Updates on management of

Adolescent PCOS An evidence based approach

Aboubakr Elnashar Benha university, Egypt

ABOUBAKR ELNASHAR

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)

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CONTENTS

1.Diagnosis

2.Evaluation

3.Treatment

Conclusion

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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. ABOUBAKR ELNASHAR

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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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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

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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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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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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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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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