1. Polycystic Ovarian
Disease & Hyperandrogenism
Evidence Based
Update on Diagnosis & Consequences
DR. SHARDA JAIN
Dr. Jyoti Agarwal
Dr. Jyoti Bhaskar
Dr. Abhishek Parihar
Directors :

2. PCOD & Hyperandrogenism
There is Need to Update as
Lately it is confusing
The Gynaecologists !!

3. Learning Objectives
• Prevalence and onset
• Etiology / Pathophysiology ( Partial Story)
• Update on clinical presentation
• Update of diagnostic criteria for PCOD.
• Short & long term consequences PCOD

4. IMPORTANCE OF PCOD
• One of the MOST COMMON endocrine
disorders of women
• Most frequent cause of anovulatory
infertility
• PCOD strongly associated with Insulin
Resistance which puts patients at risk
for DM, CVD, HTN, OSA (sleep apnea),
etc.

5. PCOD PREVALENCE
• PCOD is the most common endocrine
disorder affecting
4 - 12% of women of reproductive age.
• PCOD appears to effect all races &
nationality
Incidence is definitely more in Asian Indians
& seem to be increasing

6. Prevalence of PCOD In India

7. TYPES OF PCOD PATIENTS
Seen in Our Practice
Young
adolescent
Reproductive
age group
Women with
family
completed
Oligo/
amenorrohoea
Anovulatory
infertility
DUB
Hirsutism / Acne Obesity Metabolic
syndrome
Obesity Prevention of
metabolic
syndrome
Endometrial
neoplasia/hyper
plasia

8. Etiology of PCOD
• Exact etiology of PCOD is still UNKNOWN
– likely due to a steady state of high estrogen,
androgens, luteinizing hormone (LH) and insulin
levels.
• High estrogen levels can cause suppression
of pituitary FSH and relative increase in LH.
• Increased LH stimulates the ovary, which
results in anovulation, multiple cysts and theca
cell hyperplasia with excess androgen output.
• High insulin levels may also increase the
production of testosterone by the ovaries.

9. Genetic Basis
• A genetic basic that is both multifactorial
and polygenic is highly suspected, as there
is a well – documented aggregation of the
syndrome within families
(Franks, et al human reprod 12:2641,1997))
• An increased prevalence has been noted
between affected individuals and their
SISTERS (32 to 66 %) and MOTHER (24- 52%)
(Govind et al j clin endocrinol metab 84:38,1999)

10. Autosomal Dominant Inheritance
May have expression in both females and
males as it is seen in first – degree male
relatives of women with PCOS - have
significantly higher rates of elevated
circulating DHEA levels , early balding
and insulin resistance compared with
control males

11. INSULIN RESISTANCE
A Pathopysiological Contributor in
50-80% of the PCOD Women

12. Complete Pathophysiology of PCOD

13. Newer Concepts on PCOD & its
Management
With Myo- Inositol
Is also uploaded today
By Lifecare Centre Team in slideshare.net

14. The story is still not over …
Pandora Box
on
Myoinositol, D- Chiroinositol (40:1)
& Vitamin – D
In PCOD will be Uploaded soon

15. Vitamin D Deficiency is an
Independent Predictor of Obesity
80% PCOS women are obese
PCOS Women with vit D deficiency
• Higher mean BMI
• Hypertension
• Hypertriglyceridemia
• Lower high-density cholesterol
(all p<0.05)
Exp Clin Endocrinol Diabetes. 2006 Nov;114(10):577-83.)
ACOG

16. PCOD Presentation
• Symptom / Prevalence:
– Infertility 75%
–Hyperandrogenism 70%
–Obesity 60-80%
– Amenorrhea 50%
– Abnormal uterine bleeding 30-40%
– Normal menstruation 20%

17. Clinical Manifestation of PCOD
AAccnnee AAccaanntthhoossisis HHirirssuuttisismm OObbeessitityy
HAIR
LOSS
HAIR InInffeerrttiliiltityy
LOSS
IRREGULAR
MENSES
IRREGULAR
MENSES

18. Common Signs and Symptoms of PCOD

19. Symptoms of PCOD

20. Challenges of PCOD in Different Age
Groups
But the Root Cause is The Same

21. Challenges of PCOD in Different Age
Post
Groups
• Irregular Periods
• Endometrial Cancer
• Hypertension
• Diabetes
• Dyslipidemia
• OSA
•Dibetes mellitus
•Endometrial cancer
•Cardiovascular disease
•Metabolic Syndrome
Peri

22. DIAGNOSIS

23. PCOD DIAGNOSIS
• No single confirmatory
test for PCOS.
• It is a clinical diagnosis.
• Unlike past Ovarian
cysts alone are not
required for diagnosis.
• Cysts are present on
ultrasound in more than
90% of women with
PCOS but also present
in up to 25% of normal
women.

24. Bio chemical and Diagnostic
Markers of PCOD
Accepted everywhere
– Elevated androgen (i.e. testosterone > 60 or free
testosterone >0.75) levels
– Elevated LH:FSH ratio > 2:1
– Increased Insulin levels
– Insulin resistance , (Clinical / Lab)
– Ultrasound appearance of PCO

25. Diagnosis of Polycystic Ovarian Disease
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)
AE – PCOS (2009)
1. Hyperandrogenism : hirsutism and / or hyperandrogenemia
and
2. Ovarian dysfunction : oligo – anovulation and / or polycystic
ovaries and
3. Exclusion of other androden – excess or related disorders

26. Our Main focus will be on Diagnosis
of PCOD According to
Androgen Excess & PCOS society 2009
– Hyperandrogenism
• Elevated serum androgen levels or
• Biological expression of hyperandrogenism (acne or
hirsutism)
– Ovarian Dysfunction
• Anovulation or oligo-ovulation or
• Polycystic ovaries
– Absence of other causes of anovulation
• Thyroid disorders
• Hyperprolactinemia
• Cushing’s syndrome
• Late onset congenital adrenal hyperplasia (CAH)
• Ovarian and adrenal tumors

27. Hyperandrogenism

28. Hyperandrogenism
• Non-virilizing symptoms /signs include:
– Hirsutism: course hair growth in androgen-dependent
body areas such as sideburn area,
chin, upper lip, periareolar area, chest, lower
abdominal midline and thigh.
– Acne
– Oily skin
– Abnormal menstrual cycles
– Infertility

29. Hyperandrogenism
Virilizing symptoms /signs include:*
– Clitorimegaly
– Deepening of the voice
– Male pattern balding
– Masculinization of body habitus
– Increased libido
Less commonly seen than non-virilizing S/S
VIRILIZATION reflects higher androgen levels and should
prompt investigations
for an Androgen- producing tumor of the ovary or the
adrenal gland

30. Clinical

31. Ferriman Gallway Evaluation of Hirsutism
Hardly Used

32. Physical Exam – Significant Findings
• 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 50%

33. EExxcclluussiioonn ooff RReellaatteedd DDiissoorrddeerrss
• Thyroid disorders
SSrr..TTSSHH,,SSrr..PPrrll
• Hyperprolactinemia
• Cushing’s syndrome
DDeexxaa ssuupprreessssiioonn tteesstt
• Late onset congenital adrenal hyperplasia (CAH)
• Basal morning 17-OHP,(2-3 ng/ml))
• Ovarian and adrenal tumors DHEAS
• WHO I &III –FSH,LH,E2
• Syndromes of severe insulin resistance(HAIRAN
syn)

34. Hyperandrogenism
Differential Diagnosis

35. Screening Tests For Pcod
ACOG Recommendation
• ACOG recommends that all women
with a suspected diagnosis of PCOD
should be screened with
–17-hydroxyprogesterone level to
R/O late onset CAH (Level C).
• PCOD and late onset CAH are
distinguished from each other only by
laboratory testing.

36. A word about
Congenital Adrenal Hyperplasia (CAH)
• Late-onset presents in early adulthood.
• Autosomal Recessive.
• Presents with oligomenorrhea and/or hirsutism.
• 90% due to 21-hydroxylase deficiency.
• Patients with 21-hydroxylase deficiency do not form
cortisol in normal amounts.
DIAGNOSTIC TEST is
fasting 17-hydroxyprogesterone. always > 2 ng/mL .
All abnormal tests should be confirmed with
ACTH stimulation test. Consider endocrine
referral.

37. A Lab Tests suggested for
SUDDEN onset of Hyperandrogenism
Test Result
Total testosterone level Slightly elevated in PCOS
Total testosterone > 200 ng/dL -- suspicious for adrenal or ovarian tumor
therefore additional evaluation with pelvic US, CT or MRI indicated
Serum DHEAS level Slightly elevated in PCOS
DHEAS level > 8 ng/ml -- suspicious for adrenal tumor therefore
additional evaluation should include adrenal gland imaging with CT or MRI
24 hour urine cortisol or overnight dexamethasone
Urine free cortisol >20 ug/d is suggestive of
Cushing’s Syndrome

38. Hyperandrogenism
Hirsutism, acne, alopecia
BIOCHEMICAL Testing
• Free Testosterone –NO ROLE &
10 times costly
• ANDROSTENADIONE-NO ROLE
SUDDEN ONSET of these symptoms suggests other D/D
* Cushing’s syndrome
* Adrenal or ovarian tumor.

39. Summary
of Suggested Lab Test by
ACOG
 Prolactin level
 Testosterone level
 LH and FSH
 TSH
 Fasting glucose level or 2 hr OGTT
 Lipid profile, including total, LDL,HDL
 17-hydroxyprogesterone level*
*--Fasting level to r/o CAH

40. You Should know Prevalence of
Uncommon Conditions
to be Ruled Out before Making
Diagnosis of PCOD
• Adrenal tumors 2 per million
• Cushing’s Syndrome 2 per million
• Androgen secreting ovarian tumors < 1 per million
PCOD 1/3 girls in India
10% global

41. AAEESS RREECCOOMMMMEENNDDAATTIIOONNSS
• PPCCOOSS iiss aa HHYYPPEERRAANNDDRROOGGEENNIICC
DDIISSOORRDDEERR
• TThhee oovvaarriiaann mmoorrpphhoollooggyy sshhoouulldd bbee
ccoonnssiiddeerreedd wwhheenn eessttaabblliisshhiinngg tthhee
ddiiaaggnnoossiiss bbeeccaauussee ppoollyyccyyssttiicc oovvaarriieess
aarree ffoouunndd iinn tthhee mmaajjoorriittyy,, aalltthhoouugghh nnoott
aallll,, wwoommeenn wwiitthh PPCCOOSS

42. AAEESS CCOONNCCLLUUSSIIOONN
• PPCCOOSS sshhoouulldd bbee ffiirrsstt ccoonnssiiddeerreedd aass aa ddiissoorrddeerr ooff
aannddrrooggeenn eexxcceessss..
• AABBSSEENNCCEE OOFF CCLLIINNIICCAALL//BBIIOOCCHHEEMMIICCAALL
HHYYPPEERRAANNDDRROOGGEENNIISSMM IINN UUNNTTRREEAATTEEDD SSTTAATTEE OORR
IINN WWOOMMEENN <<4400YYRRSS ,,MMAAKKEESS AA DDIIAAGGNNOOSSIISS OOFF
PPCCOOSS LLEESSSS CCEERRTTAAIINN,,RREEGGAARRDDLLEESSSS OOFF TTHHEE
PPRREESSEENNCCEE OOFF OOVVUULLAATTOORRYY//MMEENNSSTTRRUUAALL
DDYYSSFFUUNNCCTTIIOONN //TTHHEE PPRREESSEENNCCEE OOFF PPCCOO..
IIff wwoommeenn wwiitthh oolliiggoommeennoorrrrhheeaa && PPCCOO oonn
uullttrraassoouunndd ddooeess nnoott hhaavvee hhyyppeerraannddrrooggeenniissmm
-- ddoo nnoott llaabbeell PPCCOOSS

43. UUSSGG
PPOOLLYYCCYYSSTTIICC OOVVAARRIIEESS
• PPrreesseennccee ooff 1122 oorr mmoorree ffoolllliicclleess iinn eeaacchh
oovvaarryy ,,22--99 mmmm iinn ddiiaammeetteerr aanndd oorr
iinnccrreeaasseedd oovvaarriiaann vvoolluummee >> 1100 mmll
• NNoo ssuubbjjeeccttiivvee aasssseessssmmeenntt
• OOmmiitt ssttrroommaall eecchhooggeenniicciittyy aanndd vvoolluummee
• WWoommeenn oonn OOCC ppiillll--??

44. PPOOLLYYCCYYSSTTIICC OOVVAARRIIEESS--UUSSGG
PPRRAACCTTIICCAALL CCOONNSSIIDDEERRAATTIIOONNSS
• IIff DDoommiinnaanntt FFoolllliiccllee oorr CCoorrppuuss LLuutteeuumm sseeeenn ---- ssccaann
rreeppeeaatt iinn nneexxtt ccyyccllee
• IIDDEEAALL--TTVVSS
• iiff rreegguullaarr ccyyccllee –– DDaayy 33 -- 55
• OOlliiggoommeennoorrrrhhooeeiicc wwoommeenn----pprrooggeessttiinn wwiitthhddrraawwll bblleeeedd
DDaayy 33 -- 55 oorr aannyy ddaayy
• FFoolllliiccllee nnuummbbeerr && ssiizzee--
• lloonnggiittuuddiinnaall aanndd AAPP ddiiaammeetteerr aanndd ssiizzee eexxpprreesssseedd aass
mmeeaann
• RRuullee oouutt eennddoommeettrriiaall hhyyppeerrppllaassiiaa
• AAsssseessss rriisskk ooff OOHHSSSS

45. SSCCRREEEENNIINNGG FFOORR MMEETTAABBOOLLIICC
SSYYNNDDRROOMMEE--RROOTTTTEERRDDAAMM
CCOONNSSEENNSSUUSS
•NNOO TTEESSTTSS FFOORR IIRR------??????
• OOBBEESSEE PPCCOOSS -- ssccrreeeenn iinncclluuddee OOGGTTTT
• NNOONNOOBBEESSEE PPCCOOSS -- CCoonnssiiddeerr iiff aaddddiittiioonnaall
rriisskk ffaaccttoorrss

46. SSccrreeeenn ffoorr MMeettaabboolliicc SSyynnddrroommee
UUssiinngg tthhee RRootttteerrddaamm CCrriitteerriiaa..

47. Indian 80cm

48. IInnssuulliinn RReessiissttaannccee
• IINNTTEERRPPRREETTAATTIIOONN
--NNoorrmmaall ffaassttiinngg→→<<1155 mmiiccrroo IIUU//mmll
AAfftteerr 22hhrr PPPP <<3300 mmiiccrroo IIUU//mmll
-- IINNSSUULLIINN RREESSIISSTTAANNCCEE lliikkeellyy →→ 110000 --115500
-- IINNSSUULLIINN RREESSIISSTTAANNCCEE →→115511 –– 330000
-- sseevveerree iinnssuulliinn rreessiissttaannccee →→ >> 330000
• FFaassttiinngg gglluuccoossee ttoo ffaassttiinngg iinnssuulliinn rraattiioo iiss
nnoo lloonnggeerr rreeccoommmmeennddeedd bbeeccaauussee ooff iittss
vvaarriiaabbiilliittyy

49. Androgen EExxcceessss SSoocciieettyy ssccrreeeenniinngg aanndd
ttrreeaattmmeenntt rreeccoommmmeennddaattiioonn ffoorr IIGGTT iinn PPCCOODD

50. f Screening foorr GGlluuccoossee IInnttoolleerraannccee--
RReeccoommmmeennddaattiioonnss ((jjcceemm--22000077)
• AAAACCEE----OOGGCCTT iinn oobbeessee PPCCOOSS aanndd ffaammiillyy hh//oo
• AACCOOGG——aallll PPCCOOSS--FFBBSS aanndd 22 hhrrgglluu lleevveell aafftteerr
7755gg ooff gglluuccoossee llooaadd
• AADDAA---------- << 4455 YYRRSS&& BBMMII>>2255 PPCCOOSS--FFBBSS ,,iiff
rraaiisseedd tthheenn OOGGTTTT
• AASSRRMM &&EESSHHRREE &&EEnnddooccrriinnoollooggyy PPCCOOSS
CCoonnsseennssuuss----------oobbeessee PPCCOOSS--SSccrreeeenn ffoorr
mmeettaabboolliicc aanndd gglluu iinnttoolleerraannccee wwiitthh aann OOGGTTTT..
NNoonnoobbeessee PPCCOOSS iiff aaddddiittiioonnaall rriisskk ffaaccttoorrss..

51. PCOD & Ovarian Dysfunction
Presentation
• Initial onset in the peri-pubertal
years and progressive in nature.
• PCOD with OVARIAN DYSFUNCTION
may have a wide range of clinical
symptoms.
– Menstrual irregularities,
– Hirsuitism, acne, or
– Infertility are the most common reasons
for seeking medical care.

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

53. Consequences of PCOD
(Listed in order from most common to least common)
• INFERTILITY
• Recurrent spontaneous abortion
• Depression/anxiety
• Dyslipidemias
– Total cholesterol (elevated)
– LDL cholesterol (elevated)
– HDL cholesterol (decreased)
– Triglycerides (elevated)
• Hypertension
• Type 2 diabetes mellitus
• Coronary atherosclerosis
• Cerebrovascular accidents
• Endometrial carcinoma

54. Insulin Resistance & 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
Because all are interrelated

55. Major Consequences of PCOD
• INSULIN RESISTANCE- up to 75%
–Evaluate for
–Hypertension
–Type 2 diabetes
– Dyslipidemias
–OSA (Sleep apnea)
–NASH, (Non-alcoholic fatty liver disease)
–Metabolic Syndrome X, etc.

56. Major Consequences of PCOD
• Endometrial Hyperplasia
– Chronic anovulation, obesity and
hyperinsulinemia are
associated with endometrial hyperplasia
and endometrial cancer.
– This is likely due to prolonged exposure to
unopposed estrogen.
– Endometrial cancer risk is 3 times that of
general population.

57. Major Consequences of PCOD
• Dyslipidemias
– 70% of women with PCOS will have abnormal
lipid panels.
– Elevated triglycerides and LDL and low HDL
are the most common abnormalities.
– All women with PCOS should be screened
with fasting lipid panel ( Level A).
Now endocrinologist feel that lipid profile can
be done any time of the day just like TSH

58. Major Consequences of PCOD
–CENTRAL OBESITY
android,
APPLE SHAPE
Central Obesity is High Risk
For Co-Morbidities /
Complications
– LOWER BODY OBESITY
Gynecoid
PEAR SHAPE
60-80% of women with PCOS are obese.

59. BMI Cutoff for INDIAN
-2.5 in each category
BMI Cutoff Weight Status Comments
<18.5 UNDERWEIGHT Being underweight also puts you at risk
for developing many health problems.
18.5 - 23.9 HEALTHY WEIGHT
RANGE
Your weight is within normal range. You can
continue to keep a healthy weight through physical
activity and healthy eating. Keep up with the good
work!
24 - 26.9 OVERWEIGHT Being overweight can put you at risk for
developing many chronic diseases
>27 OBESE
Obesity increases risks for developing many
chronic diseases such as heart disease and
diabetes, and decreases overall quality of
life.

60. 60-80% of women with PCOS are obese.
Anthropometric measurements
•Waist Circumference
•> 40” in males
•>35” in Females
•Waist HIP Ratio
–>1.0 in males
–>0.8 in Females

61. Target WAIST Circumference
for Indians
Sometimes even when BMI is within
Normal range, having too much fat
around the abdomen (APPLE SHAPE BODY)
will still put one at risk for heart disease and diabetes.
Below are the target goals for waist circumference
measurements.
INDIAN WOMEN
Equals or less than
80cm (31.5 in)

62. Major Consequences of PCOD
• 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.

63. Summary of presentations and
Consequences of PCOD
The Most
Common
Endocrine
disorder
In women
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

64. Left you with many Q unanswered

65. Management
of
Adolescent PCOD
Made Easy
Is also uploaded today
By Lifecare centre team
In slideshare.net

66. Management Guidelines
of INFERTILITY an ART
in PCOD Based on
A ESHRE/ASSRRMM--SSppoonnssoorreedd PPCCOOSS
CCoonnsseennssuuss WWoorrkksshhoopp GGrroouupp
((FFeerrtt SStteerrtt--22000088))
WWiillll bbee uuppllooaaddeedd sshhoorrttllyy

67. ADDRESS
11 Gagan Vihar, Near Karkari
Morh Flyover, Delhi - 51
CONTACT US
9650588339, 011-22414049,
WEBSITE :
www.lifecarecentre.in
www.drshardajain.com
www.lifecareivf.com
E-MAIL ID
Sharda.lifecare@gmail.com
Lifecarecentre21@gmail.com
info@lifecareivf.com
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