This document provides guidance on diagnosing and managing polycystic ovarian syndrome (PCOS) in adolescents. Key points include: - Adult PCOS diagnostic criteria are not applicable to adolescents due to normal irregular periods and cystic ovaries during puberty. - Recommended diagnostic approach involves assessing for unexplained hyperandrogenism and ovarian dysfunction after ruling out other conditions. - Management involves lifestyle changes like weight loss, exercise and diet, as well as symptom-focused treatments like birth control pills, anti-androgens and insulin-sensitizing agents. - The goals are to alleviate current symptoms, decrease future health risks of PCOS like infertility, metabolic syndrome and diabetes. Care must be taken to

1. Prof. Rokeya Begum
Director
Surgiscope fertility center
&
Adviser
USTC
Bangladesh.

2. Adolescent PCOSDi
DIAGNOSIS AND MANAGEMENT
OF ADOLESCENT PCOS

3. Polycystic ovarian syndrome is most common
endocrine disorder of reproductive aged women
(15-45 yrs).

4. The classic syndrome originally was described by
stein and leventhal as the association of amenorrhoea
with polycystic ovaries and variably hirsutism and
obesity.
(J.obstet gynecol 1935)

5. It is now recognized that PCOS represents a
spectrum of disease characterized primarily by the
following features.

6. Etiology
Multifactorial disease with full clinical expression being
the result of synergistic pathological interaction of :
1. Genetic,
2. Epigenetic
3. Environmental factor.

7. Genetic link
1. Familial genetic disorder related to a single gene defect.
2. 16 loci for PCOS (Jones and Goodarzi Fertil steril 2016)
3. Gene polymorphism
4. Familial clustering of PCOS common.
- First degree relatives of patients with PCOS may be at high risk for diabetes and
glucose intolerance.
- Inherited cell dysfunction
- Mother and sister of PCOS

9. Criteria for Diagnosis of PCOS
PCOS definition
NIH 1990
Patient demonstrates
both:
1. Clinical and/or
biochemical signsof
hyperandrogenism
2. Oligo- orchronic
anovulation
Rotterdam
criteria 2003
(ESHRE/ASRM)
Two of the following
three manifestations:
1.Irregular or absent
ovulation
2.Hyperandrogenism
(clinical or
biochemical)
3 PCO on USG
AES Criteria
2006
Patient demonstrates
both:
1. Hirsutism and/or
hyperandrogenemia
2. Oligo-anovulation
and/or polycystic
ovaries
Azziz et al. JCEM 2006; 91: 4237-45
Exclude other etiologies of androgen excess – Late onset congenital
adrenal hyperplasia, Androgen secreting tumours, Cushing’s
syndrome

10. Can we use these criteria to diagnose PCOS
in Adolescence?
Normal Adolescents
- Oligomenorrhoea
- Amenorrhoea
- Acne
- Multicystic” ovaries
NO

11. Adolescence
From Latin adolescere meaning to grow up
1.Transitional stage of physical and psychological
development from puberty to adult hood.
2.Adolescent young people between the age of 10 -19 years.

12. DIAGNOSTIC
APPROACH
Unexplained clinical
and /or biochemical
hyperandrogenism
Ovarian dysfunction

13. PCOS patient presents during
adolescents
30% menstrual irregularities
60% adrogen excess
84% over weight
9% IGT or T2 DM

14. Obesity
Typical obesity of PCOS is described as centripetal or apple type
of fat distributions center of body as apposed to thighs and legs.
Waist circumference > 88cm marker of central / visceral obesity
Body weight primary factor affecting quality of life.

15. Why adult criteria not applicable to young PCOS.
Anovulation
 85% of cycles anovulatory in first year of menstruation.
 59% of cycle anovulatory in third year.
 25% of the cycle still anovulatory by the 6th year.
Normal adolescent
PCOM at USG
2 years after Menarche – 40%
3 years 35%
4 years 33.3%

16. Abnormal menstrual patterns painting out anovulation in adolescents.
Secondary amenorrhea > 90 days
Oligomenorrhoea
Postmenercheal
1st year > 90 days < 4 periods/yr
2nd year > 60 days < 6 periods/yr
3-5 yrs > 45 days < 8 periods/yr
>6yrs > 35-40 days < 9 periods/yr
Menorrhagia bleeding <21 days or> 7 days and one pad per 1-2 hours.

17. Adolescent have functional ovarian cysts
High ovarian volume occurs in adolescence.
Transabdominal sonography is inaccurate
Clinical evidence of androgen excess (especially acne) is common
during puberty as resolves over time.

18. Metabolic features
Insulin resistance
- Increase insulin level due to high growth hormone leading to
obesities
- BMI > 24.
- Hyperpulsatile GnRh secretion.
- Decrease SHBG increase the androgen level.
Return to normal at the end of normal puberty but remain elevated
in PCOS.

19. How to evaluate hyper androgenemia in the adolescent girl.
 Hirsutism – good marker
 Alopecia – from the bolding and anterior hair line recession
seen only in more severe cases of androgen excess.
 Acne and seborrhea.
Sexual hair growth is commonly graded by
semiquantitative Ferriman-Gallway (F-G score)

20. Ferriman-Gallway (F-G score)

21. Recommendation:
Clinical:
1. Isolated mild hirsutism – in early post menarched year may be development.
2. Moderate to severe hirsutism constitutes clinical evidence of hirsutism.
3. Girls with acne that is persistent and poorly responsive to topical dermatologic
therapy should be evaluated for the presence of hyper androgenaemia before
initiation of any medical therapy.
Biochemical hyperandrogenic:
Measurement of total and free testosterone.

22. Precaution
1.Best assessed in early morning.
2.Early follicular phase.
3.Oral pill interface with the assessment of androgen.
4.After discontinuation wait for 6 weeks.

23. Total testosterone level
The normal upper limit for semen total testosterone in woman is
approximately 60ngm/dl (2.0nmol/L).
Free testosterone level an elevation in serum or plasma free
testosterone is the single most sensitive test to establish the
presence of hyper androgenemia.

24. Evidence of Oligo anovulation
It is difficult to differentiation of adolescent with physiological
anovulation from those with true ovulatory dysfunction in PCOS.

25. Recommendation
1.Menstrual interval persistently shorter than 20 days or greater
than 45 days in individuals two or more years after menerche
are evidence of oligo-anovulation.
2.A menstrual interval greater than 90 days is unusual even in
first year after menerche – Require further investigations.
3.Lack of onset of menes by the age of 15 years or by more than
2-3 years after thelarche regardless of chronological age.

26. Evaluation of polycystic ovarian morphology in an adolescent
(PCOM)
1. No compelling criteria to define PCOM have been established for adolescent
- ovarian volume
- follicle count
2. Multifollicular pattern which is defined by the presence of large follicle distributed throughout the
ovary does not have relation with hyper androgenaemia is more common in adolescent and should not
considered a pathological finding.
3. Regular menstruation with hyper androgenaemia – may show PCOM.
4. Abdominal US is Adolescent particularly obese girl may yield inadequate information.
5. AMH should not be used as diagnostic criteria for PCOS in adolescent.
6. Till now ovarian image can be deferred during the diagnostic evaluation of PCOS.

27. What are the other disease mimcs PCOS
1. Hypothyroidism
2. Hyper prolactineamia
3. Nonclassical CAH
4. Androgen secreting neoplasm
- ovary
- Adrenal
1. Cushing’s syndrome
2. Acromegaly
3. Gluco corticoid resistance
4. Drug – sodium valproate
The incidence is less

28. Hypothyroidism
Primary – increase TRH
Increase FSH/LH
Increase prolactin
Secondary
PCOS – obesity – Leptin
Increase TRH level

29. Hyper prolactinaemia causes PCOS phenotype
Hyper prolactinaemia
1. Central neurotransmitter dysregulation.
2. Positive feed back of estrogen
3. Drug OCPS, Antipsychotic
4 Other
- Pituitary cause
- Hypothyroidism
- Physiological
PCOS – causes mild hyper prolactnaemia

30. Congenital Adrenal Hyperplasia(CAH)
Mainly nonclassical form – phenotypical like PCOS
Premature pubarche
Peripubertal onset
Consanguinity
Virilisation
Total testosterone > 1.5ngm/L

31. 17 OH progesterone measurement in follicular phase
Due to 21 hydroxylase deficiency.
Less than 2ngm/ml - No NC CAH
More than10ngm/ml- NC CAH
2-8 ngm/ml – ACTH stimulation test
< 10ngm/nl – rule out
>15ngm/nl – NC CAH

32. Androgen secreting tumour – Malignant potential
 Rapid onset hirsutism
 Virilisation
 Total testosterone > 2ngm/ml
 DHEAS – Adrenocortical carcinoma.
 Imaging – USG, CT/MRI

33. Cushing syndrome
Acromegaly
 IGF- 1
 Post glucose growth hormone suppression test

34. Following investigations has to be done.
1. TSH and prolactin
2. Serum 17OH progesterone
3. Serum testosterone more than 2ngm/ml
4. DHEA
5. Imaging of abdomen to rule out Androgenic tumour.

35. Once the diagnosis of PCOS has been established
identify the other risk factors.
- Early development of type-2 DM
- Metabolic syndrome
- Sleep disordered
- Breathing difficulty
- Cardiovascular risk sequence
- Endometrial carcinoma

36. Family evaluation
There is a high frequency of PCOS and metabolic syndrome
among immediate relatives of individual with PCOS.

37. Management of adolescent girls with PCOS
• Psychological support
• Life style change
- Weight loss and exercise
- Healthy approach to eat
• Symptom oriented treatment
• Anti androgens and Insulin sensitizing agent

38. Psychological intervention
1. Counselling
Individual
- Group
2. Behavioral problem
Abnormal eating patterns (21% vs 2.5%)
3 .Damaged self confidence
Acne
hirsutism
obesity
Increased level of anxiety and depression.

39. Weight loss of only 5% of total body weight is associated with
- Decreased insulin and LH level
- Increased SHBG and decreased free androgen
- Improved menstrual function
- Reduced hirsutism and acne
- Lower testosterone level

40. Metformin
1.Reduced insulin level by direct inhibition of hepatic glucose
output.
2.Suppress appetite and enhance weight reduction.
3.Metformin is used as an adjuvant to
- Management of obesity
- Insulin resistant metabolic abnormalities

41. Dose
 lean – 850mg/daily
 over weight and obese 1.5-2.5gm daily

42. Menstrual irregularity
Chronic anovulation – Oligomenorrhoea
Abnormal bleeding - Anaemia

43. Combination OCPS
 First line treatment
 OCP induced menstrual period with a higher degree of reliability than other
form of treatment.

44. Combinations of OCPS
Progesterone
Inhibits endometrial proliferation
Prevent hyperplasia
Estrogen
Inhibits the activity of the H-P-O. axis
Reducing ovarian androgen production
Increase level of SHBG
Decrease gene of unbound testosterone
OCP will normalize androgen level within
18-21 days

45. Combinations OCPS
After three months – The efficacy of treatment is assessed by evaluation
- clinical symptoms
- Androgen level
How long
Till patient is gynecologically nature – 5 years post menercheal.
or loss of substantial amount of excess weight
At that point withholding treatment for a few months
-To allow recovery of suppression of H-P-O
-Persistent of abnormalities

46. Limitation of OCP
1.Weight loss difficult
2.Epiphyseal closure
3.Post pill amenorrhoea

47. Progesterone
- Menstrual irregularity can be controlled with cycle progesterone alone
GnRh agonist
Cannot tolerate OCP
Progesterone not sufficient
Not use before the case of 16 yrs
Pt receive GnRn agonist therapy also should be treated with
low dose estradiol and progesterone add back therapy
Bone mineral density should be monitored during therapy

48. Hyper adrogenism
This is manifested in 2/5 of cases by
Hirsutism
Equivalent cutaneous findings
Acene vulgaris
Alopecia
Seborrhoea
Hyperhidrosis
Hidradenitis suppurative

49. Hirsutism treated
Cosmetic and dermatological measure
Medical endocrine therapy
Cosmetic and physical measures
 Shaving
 Eflornithine cream (vanique) is a tropical agent that is FDA approved for the
removed of unwanted facial hair in women.

50. Laser therapy
 Removes hair permanently by thermal destruction of dermal papilla.
 Reduce hair density by 30% or move with 3-4 treatment cycle
Medical therapy
Reduced productions of androgen
Increase SHBG
Block androgen action at largest organs.

51. OCP
1. Suppress ovarian androgen production
2. Increase sex hormone binding globulin (SHBG) level
3. Decrease DHEA sulfate.
4. Transformation of vellus to terminal-reduced.
OCP
1. Arrest progression of hirsutism
Reduced the shaving by about half
1. Improve acne – with in 3 months

52. Androgen level has to be checked after 3 months of therapy.
Anti androgen
Suboptimal response after 6 months
Inhibits the androgen induced transformation of vellus to terminal hair.
Individual variation antiandrogen therapy reduces hirsutism by one third on average.
Antiandrogen should be prescribed with an OCP
Cause menstrual disturbance
Potential teratogen for fetus.

53. Anti androgen
1. Cyproterone acetate -progesterone with anti androgenic effect.
2. Spironolactone – Safe and potent
Starting with l00mg twice day until maximum effect than
reduce the dose to 50mg twice day
Causes fatigue and hyper kalamia
Laboratory test
Electrolytes
Liver function
- one to two week after initiation of Spironolactone

54. Flutamide
250mg TDS for 3 months
Gradually lowering the dose
Hepatocellular toxicity
Finasteride
5 reductase inhibitor

55. Acne
- Antibiotics and topical therapies
 Tetracycline, erythromycin and minocycline
 Used in conjunction with anti androgen treatment
 Topical non steroidal anti androgen
 Oncogenomic acetate
 Benzoyl peroxide.
Alopecia
- 2% minoxidil BD with anti androgen treatment

56. Over diagnosis of PCOS
Unnecessary psychological distress of having a
diagnosis associated with future subfertility.

57. Under diagnosis
Transition to adult hood and suffer the
long term consequence of PCOS.

58. Long term health hazard
 Infertility
 Metabolic syndrome
 Obesity
 Diabetes
 Heart disease

60. Take home message
1. The overlap between normal pubertal development and characteristic
features of PCOS.
2. Other diagnosis associated with irregular menses hyper adrogenaemia need
to excluded from diagnosis.
3. Even in the absence of definitive diagnosis
- Alleviation of current symptoms
- Decrease the risk
for subsequent associated co-morbidities