence of androgen exces.
However, we do not use it in day to
day practice to grade our patients

46. Q10 (B).
COSMETIC CONCERNS
HIRSUTISM , ACNE, ALOPECIA
what all tests are needed to
diagnose HYPERANDROGENEMIA?

47. What All Test Are Needed To Diagnose
Hyperandrogenism
(Hirsutism, acne, alopecia)
BIOCHEMICAL TESTING
Total Testosterone
& 17 – hydroxyprogesterone level to
R/O late onset CAH is all that is needed
Free Testosterone &
% Free Androgen index have NO ROLE in
diagnosis. It is 10 times costly & is not standard in all
labs.
• ANDROSTENADIONE-NO ROLE

48. NORMAL VALUES OF SERUM ANDROGENS
Testosterone (Total) 20-80 ng/dl
DHEAS 100-350 mg/dl
17 – hydroxprogesterone
(Follicular phase)
30-200 ng /dl
Over 800 diagnostic of
adult onset CAH

49. Q10C
Hirsutism – Virilisation
SUDDEN ONSET of these symptoms suggests
other D/D
* Cushing’s syndrome
* Adrenal or ovarian tumor.

50. Q11
COSMETIC CONCERNS
Does ACNE require systemic treatment
or only topical is sufficient?

51. ACNE
• Grade 1: Acne are classified
non inflammatory
• Topical Retinoids
• Grade 2: Inflammatory
•Antimicrobial aqents +
•topical ratinoids
• Grade 3 : Combination of
above (Severe)
TREATMENT MEDICAL ENDOCRINE THERAPY +
TOPICAL / ORAL RATINOIDS

52. Management Topical
Retinoids
1. Apply the preparation over the whole affected
area and not just spot application
2. Apply the product very miserly as Acne
treatments are often irritating and drying
3. Excessive washing of face is to be avoided as it
further aggravates the irritation
4. Stop application the moment excessive drying
or irritation develops
5. Cream based applications should be preferred
as they reduce the concomitant dryness
ACNE GRADE - I

53. Systemic – Management
is needed for infected or severe acne
• ORAL ANTIBIOTICS – Minocycline,
Doxycycline, Azithromycin,
CEPHALOSPORINS
• Isotretenoin – 0.5 -1 mg/ Kg body
weight. Cumulative dose of 120 – 150
mg /Kg over a period of 6 – 9 months.
• Low dose OCP
Acne / Grade II & III

54. Hormonal Therapy in Acne
– Recalcitrant acne (severe Acne)
– Acne not responding to topical /oral
Isotretenoin
– Co- prescribed with Isotretenoin
•OCP
•6-9 MONTHS
•Any pill

55. Acne Treatment – Other Modalities
• Chemical peels
• Comedon removal
• IPL
• Cryotherapy
• Microneedling
• Use of steroids
Good Dermatologist
help is needed.
Gynaecologist can’t
treat on there own

56. Q12
COSMETIC CONCERNS
How common is ALOPECIA ?
Treatment ?

57. Alopecia
Incidence
in adolescent PCOS
Dermatologist feel that it is not all that uncommon
• Diffuse thinning
With preservation
of frontal line
• Bitemporal
recession
CAUSE
• Decrease in 5a
reductase -
• in DHT
DERMATOLOGIST To Be Care

58. Q 13
COSMETIC CONCERNS
Guidelines to Gynaecologist on
treatment of
HIRSUTISM

59. Treatment Hirsutism
IS CHALLENGING

60. TREATMENT - HIRSUTISM
• All combination OCPs are effective
• OCPs decrease androgen levels by
suppressing LH and stimulating sex
hormone binding globulin (SHBG).
• It takes almost 6 months when decrease
growth of hair is noted.
•OCPs with low androgenic
Progestins (norgestimate, desogestrel)
may be Most effective for acne and hirsuitism

61. Hirsutism Treatment
• METFORMIN perse are not needed
– To reduce hirsuitism.
Anti ANDROGENS (RECEPTOR BLOCKERS)
– Spironolactone 100mg twice daily (max dose
200 mg/day).
– A full clinical effect may take 6 months or
more
– After a periods of time, maintenance dose of
25-50 mg daily.

62. Q 14 B
Any Special Choice of OCPs for
hirsutism in PCOS ?

64. Q -14 C
TOPICAL HAIR GROWTH RETARDANTS
• EFFORNITHINE HYDROCHLORIDE CREAM are
effective & take almost 3 months to show effect.
Dosages & Applications
• Remove the heir from the affected areas and wait for minimum 5
minutes
• Apply a thin layer of hinder cream to the affected areas of the face
and adjacant involved areas under the chin
• Rub in thoroughly
• The treated area should not be washed for 4 hours
• Cosmetics and sunscreens may be applied over the treated areas
after the cream has dried
• To be used twice daily at least 8 hours apart
• For optimal results, use hinder fo a minimum of 6-12 months along
with other methods of hair removal

65. Q -14 D
Great TIPS on Solution of Hirsutism
• Temporary Methods – Remove the hair
shafts but leave the hair follicle intact.
Example – waxing, shaving, depilatory
creams & plucking
The process needs to be repeated indefinitely.
Though cheap & effective, are time consuming,
repetitive and often lead to pigmentation and
thickening of skin.
OCP & ALDACTONE ARE NEEDED

66. Q -14 D
Great TIPS on Solution of Hirsutism
ELECTROLYSIS IS GOING OUT
(Burns / Scarring)
LASER THERAPY is not permanent.
Repeated sittings may be needed
OCP & ALDACTONE ARE NEEDED

67. Q -15.
CHOICE OF COC
Menstrual Irregularity / Hirsutism / Acne
Which COC is most preferred?
Containing
• Levonorgestrel / Desogestrel
• Cyproterone acetate
• Drospirenone

68. CHOICE of COC
ANY LOW DOSE COC CAN BE GIVEN
• OC’s containing progestins such as NORGESTREL
/ LEVONORGESTREL / DESOGESTREL are preferable.
• If HIRSUTISM is a problem then
Cyproterone Acetate (CPA) is preferred.
•DROSPIRENONE HAS NO ADVANTAGE

69. Two Types OF OCPs
NON ANDROGENIC PROGESTOGENS
Desogestrel 0.15 mg + EE 30mcg(novelon)
Desogestrel 0.15 mg + EE 20mcg( femilon)
ANTIANDROGENS WITH PROGESTATIONAL ACTIVITY
Cyperoterone acetate
(EE 30 mcg + C 2 mg - Diane35)
Drosperinone- (EE 30 mcg + D 3 mg -Yasmin)

70. Q 15 B
What are the
DRAWBACK OF OCP
IN PCOS
• Menstrual Problem
• Hirsutism

71. What are the DRAWBACK OF OCP
IN PCOS
• Cause salt & water retention making weight
loss more difficult.
• In permenarcheal girls with short stature who
have open epiphyses, OCPs are
contraindicated bcz OCPs contain growth –
inhibitory amounts of estrogen
• In Incompletely mature girls - increase risk of
post pill amehhnoria
• VTE with OCP is primarily related to dose &
duration of estrogen use & progesterone like
DROSPERINONE (Twofold increase)

72. Q15 C
Combination OCPs
FOR HOW LONG in adolescents
PCOS?
Hirsutims / Menstrual

73. OCPs FOR HOW LONG ??
in Adolescents PCOS?
Hirsutims / Menstrual
By three months the bleeding problems gets
stabilized & by six month markedly decrease
growth hair is noticed.

74. As a general rule, OCPs should be
continued until the girls is gynaecologcally
mature (Five years postmenarcheal) or
has lost substantial amount of excess weight.

75. DURATION OF TREATMENT with
OCP is Controversial
Gynaecologists are confused & use it for
variable periods but
sr. DERMATOLOGISTS feel it should not be
discontinued unless girls wants to become
pregnant .

76. Q16.
ETHINYLESTRADIOL – HOW MUCH in
OCP?
What is the patient profile for
choosing COCs containing 35, 30,
20 mcg ethinylestradiol ?

77. ETHINYLESTRADIOL in OCP
– HOW MUCH?
Low Dose COC pill is the choice
(<35 ug EE is the choice).
In adolescent people start with EE 20 ug pill
– if BTB – occurs, higher dosage pill is used

78. Q-17
CHOICE OF PROGESTIN in OCP
What is the patient profile for
choosing the type of
PROGESTERONE in COCs?

79. CHOICE OF PROGESTIN
Safety of the pill is most important
Like venus thromboembolism , mycardial
infaction & cancer etc.

80. SAFETY of OCP is key
1st
Noethindrone
Gen.
Norgestril / Levonorgestril Low DVT • Non Androgenic Progestogens
Desogestrel 0.15 mg + EE 30mcg(novelon) ,
Desogestrel 0.15 mg + EE 20mcg( femilon)
•Antiandrogens with progestational activity
• Cyperoterone acetate
• (EE 30 mcg + C 2 mg - Diane35)
Drosperinone DVT twofold increase (BMJ)
2nd
Gen.
DVT
?
Drosperinone- (EE 30 mcg + D 3 mg Yasmin)

81. Q18.
CONCERNS WITH COC
Q. What are common complaints with the use of
COCs?
* HYPERTENSION * WEIGHT GAIN * ACNE

82. CONCERNS WITH COC
HYPERTENSION – in few 10 mm rise of BLOOD
PRESSURE may be there which settles once the drug is off
WEIGHT GAIN is not the complication with low dose
COC pills.
ACNE : Infact OCP is the treatment. We preferred pill with
Antiandrogens with progestational activity

83. Q19.
ROLE OF PROGESTIN
in menstrual irregularity

84. Role of Progestin in Menstrual
Irregularity
• MICRONIZED PROGESTERONE
(100 to 200 mg given orally at bedtime)
• MEDROXPROGESTERONE ACETATE
(10mg given orally at bedtime)
can be used for 7 to 10 days out of each month of cycle.
SIDE EFFECTS of progestin include * mood symptoms
(depression) * Bloating * Breast soreness
Patients must be informed that oral progestin
Prescribed in this manners (i.e. 7 to 10 days each month)
is not a means of contraception

85. Q20
INSULIN RESISTANCE
How frequently do you see IR in your
PCOS patients?
• Why we are worried ?
• Various syndrome with IR
• Special signature of IP
• Role of metformin
?

86. INSULIN RESISTANCE
Ans. In Research situations IR is seen in
good 65 to 70% patients among whom
70 to 80% are obese (BMI > 30) & 20 to
25% are normal weight.
It is the biggest risk factor for type 2 DM
and cardiovascular disease
Ref.http:www.uptodate.com

87. You should Know
Insulin Resistance is present
Various Clinical Syndrome
• Type 2 diabetes
• Cardiovascular disease
• Essential hypertension
• Polycystic ovary syndrome
• Non-alcoholic fatty liver disease (NASH)
• Certain forms of cancer -
breast,colon,liver,prostate
• Sleep apnea
All are interrelated

88. Significant Findings Insulin Resistance
which gynaecologits should always note
• SKIN : Acanthosis nigricans (darkly shaded skin in the
flexures of the neck , axilla, or groin – IR/DM)
Skin tags – IR/DM
10 %
Acanthosis nigricans
Over 20% obese
5% in lean

89. Q20(B).
INSULIN RESISTANCE
Q. Are insulin sensitizers prescribed
to all women with PCOS or only those
with insulin resistance?

90. Gynaecologist are Not Clear and
use metformin Left & Right
Both ESHRE & ASRM consensus is that
no clear role for insulin sensitizing in
management of PCOS except in patients
with glucose or type 2 diabetes
Therefore, on current evidence -
metformin is not a first line treatment of
choice in the management of PCOS for
any clinical manifestation

91. INSULIN RESISTANCE
Insulin sensitizers like metformin is
used in patients with impaired
glucose tolerance patients & not
otherwise

92. IImmppoorrttaannccee &&
HHooww ttoo DDiiaaggnnoossee IInnssuulliinn RReessiissttaannccee ––
JJuusstt DDoo FFaassttiinngg GGlluuccoossee && 7755 ggmm 22 hhrrss oorraall GGTTTT
• IMPAIRED Glucose Tolerance /
Type 2 Diabetes
– Up to 40% of women with PCOS have impaired
glucose tolerance (IGT).
– Risk of IGT and Type 2 Diabetes Mellitus (DM) is
increased in both obese and non-obese women
with PCOS.
– Retrospective studies have shown 2 to 5 fold
increase of type 2 diabetes in women with PCOS.

93. Q21.
Place of INSULIN SENSITIZERS in- YOUR
OPINION?
Q(A) In patients who do not respond to one
COC, do you change the COC (consisting of
another progestin) or shift them to or add an
insulin sensitizer?
Q(B). Metformin / Myoinositol

94. METFORMIN—PRESENT ROLE
• Although there had been widespread enthusiasm to use
metformin left & right – but clinical data no longer
support this approach
• Use of metformin in PCOS
should be restricted to those
patients with glucose intolerance
ESHRE/ASRM-Sponsored PCOS Consensus
Workshop *,2007, Thessaloniki, Greece

95. Dose of Metformin
• When metformin is given , therapy is started
with 500 mg daily before the evening
meal, with an increase in the dose by 500
mg per week to the effective dose of 1500
to 2000 mg daily , as tolerated .
• The greatest dose (1500 to 2000) often
are better tolerated when divided into two
daily doses or when given in an extended
release form

96. MYOINOSITOL in PCOS
advantage will be known
5 yrs down the line - at
present it is only a
concept
2014

97. Q 22
PREGNANCY & PCOS
If the female wishes to conceive, when
would you advise
her to stop taking the insulin
sensitizers and / or COCs?

98. PREGNANCY & PCOS
COCs need to be stopped, FOLIC ACID
started & drugs for ovarian stimulation to be
used.
CLOMIPHENE CITRATE IS
Widely used Simple to use
Minimal side effects Cost effective

99. Clomiphene in
ANOVULATORY PCOS
• 50-80% will ovulate on CC
• Only 40-50%will conceive

100. Q 23
What are INFERTILITY
Guidelines ??

101. THESSALONIKI CONSENSUS ON INFERTILITY
TREATMENT IN PCOS, GREECE 2007
FFIIRRSSTT LLIINNEE
CLOMIPHENE CITRATE
SSEECCOONNDD LLIINNEE
LOD/GONADOTROPINS
TTHHIIRRDD LLIINNEE
IVF
The Thessaloniki ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group March
2–3, 2007, Thessaloniki, Greece. Human Reproduction 2008
RR
EE
SS
II
SS
TT
AA
NN
CC
EE
RR
EE
SS
II
SS
TT
AA
NN
CC
EE
FF
AA
II
LL
UU
RR
EE

102. PCOS & INFERTILITY
Q (a) Ovulation induction aim
(B) First & second line management of
infertility in women with PCOS?
(c) Role of LOD
(D) Role Luteal phase support
(E) OHSS

103. Suggested a step by step approach to
ovulation induction in women with PCOS
Steps Approach
1 If BMI is elevated - loss at least 5% of current body
weight
2 Ovulation induction with clomiphene citrate
3 Metformin in combination with clomiphene
citrate in CC resistant cases or
BMI > 27 ???
4 Gonadotropin Therapy (OHSS / multiple
pregnancy)
5 Laparoscopic Ovarian Drilling
6 IVF ± Metformin Insulin sensitizer in combination with
gonadotropin therapy to decrease OHSS

104. Goals of Ovulation induction
in IUI / IVF
Minimize Complications &
Risk
AIM
Ideal Outcome
Singleton live
Birth at term
Cycle
Cancellation
Multiple
Pregnancy OHSS

105. 1. First Line Management
Clomiphene is drug of Choice
2. In CC Resistant cases
metformine has a role
3. 2nd line treatment Lap. Ovarian
drilling has a role for women who
can’t came for closed follow – up
pregnancy role is 50%
4. Gonadotrophines in PCOS have
promise, but OHSS & multiple
pregnancy, should never before
gotten complication
•Tamoxiphene
people have just
staring using it
•Letroz is
banned in india
•Metformine role
dealt

106. The Truth is that
OHSS MUST
BE PREVENTED RATHER than
treated

107. HCG TRIGGER PLAYS THE KEY
ROLE

108. METFORMIN
ROLE IN INFERTILITY
Metformin may be added to CC in
women with clomiphene resistance who
are older and have visceral obesity (I-A)
SOGC guidelines, 2010

109. Q 24
PREGNANCY & PCOS
What is the line of treatment in women
with PCOS who have
CONCEIVED NATURALLY ?

110. PREGNANCY & PCOS
• PCOS patients have high chance of
miscarriages so they need TLC +
micronised vaginal progesterone
• If they have conceived while taking
Metformin - it has to be continued for 3
months. This decreases miscarriage
rate.
• Few caution throughout pregnancy

111. Q 25
Can we do
LAPAROSCOPIC OVARIAN DRILLING
in ADOLESCENTS who do not respond to
OCP
Not
Recommended
except for infertility problems

112. Q26.
LONG-TERM COMPLICATIONS
Q. Are the women sensitized to the
long- term complications of PCOS?
Infertility, Diabetes, Cardiovascular diseases,
Cancer…

113. LONG-TERM COMPLICATIONS
COUNSELING IS IMPORTANT AT THE FIRST VISIT
detailing them of short term & long term
consequences.
It helps them in REDUCING WEIGHT, strictly
following life style modifications & become
proactive about conception & metabolic
disorders timely.

114. Consequences of Polycystic
Ovarian disorders
Short Term consequences
• Obesity
• Infertility
• Irregular menses
• Abnormal lipid levels/ Hypertension
• Hirsutism/acne/androgenic alopecia
• Glucose intolerace / acanthosis nigricans
• Increase early pregnancy loss / GDM
Long – Term consequences
• Dibetes mellitus
• Endometrial cancer
• Cardiovascular disease

115. Long Term Complications &
The Most
Common
Endocrine
disorder
In women
Consequences
Symptoms may
Include chronically
irregular and / or
Absent or delayed
periods
Symptoms may
include facial
hair , central
obesity and
acne
Let untreated it
may lead to
Heart
Disease
Left untreated,
it may lead to
Uterine cancer
Leading cause
of
Infertility
P C O D

116. Q27
Counseling
Counseling also helps them to get
regular screening / monitor from time to
time detect problems early.
•Infertility ,
•Diabetes
•Cardiovascular disease,
•Endometrial Cancer..

117. Q28.
CANCER
in women & PCOS
Would you like to comment on
a) Endometrial Cancer
b) Breast cancer in PCOS
c) Your Pregnancy Experience

118. Ans. 28 A
Endometrial Cancer in PCOS
• Gynaecologists should not forget that
there is 3 fold increase in incidence of
endometrial cancer.
• There Should be screening &
monitoring for the same from time to
time with TVS & EB

119. Ans. 28 B
PCOS & Breast Cancer ??
Limited data exist that Do Not Support the
conclusion that women with PCOS are a
increased risk for BREAST CANCER.

120. Q 29
OBESITY IN PCOS
ASSOCIATION IS
THERE
NOT THE CAUSATIVE
FACTOR
Not included in
diag. criteria

121. OBESITY & PSYCHOSOCIAL
HEALTH in WOMAN
1. Poor body image
2. Social stigmatisation (‘a laughing
matter’)
3. Lower education levels
4. Lower rates of marriage
5. Lower socio economic levels
Neglected Area

122. Management of Obesity
in general
1st LINE OF MANAGEMENT : Lifestyle changes like
modification of diet , physical activity and daily habits
2nd line of Management : introduction of pharmacotherapy
for patients with BMI above 24 with co – morbidities and
BMI above 27.5 with no co- morbidity
BARIATRIC SURGERY : may be an option for treatment
of morbid obesity (BMI > 32.5) when diet and exercise
do not work
1
2
3

123. Q30
ROLE OF VIT – D ?

124. Vitamin – D Role
in PCOS
was suggested by
all Panelist

125. ADD VITAMIN D Too
GIVE HER A GIFT FOR LIFE TIME

126. Q 31
Prevention of Endometrial Ca.
Monitoring of PCOS patients to prevent
occurrence of Endometrial Carcinoma
Guidelines
• Frequent TVS
• Endometrial Sampling
• Progesterone for periods

127. CONCLUSION
• TAILOR MADE THERAPY in
Adolescent PCOS is our attempt
in this panel discussion

128. CONCLUSION
Pre-Diabetes Fatty Liver
Diabetes type II Hyperlipidemia
Insulin Resistance Hypo-Thyroidism
Metabolic Syndrome Vitamin-D Deficiency
Cancer screening – Endometrial Ca.
RULE OUT Diagnosis:

129. CONCLUSION
COUNSELING & MONITORING of
short & Long term sequalae of
PCOD is the key

130. More & More PCOS CLUBS
should be formed
To shoot
Information for
teens & young
PCOS patients on
its
various aspects

132. ADDRESS
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