Updates on management of Adolescent PCOS An evidence based approach

1. Updates on management of
Adolescent PCOS
An evidence based approach
Aboubakr Elnashar
Benha university, Egypt
ABOUBAKR ELNASHAR

2. GUIDELINES
 In 2012:
ESHRE/ASRM-sponsored 3rd PCOS
In 2013
Endocrine Society Clinical Practice
 In 2015
1. Androgen Excess PCOS Society, Pediatric
endocrine Society
2. Italian society of endocrinology
3. American Association of Clinical
Endocrinologists (AACE) and the Androgen
Excess and PCOS Society (AES)
ABOUBAKR ELNASHAR

3. CONTENTS
1.Diagnosis
2.Evaluation
3.Treatment
Conclusion
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4. Grading of Recommendations, Assessment,
Development, and Evaluation (GRADE)
Endocrine Society Clinical Practice (2013)
Strength of the recommendation
strong recommendations use the phrase “we
recommend” and the number 1
weak recommendations use the phrase “we
suggest” and the number 2.
Quality of the evidence, Cross-filled circles
+OOO: very low quality evidence
++OO: low quality
+++O: moderate quality
++++: high quality.
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5. 1. DIAGNOSIS
Androgen Excess PCOS Society, Pediatric endocrine society(2015)
Great caution
before diagnosis with clinical features of androgen
excess (hirsutism and biochemical hyperandrogenism) if
oligomenorrhea has not persisted for ≥2 ys.
These girls can be considered to be at risk for
PCOS.
{avoid misdiagnosing physiological pubertal changes as
PCOS}
Postpone diagnosis
Frequent longitudinal re-evaluations
(Level C).
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6. ESHRE/ASRM (2012)
All 3 elements of the Rotterdam criteria should be
present
Oligomenorrhea or amenorrhea:
should be present for at least 2 ys after menarche or
primary amenorrhea at age 16 ys
US Diagnosis of PCO:
should include increased ovarian size (>10 cm3)
{multifollicular ovaries are a feature of normal puberty that
subsides with onset of regular menstrual cycling and may be
difficult to distinguish from PCO morphology }
Hyperandrogenemia:
rather than just signs of androgen excess should be
documented.
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7. Endocrine Society Clinical Practice (2013)
For diagnosis:
Clinical and/or biochemical evidence of
hyperandrogenism (after exclusion of other
pathologies) plus
Persistent oligomenorrhea
Anovulatory symptoms and PCO morphology:
not sufficient to make a diagnosis
{±evident in normal stages in reproductive
maturation}
(2++OO).
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8. Hyperandrogenemia
Extremely important
No established normal ranges.
FT ≥ 1.3 ng/dL,
(Piltonen et al, 2005)
TT >1 µg/ml
(The Rotterdam consensus workshop group, 2004).
Adult cutoffs should be used until appropriate
pubertal levels are defined.
(Endocrine Society Clinical Practice , 2013)
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9. AMH:
elevated AMH may serve as a noninvasive
screening or diagnostic test for PCO,
although there are no well-defined cutoffs
(Pawelczak et al, 2012; Rosenfield et al, 2012).
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10. 2. EVALUATION
1. Cutaneous manifestations
Physical examination should document cutaneous
manifestations of PCOS:
Terminal hair growth
Acne
Alopecia,
Acanthosis nigricans
Skin tags
(1+++O).
(Endocrine Society Clinical Practice, 2013)
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11. 2. Obesity
{Increased adiposity, particularly abdominal, is associated
with hyperandrogenemia and increased metabolic risk }
Screening for increased adiposity, by
BMI calculation
measurement of waist circumference
(1+++O).
(Endocrine Society Clinical Practice, 2013)
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12. 3. Depression
screening for depression and anxiety by
history and,
if identified: referral and/or treatment
(2++OO).
(Endocrine Society Clinical Practice, 2013)
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13. 4. Sleep-disordered breathing/obstructive sleep
apnea (OSA)
screening overweight/obese adolescents for
symptoms suggestive of OSA
when identified: definitive diagnosis using
polysomnography: referred for treatment
(2++OO).
(Endocrine Society Clinical Practice, 2013)
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14. 5. Type 2 diabetes mellitus (T2DM)
OGTT to screen for IGT and T2DM
{they are at high risk for such abnormalities}
(1+++O).
HgbA1c test if a patient is unable or unwilling to
complete an OGTT
(2++OO).
 Rescreening:
/3–5 y
more frequently if:
central adiposity
substantial weight gain, and/or
symptoms of diabetes develop
(2++OO).
(Endocrine Society Clinical Practice, 2013)
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15. 6. Cardiovascular risk
screened for the following CVD risk factors:
family history of early CVD
cigarette smoking,
IGT/T2DM
hypertension,
dyslipidemia,
OSA, and
obesity (especially increased abdominal adiposity)
(1++OO).
(Endocrine Society Clinical Practice, 2013)
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16. 3. TREATMENT
Indications
Even in the absence of a definitive diagnosis:
treatment that
alleviate symptoms
decrease the risk for subsequent associated
comorbidities are recommended
(Level B).
(Androgen Excess PCOS Society; Pediatric endocrine society, 2015)
Individual PCOS manifestations: obesity, hirsutism,
irregular menses should be treated.
(level B)
(ESHRE/ASRM; 2012)
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17. Lines of therapy
1. lifestyle therapy:
 First-line strategy
Weight loss
Calorie-restricted diets (with no evidence that
one type of diet is superior)
(2++OO).
Beneficial for both reproductive and metabolic
dysfunction.
(Endocrine Society Clinical Practice, 2013)
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18. Exercise
use of exercise therapy in the management of
overweight and obesity in PCOS
(2++OO).
{ improves weight loss
reduces CV risk factors and diabetes risk}.
(Endocrine Society Clinical Practice, 2013)
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19. 2. Hormonal contraceptives (HCs):
Indications:
First-line management for the
menstrual abnormalities
hirsutism/acne
(1++OO).
(Endocrine Society Clinical Practice, 2013)
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20. Types:
oral contraceptives, patch, or vaginal ring
do not suggest one HC formulation over another
(2++OO).
OCPs either containing or not containing an
antiandrogen
(Italian society of endocrinology, 2015)
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21. Metabolic effects of COC containing 30ug or less
of EE: mild
Deterioration of glucose tolerance
Worsening of lipid profile
should not influence the choice
(Italian society of endocrinology, 2015)
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22. VTE risk is not studied
Odds ratio
1.65 for BMI 25–30 kg/m2
1.84 for BMI 30–35 kg/m2
4.34 for BMI >35 kg/m2
[Murthy, 2010].
risk is further increased in CPA or 3rd generation
progestins, including drospirenone
[Lenzer, 2011].
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23. Screening for contraindications
 via established criteria
(1+++O).
lipid profile and the glucose tolerance should be
evaluated before and after 3 months of higher dose
OC containing cyproterone acetate
(Italian society of endocrinology, 2015)
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24. BMI: ≤35 kg/m2 with no specific metabolic and/
or CV abnormalities
choose from various OC formulations, acc to the
preferences of the physician and patient, and the
specific clinical characteristics of the patient.
(Italian society of endocrinology, 2015)
BMI
≥35 kg/m2 : OC should be prescribed with caution
≥40 kg/m2: not used
(RCOG, 2011). If contraception is needed, alternative
measures should be preferred, such as progestin-only
methods.
(Italian society of endocrinology, 2015)
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25. 3. Metformin:
Indications
if the goal is to treat IGT/metabolic syndrome
(2++OO).
who wish for long-term resumption of ovulation,
especially those with metabolic alterations with an
inadequate response to lifestyle intervention
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26. Met and COC have comparable therapeutic
effectiveness on cycle regularity and hirsutism.
Met was associated with a sig improvement in
insulin sensitivity
COC was associated with a deterioration of
insulin sensitivity ABOUBAKR ELNASHAR

27. 4. Combined metformin and OC
:
attenuating the adverse metabolic effects of OC
improving body composition
, as compared with OC alone
[Glintborg et al, 2014].
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28. Duration of HC or metformin
Not yet been determined.
OCPs should be continued until the patient is
gynecologically mature (5y postmenarcheal) or
has lost a substantial amount of excess weight.
(Rosenfield; 2015)
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29. CONCLUSIONS
Diagnosis:
Criteria for the diagnosis differ from those used for
older women of reproductive age
Hyperandrogenaemia: the most consistent marker
Early diagnosis for timely initiation of therapy,
outweighs harms and burdens of misdiagnosis.
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30. Evaluation:
metabolic and CV risks,
psychologic and dermatologic .
Treatment
should be individualized depending on
Age
Stage in life
Symptoms
Personal and familial risk indices
Choices.
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31. ABOUBAKR ELNASHAR
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