International Guidelines 2018 PCOD DIAGNOSTIC ASSESSMENT TOOLS + What we have learnt in last 50 years OVERVIEW of PCOD HISTORY PREVALENCE ETIOPATHOGENESIS as we understand it. SYMTOMS & SIGNS 2018 GUIDELINES DIAGNOSTIC criteria, assessment, investigations , monitoring & short / long term impact of untreated PCOD

1. DIAGNOSTIC ASSESSMENT TOOLS
+
What we have learnt in last 50 years
International Guidelines 2018
DR SHARDA JAIN
Dr Jyoti Agarwal
…Caring hearts, healing hands

2. OBJECTIVES
• OVERVIEW of PCOD
• HISTORY
• PREVALENCE
• ETIOPATHOGENESIS as we understand it.
• SYMTOMS & SIGNS
• 2018 GUIDELINES DIAGNOSTIC criteria,
assessment, investigations , monitoring &
short / long term impact of untreated PCOD

4. • Single most common heterogenous & multi-system endocrine
abnormality of women of reproductive age group.
• Incidence : 2-20% depending on how it is defined & 70% remain
undiagnosed.
• It is a disorder of the adrenal-ovarian endocrine axis.
• It may present with a variety of symptoms that can remit or
relapse over time.
• These include; menstrual disorders , excess facial and/or body
hair,acne , subfertility / infertility, truncal obesity, difficulty losing
weight (due to insulin resistance).
OVERVIEW

5. • It is one of the leading causes of infertility.
• Associated conditions include; Type 2 Diabetes ,
obstructive sleep apnoea, mood disorders, and
endometrial cancer.
• Other metabolic sequelae include; hypertension,
dyslipidaemia, visceral obesity, insulin resistance,
hyperinsulinaemia and CHD.
OVERVIEW

6.  1721 : First published description in Italy.
 1844 : Cyst-related ovarian changes described.
 1935 : Dr Irving Stein & Dr. Michael leventhal
Coined Stein – Leventhal disorder
 1980 : Linked to hyperinsulineemia & impaired GTT
 2003 : Rotterdom Criteria
 2006 : What causes PCOS ?
 2007 : The Thessaloniki ESHRE/ASRM-Sponsored PCOS
Consensus Workshop Group INFERTILITYThessaloniki,
Greece
 2018 : INTERNATIONAL GUIDELINES PCOD ( BARCILONA )
History of

7. History of

8. • The prevalence of PCOS depends on the choice of diagnostic criteria.
• The WHO estimated that 116 million women worldwide (3.4%) were affected in 2010.
• One community-based prevalence study using the Rotterdam criteria found that
about 18% of women had PCOS, and 70% were previously undiagnosed.
• Ultrasound findings of PCO are found in 8–25% of normal women.
• 15% women on oral contraceptives are found to have PCO.
INCIDENCE of
Between 3 to 20% & 70% of them remain undiagnosed

9. Understanding
in last 50 years (1970 -2018)
• It is combination of INSULIN RESISTANCE,
Genetic & environmental factors .
• Risk factors include obesity ,lack of physical
exercise ,family h/o someone with the
condition.

10. ETIOPATHOGENESIS in
Disease of many Theories
Most accepted is this Insulin
resistance,hyperinsulinemia
Increased free testosterone & androgens,
Increased LH .
High androgen levels cause symptoms of
androgen excess & inhibit growth of dominant
follicle & prevent apoptosis of smaller follicles
causing polycystic ovaries .

11. - Insulin Resistance

12. Fetal Growth Restriction &

13. • PCOS is a HETEROGENOUS disorder of unknown aetiology.
• FAMILIAL CLUSTERING and concordance in monozygotic
twins suggests some genetic component inherited in an
autosomal dominant manner with high penetrance but
variable expressivity.
• Each child thus has a 50% chance of inheriting the
predisposing genetic variant(s) from a parent, and, if a
daughter receives the variant(s) she will have the disease
to some extent.
GENETICS &

14. • The genetic variant(s) can be inherited from father or mother and passed
along to both sons & daughters
• These may be ASYMPTOMATIC CARRIERS OR HAVE SYMPTOMS such as early
baldness and/or excessive hair) and daughters, who show signs of PCOS.
• The phenotype manifests itself at least partially via raised androgen levels
secreted by ovarian follicle theca cells .
• The exact gene has not yet been identified. In In rare instances, single-gene
mutations can give rise to the phenotype of PCOS.
• CURRENT UNDERSTANDING OF THE PATHOGENESIS SUGGESTS-- IT IS A
COMPLEX MULTIGENIC DISORDER.
GENETICS &

15. OVERVIEW OF

16. CLINICAL PRESENTATION

17. Women with PCOS present with features
 Irregular menstrual cycles(delayed-85%/HMP-15% /
Prim Amen-2%)
Hyperandrogenism : Hirsutism 65-75%,Acne 30 %
Alopecia-5%
Heterogeneity + + + , from etiology to clinical
presentation and long term prognosis, is intrinsic
to PCOS
Nature reviews -endocrinology 2018 14,270

18. AcneAcne ObesityObesityHirsutismHirsutismAcantosisAcantosis
InfertilityInfertilityHAIR LOSSHAIR LOSSIRREGULAR MENSESIRREGULAR MENSES
Heterogeneous Clinical MANIFESTATION OF

19. A Changing paradigm in
Human Reproduction 27:14:24(2012)

20. 2018 INTERNATIONAL GUIDELINES
What is New
(It is totally evidence based ,
there is no controversy ,no arguments)
DIAGNOSTIC CRITERIA
• MENSTRUAL DISORDERS—
• HYPERANDROGINISM - BIOCHEMICAL/CLINICAL
• PCOM
• MONITORING IN PCOD
• ENDOMETRIAL CANCER
• CVD RISK / INSULINE RESISTANCE
• OBSTRUCTIVE SLEEP APNEA

21. INTERNATIONAL consensus Guidelines 2018
THE DIAGNOSTIC CRITERIA
is same as Rotterdam criteria
(ESHRE/ASRM 2003)

22. Guidelines 2018= Rotterdam criteria
(ESHRE/ASRM 2003)
at least 2 of the following 3
Lets Focus on Menstrual symtoms
1. Oligo-ovulation/or anovulation
2. Clinical orbiochemicalHyperandrogenism
3. PCOM on USS
X

23. IRREGULAR PERIODS IN
IRREGULAR MENSTRUAL CYCLES ARE DEFINED AS:
● NORMAL IN THE FIRST YEAR POST MENARCHE AS PART OF
THE PUBERTAL TRANSITION
> 1 to < 3 years post menarche: < 21 or > 45 days
> 3 years post menarche to perimenopause: < 21 or
> 35 days or < 8 cycles per year
 > 1 year post menarche > 90 days for any one cycle

24. When irregular menstrual cycles are present a
diagnosis of PCOS should be considered and assessed
according to the guidelines.
by age 15 or > 3 years post thelarche
(breast development)
PRIMARY AMENORRHEA in

25. Ovulatory Dysfunction in
Ovulatory dysfunction can still occur
with regular cycles and if Anovulation
suspected-- needs to be confirmed by
serum progesterone levels .

26. Guidelines 2018
at least 2 of the following 3
Lets Focus on Hyperandrogenism
1. Oligo-/anovulation
2. Hyperandrogenism
3. PCO on USS
X

27. • Assessment of biochemical
hyperandrogenism is most useful in
establishing the diagnosis of PCOD and/or
phenotype of PCOD
where clinical signs of
Hyperandrogenism (in particular
hirsutism) are unclear or absent.
BIOCHEMICAL hyperandrogenism in

28. Biochemical Hyperandrogenism in

29. Testosterone and dihydrotestosterone (DHT
Unbound (free
fraction
approximately 2 -3%)
bound
specific plasma
proteins
nonspecific
proteins
SHB
G
Albumi
n
biologically
inactive
weakly
bound
Free

30. BIOCHEMICAL HYPERSANDROGENISM IN
• Calculated free testosterone,
• Free androgen index or
• Calculated bioavailable testosterone should
be used to assess biochemical
Hyperandrogenism in the diagnosis of PCOS.

31. Total Testosterone levels may be normal but there is
elevated free testosterone levels due to decrease in
SHBG level.
Serum testosterone levels is more than 150 ng /dl
DHEAS is also marginally raised.
Androstenedione is also raised.

32. • ANDROSTENEDIONE and
• DEHYDROEPIANDROSTERONE SULFATE (DHEAS)
could be considered if TOTAL OR FREE
TESTOSTERONE are not elevated; however,
these provide limited additional information in
the diagnosis of PCOS.
Biochemical Hypersandrogenism in

33. Where assessment of biochemical Hyperandrogenism
is needed in women on
HORMONALCONTRACEPTION,
Drug withdrawal is recommended for three months
or longer before measurement to get correct values
and Contraception management with a non-
hormonal alternative is needed during this time.
BIOCHEMICAL HYPERSANDROGENISM IN
IMPORTANT TIP

34. • Where androgen levels are markedly above laboratory
reference ranges, other causes of biochemical
hyperandrogenism need to be considered.(androgen producing
tumors from ovary /adrenal ,cong.adrenal hyperplasia or exog
androgen )
• History of symptom, onset, and progression is critical in
assessing for androgen secreting NEOPLASMS,
• however, some androgen-secreting neoplasms may only induce
mild to moderate increases in biochemical Hyperandrogenism
BIOCHEMICAL HYPERSANDROGENISM IN
IMPORTANT TIP

35. CLINICAL HYPERANDROGENISM in
• A comprehensive history and physical
examination should be completed for symptoms
and signs of clinical Hyperandrogenism, including
acne, alopecia and hirsutism ,
• in adolescents, severe acne
and hirsutism

36. Standardized visual scales for scoring HIRSUTISM in
Shoud be used when assessing Hirsutism, such
as the modified Ferriman Gallwey score
(mFG) with a level ≥ 4 - 6 indicating Hirsutism
depending on ethnicity.
We must know local self-treatment of hirsutism
is common and can limit clinical assessment.

37. HIRSUTISM ASSESSMENT
Ferriman Gallway Score
O Bulent et al. Diagnosis of hyperandrogenism: clinical criteria. Best Practice & Research Clinical Endocrinology & Metabolism Vol. 20, No. 2, pp. 167–176, 2006
Best Practice & Research Clinical Endocrinology &
Metabolism Vol. 20, No. 2, pp. 167–16, 20067

38. LEVEL ≥ 4 - 6
INDICATING
HIRSUTISM,
DEPENDING
ON ETHNICITY,
2018
PCOD GUIDELINES
Modified Ferriman Gallway score

39. The Ludwig visual score is
preferred for assessing the
degree and distribution of
Alopecia.

40. Acne
• There are no universally accepted visual
assessments for evaluating acne.

41. Guidelines 2018
at least 2 of the following 3
Lets Talk PCOM
1. Oligo-/anovulation
2. Hyper Androgenism
3. PCOM on USS
X

42. ULTRASOUND AND POLYCYSTIC OVARIAN
MORPHOLOGY
• Ultrasound should not be used for the
diagnosis of PCOS in those with a
gynaecological age of < 8 years (< 8 years after
menarche), due to the high incidence of multi-
follicular ovaries in this life stage.

43. MULTI-FOLLICULAR
OVARIES
fewer cysts (~6 or more
per ovary), which tend to
be larger (up to 10 mm in
diameter) and distributed
throughout the ovary with
no stromal hypertrophy
PCOM 2003
12 or more subcapsular
follicular cysts (2-
9mm) ,Hyperechogenic
ovarian central stroma or
volume ≥10 cm3

44. New Rregulations 2018 on
• Using endovaginal ultrasound transducers with
a frequency bandwidth that includes 8MHz,
the threshold for PCOM should be on either
ovary, a follicle number per ovary of >
20 and/or an ovarian volume ≥ 10ml,
ensuring no corpora luteam, cysts or dominant
follicles are present.

45. ≥ 8 years after menarche
Ultrasound should
not
be used for the
diagnosis of PCOS
< 8 years after menarche
8MHz Probe,
The threshold for PCOM
should be on either ovary,
a follicle number per
ovary of > 20 and/or an
ovarian volume ≥ 10ml
New Regulations 2018

46. TVS approach is
preferable in
diagnosis of PCOS
In Transabdominal ultrasound reporting is
best focused on ovarian volume with a
threshold of ≥ 10ml, given the difficulty of
reliably assessing follicle number
with this approach.
IMPORTANT TIPS
In patients with irregular menstrual cycles and
Hyperandrogenism, an ovarian ultrasound is
not mandatory for PCOS diagnosis

47. How to report on
According to 2018 Guidelines?
• Clear protocols are recommended for reporting follicle number per ovary and
ovarian volume on ultrasound.
• Recommended minimum reporting standards include:
• Last menstrual period
• Transducer bandwidth frequency
• Approach/route assessed
• Total follicle number per ovary measuring 2-9mm
• Three dimensions and volume of each ovary
• Reporting of endometrial thickness and appearance is preferred --3-layer
endometrial assessment may be useful to screen for endometrial pathology
• Other ovarian and uterine pathology, as well as ovarian cysts, corpus luteum,
• Dominant follicles ≥ equal 10mm

48. ANTI-MÜLLERIAN HORMONE (AMH) in
Serum AMH levels should not be used as an
alternative for the detection of PCOM or as a
single test for the diagnosis of PCOS.
Till now we understood that Level of > 20 pmol/L are
associated with high sensitivety& specificity in diagnosis of
PCOS

49. ETHNIC variation in the presentation and
manifestations of PCOS are ++
• Health professionals should consider ethnic variation in the
presentation and manifestations of PCOS, including:
• A relatively mild phenotype in Caucasians
• Higher body mass index (BMI) in Caucasian women, especially in
North America and Australia
• More severe hirsutism in Middle Eastern, Hispanic and Mediterranean
women
• Increased central adiposity, insulin resistance, diabetes, metabolic
risks and acanthosis nigricans in South East Asians and Indigenous
Australians
• Lower BMI and milder hirsutism in East Asians
• Higher BMI and metabolic features in Africans

50. Monitoring of
• All those with PCOD should be offered regular
monitoring for BMI , waist circumference,BP .
• BMI—NORMAL (19 TO 23 ), OVERWEIGHT >23
OBESE >27. MORBID OBESE >32 with co morbidities
> 37 without co morbidities
Monitoring could be at each visit or at a minimum 6-12
monthly if normal
Weight,, height , waist circumference,
BMI, BP is Must

51. LIPID PROFILE
Overweight and obese women with PCOS,
regardless of age, should have a fasting lipid profile
(cholesterol, low density lipoprotein cholesterol,
high density lipoprotein cholesterol and triglyceride
level at diagnosis).
 Thereafter, frequency of measurement of LIPID profile should be
based on the presence of Hyperlipidemia and global CVD risk.
All women with PCOS should have BLOOD
PRESSURE measured annually, or more frequently
based on global CVD risk.
COUNCELLING is mandatory for consequences /late sequelae like
metabolic syndrome ,coronary artery disease ,endometrial caner etc

52. Post Menopausal Life Stage in
• A diagnosis of postmenopausal PCOD
could be considered if there is a past
diagnosis of PCOS, a long-term history of
irregular menstrual cycles and
Hyperandrogenism and/or PCOM, during the
reproductive years.

53. Endometrial cancer
• A 2-6-fold ↑ risk of endometrial cancer,
• Optimal prevention for endometrial hyperplasia and
endometrial cancer is not known.
• However, routine ultrasound screening of
endometrial thickness in PCOS is not
recommended.
• persistent thickened endometrium and/or risk
factors like prolonged amenorrhea, abnormal
vaginal bleeding need investigation by TVS &
Endometrial sampling

54. All PCOS patient should be screened
for Cardiovascular disease risk (CVD)
CVD risk factors in PCOS
•obesity,
•cigarette smoking,
•dyslipidemia,
•hypertension,
•impaired glucose tolerance
•lack of physical activity.

55. Insulin Resistance &
• INSULIN RESISTANCE in
PCOS is closely related to
obesity.
• It is the driving factor that
leads to:
– type 2 diabetes
– gestational diabetes
– prediabetes.

56. Clinical presentations of
IR
• Lethargy (tiredness)
• Hunger
• Difficulty concentrating (brain fog)
• S i g n e s :
• Weight gain around the middle (belly fat)
• High blood pressure
• High cholesterol levels

57. TESTS For INSULIN Resistance
• A baseline 2 hr 75gm oral glucose tolerance test
(OGTT) is recommended for all high risk woman of
PCOS. Normal 2hr blood glucose is <140mg/dl,
impaired glucose tolerance is when blood glucose is
140-199 mg/dl while in diabetes mellitus it is ≥ 200
mg / dl.
• Normal 2hr serum insulin is <80 μiu/ml shows insulin
resistance, while a level of >300 μ IU /ml shows
severe insulin resistance fasting glucose / insulin
ratio of <4.5 shows insulin resistance ( these 2 tests
not recommended in 2018 guidelines )

58. An oral glucose tolerance test
(OGTT -75 gm)
Who is high-risk women with PCOS?
• BMI > 25kg/m2
• or in Asians > 23kg/m2,
• history of impaired fasting glucose,
• H/O impaired glucose tolerance or
gestational diabetes,
• family history ofType 2 diabetes mellitus
• hypertension or
• high-risk ethnicity

59. Thereafter, assessment should be
every 1-3 years, influenced by the
presence of other diabetes risk
factors
fasting plasma glucose//PP after
75 gm glucose or HbA1c
Glycaemic status should be assessed
at baseline workup in all women
with PCOS

60. Gestational diabetes, impaired
Glucose tolerance and type 2 diabetes
• Regardless of age,
• the prevalence of gestational diabetes, impaired
glucose tolerance and type 2 diabetes is
• 5 fold in Asia,
• 4 fold in the Americas and
• 3 fold in Europe
with risk independent of, yet exacerbated by
obesity

61. DURING PREGNANCY
• A 75-g OGTT should be offered in all women with
PCOS preconception when planning pregnancy or
seeking fertility treatment. This picks up the high
risk cases of hyperglycaemia who are associated
with co morbidities in pregnancy.
• If not performed preconception, an OGTT should be
offered at < 20 weeks gestation, and with again
should be offered the test at 24-28 weeks gestation.

62. Obstructive Sleep Apnea Syndrome
(OSAS)
• Some women with pcos, specially with OBESITY have
OSAS with episodes of apnea & hypopnea during
sleep. It is also a risk factor for Cardiovascular
disorders in patient with PCOS
• A simple screening questionnaire can be easily
done by treating doctor , preferably the Berlin tool,
could be applied.
• if positive, referral to a specialist is done.

63. TAKE HOME MESSAGE
• 2018 GUIDELINES ARE EVIDENCE BASED ....SO NO
ARGUMENTS ..,NO CONTROVERSY
• Diagnostic criteria of 2018 guidelines is same as
ROTTERDOM CRITERIA OF 2013 i.e..2/3 findings .
• many criteria are suggested in our understanding of
mentrual disorders in PCOD, ultrasound detection of pcom
& testing of biochemical hyperandronism .
• Strict monitoring with BP, BMI , Waist , Lipid profile,
75gm OGTT,+ standardised visual criteria for Hirsuitm /
Alpoecia.

64. • Long term consequences of PCOD include metabolic
syndrome (hypertension , DM , Hyperlipidymia , obesity &
coronary artery disease ) , Endometrial hyperplasia & cancer
& obstructive sleep apnea-- should be explain by health
professional in detail.
• Advice : Given on Diet & Life Style
• Psychological issues considered, evaluated & addressed.
Any questions ???
TAKE HOME MESSAGE

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