Pcod

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"Polycystic Ovary Syndrome"[MeSH Terms]

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PCOS patient information diagnosis treatment NHS

PCOD usually refers to PCOS, polycystic ovary syndrome. It is a common hormonal condition in which ovulation may be irregular and androgen hormones may be higher than usual. Despite the name, it does not necessarily mean there are true ovarian cysts.

Possible symptoms

Irregular, infrequent, or absent periods
Acne, excess facial/body hair, scalp hair thinning
Weight gain or difficulty losing weight
Trouble becoming pregnant due to irregular ovulation
Darkened skin patches, often around the neck or underarms

Diagnosis A clinician typically considers PCOS after ruling out other causes and finding at least two of:

Irregular or absent ovulation/periods
Signs or blood-test evidence of raised androgens
Polycystic-appearing ovaries on ultrasound

An ultrasound is not always required. The NHS Wales PCOS overview describes this approach.

Management depends on your goal

Regular meals, activity, sleep, and weight management if applicable can improve symptoms and metabolic health.
Combined hormonal contraceptive pills or cyclic progesterone may regulate bleeding and protect the uterine lining when periods are very infrequent.
Medicines can help acne/excess hair and insulin resistance in selected people.
If pregnancy is desired, ovulation-induction treatment can be effective.

Seek medical care promptly for very heavy bleeding, severe pelvic pain, or if you have gone more than 3 months without a period. A gynecologist or endocrinologist can arrange appropriate blood tests and discuss treatment.

In detail notes for obgy

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2023 international evidence based guideline PCOS diagnosis management summary

PCOS/PCOD: OBGYN Notes Map

Definition, terminology, epidemiology
Etiology and pathophysiology
- Insulin resistance, hyperinsulinemia, androgen excess, abnormal folliculogenesis
Clinical features
- Menstrual irregularity, infertility, hirsutism, acne, obesity, acanthosis nigricans
Diagnosis
- Rotterdam criteria, clinical evaluation, investigations, ultrasound/AMH, differential diagnosis
Adolescent PCOS
Metabolic, endometrial, cardiovascular, psychological, and pregnancy risks
Management of menstrual irregularity and endometrial protection
Management of hirsutism, acne, and obesity
PCOS-related infertility and ovulation induction
PCOS in pregnancy and long-term follow-up
Exam-oriented short notes, flowcharts, and viva questions

High-yield overview

PCOS is a heterogeneous endocrine-metabolic disorder characterized by ovulatory dysfunction, hyperandrogenism, and/or polycystic ovarian morphology. In adults, after excluding mimicking disorders, diagnosis is made when any two of the three Rotterdam criteria are present. If irregular cycles and hyperandrogenism are both present, ultrasound or AMH is not required. In adolescents, both ovulatory dysfunction and hyperandrogenism are required, and ultrasound/AMH should not be used diagnostically. This aligns with the 2023 International PCOS Guideline.

Core management is individualized according to the presenting issue: menstrual control and endometrial protection, androgen-related symptoms, metabolic health, or fertility. Lifestyle support is advised for all, while combined oral contraceptives are commonly used for irregular menses/hyperandrogenic symptoms, metformin mainly for metabolic indications, and letrozole is first-line pharmacologic ovulation induction in anovulatory infertility when no other infertility factors exist.

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Possible symptoms

Irregular, infrequent, or absent periods
Acne, excess facial/body hair, scalp hair thinning
Weight gain or difficulty losing weight
Trouble becoming pregnant due to irregular ovulation
Darkened skin patches, often around the neck or underarms

Diagnosis A clinician typically considers PCOS after ruling out other causes and finding at least two of:

Irregular or absent ovulation/periods
Signs or blood-test evidence of raised androgens
Polycystic-appearing ovaries on ultrasound

An ultrasound is not always required. The NHS Wales PCOS overview describes this approach.

Management depends on your goal

Regular meals, activity, sleep, and weight management if applicable can improve symptoms and metabolic health.
Combined hormonal contraceptive pills or cyclic progesterone may regulate bleeding and protect the uterine lining when periods are very infrequent.
Medicines can help acne/excess hair and insulin resistance in selected people.
If pregnancy is desired, ovulation-induction treatment can be effective.

Definition, terminology, epidemiology
Etiology and pathophysiology
- Insulin resistance, hyperinsulinemia, androgen excess, abnormal folliculogenesis
Clinical features
- Menstrual irregularity, infertility, hirsutism, acne, obesity, acanthosis nigricans
Diagnosis
- Rotterdam criteria, clinical evaluation, investigations, ultrasound/AMH, differential diagnosis
Adolescent PCOS
Metabolic, endometrial, cardiovascular, psychological, and pregnancy risks
Management of menstrual irregularity and endometrial protection
Management of hirsutism, acne, and obesity
PCOS-related infertility and ovulation induction
PCOS in pregnancy and long-term follow-up
Exam-oriented short notes, flowcharts, and viva questions

High-yield overview

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Diagnosis and work-up
Pathophysiology
Complete management
Infertility treatment
Full PCOS/PCOD notes in parts

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2023 International Evidence-based Guideline PCOS diagnosis management recommendations letrozole metformin adolescent

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Polycystic Ovary Syndrome (PCOS/PCOD) - Detailed OBGYN Notes

1. Definition

Polycystic ovary syndrome (PCOS) is a common, heterogeneous endocrine-metabolic disorder of reproductive-age women characterized by a combination of:

Ovulatory dysfunction: oligo-ovulation or anovulation
Hyperandrogenism: clinical and/or biochemical
Polycystic ovarian morphology on ultrasound

It is a diagnosis of exclusion. The term PCOD is commonly used in practice, but PCOS is the preferred medical term.

PCOS is a leading cause of hirsutism and anovulatory infertility and is often associated with obesity and insulin resistance.
Berek & Novak's Gynecology, p. 1919.

2. Epidemiology

Affects approximately 10%-13% of women of reproductive age, depending on diagnostic criteria.
Most common endocrine disorder in reproductive-age women.
Most common cause of:
- Anovulatory infertility
- Hirsutism
- Menstrual irregularity due to chronic anovulation
Familial clustering is common. Inheritance is multifactorial/polygenic.

3. Etiopathogenesis

PCOS is multifactorial. Important interacting mechanisms are genetic susceptibility, insulin resistance, hyperinsulinemia, ovarian androgen excess, and hypothalamic-pituitary dysfunction.

A. Insulin resistance and hyperinsulinemia

Insulin resistance is frequent, particularly with overweight/obesity, but can occur in lean PCOS.

Hyperinsulinemia causes:

Direct stimulation of ovarian theca cells to increase androgen production.
Increased LH action on theca cells.
Reduced hepatic production of sex hormone-binding globulin (SHBG).
Increased circulating free testosterone due to low SHBG.
Aggravation of anovulation and impaired follicular development.

B. Increased androgen production

Androgens are increased from:

Ovary: excessive theca-cell androgen production
Adrenal gland: increased DHEAS in some patients
Peripheral conversion in adipose tissue and skin

Main androgens:

Testosterone
Androstenedione
DHEAS

C. Hypothalamic-pituitary-ovarian axis abnormality

Increased frequency of pulsatile GnRH secretion
Increased LH secretion relative to FSH in many, but not all, patients
Increased LH stimulates ovarian theca cells to produce androgens.
Relative FSH insufficiency impairs granulosa-cell aromatase activity and follicular maturation.

Important: An increased LH:FSH ratio is neither diagnostic nor essential for PCOS.

D. Follicular arrest

Multiple early antral follicles start developing.
They fail to select a dominant follicle.
Ovulation does not occur.
This produces chronic anovulation and the typical multifollicular ovarian appearance.

E. Role of obesity

Obesity can worsen:

Insulin resistance
Hyperinsulinemia
Hyperandrogenism
Menstrual irregularity
Subfertility
Pregnancy complications

However, PCOS can occur in women with normal BMI.

4. Clinical Features

A. Menstrual and reproductive manifestations

Oligomenorrhea: cycles >35 days or fewer than 8 cycles/year
Amenorrhea
Irregular cycles
Anovulatory abnormal uterine bleeding
Infertility or subfertility due to anovulation
Recurrent pregnancy loss may occur, though other causes must be evaluated.

B. Features of hyperandrogenism

Clinical hyperandrogenism

Hirsutism
Acne
Androgenic alopecia/female-pattern hair loss
Seborrhea

Virilization signs suggest an androgen-secreting tumor rather than routine PCOS

Rapid-onset severe hirsutism
Deepening of voice
Temporal balding
Increased muscle mass
Clitoromegaly
Rapid progression over months

C. Metabolic features

Overweight or obesity, especially central obesity
Acanthosis nigricans
Insulin resistance
Dyslipidemia
Prediabetes or type 2 diabetes mellitus
Hypertension
Obstructive sleep apnea

D. Psychological features

Screen for:

Depression
Anxiety
Poor body image
Eating disorders
Reduced quality of life

5. Diagnostic Criteria

Rotterdam Criteria, 2003

In an adult, diagnose PCOS when any 2 of the following 3 are present, after exclusion of alternative causes:

Ovulatory dysfunction
- Oligo-ovulation/anovulation
- Oligomenorrhea or amenorrhea
Hyperandrogenism
- Clinical: hirsutism, acne, female-pattern hair loss
- Biochemical: raised total/free testosterone or other validated androgen measures
Polycystic ovarian morphology
- On ultrasound, or AMH may be used as an alternative in adults according to the updated guideline.

Berek & Novak's Gynecology, p. 1919.

Key point

If a patient has:

Irregular menstrual cycles, and
Clinical/biochemical hyperandrogenism

then ultrasound or AMH is not required to diagnose PCOS after excluding mimicking conditions. This is supported by the 2023 International PCOS Guideline.

6. PCOS Phenotypes

According to Rotterdam criteria:

Phenotype	Hyperandrogenism	Ovulatory dysfunction	Polycystic ovaries
A - Classic/severe	Yes	Yes	Yes
B - Classic NIH phenotype	Yes	Yes	No
C - Ovulatory PCOS	Yes	No	Yes
D - Non-hyperandrogenic PCOS	No	Yes	Yes

Phenotypes A and B generally have greater metabolic risk.

7. Diagnosis in Adolescents

Diagnosis is difficult in adolescents because irregular cycles, acne, and polycystic ovarian appearance can be physiological after menarche.

Adolescent diagnostic requirements

Both must be present:

Persistent menstrual irregularity, interpreted according to years since menarche
Clinical and/or biochemical hyperandrogenism

Also exclude alternative diagnoses.

Do not use routinely in adolescents

Pelvic ultrasound for PCOS diagnosis
AMH for PCOS diagnosis

Adolescents with some features but not fulfilling criteria can be labelled "at risk of PCOS" and followed over time.

8. History Taking

Ask about:

Menstrual history

Age at menarche
Cycle length and regularity
Duration and amount of bleeding
Amenorrhea
Abnormal uterine bleeding

Hyperandrogenism

Onset and progression of facial/body hair
Acne
Hair loss
Virilization symptoms

Fertility history

Duration of infertility
Frequency/timing of intercourse
Previous pregnancy and miscarriage
Past fertility treatment
Partner history

Metabolic history

Weight gain
Diet and activity
Diabetes, hypertension, dyslipidemia
Family history of PCOS, diabetes, cardiovascular disease

Differential diagnosis clues

Galactorrhea, headache, visual symptoms: hyperprolactinemia/pituitary disease
Cushingoid appearance: Cushing syndrome
Rapid virilization: androgen-secreting tumor
Thyroid symptoms
Eating disorder, excessive exercise, stress: hypothalamic amenorrhea
Drug history, especially valproate and exogenous androgens

9. Examination

Height, weight, BMI
Waist circumference
Blood pressure
Distribution of body fat
Hirsutism assessment using modified Ferriman-Gallwey score
Acne, alopecia, seborrhea
Acanthosis nigricans
Signs of Cushing syndrome
Signs of virilization
Thyroid examination
Breast examination for galactorrhea if indicated
Pelvic examination when indicated

10. Investigations

A. To establish hyperandrogenism

Total testosterone
Free testosterone or free androgen index, depending on laboratory availability
SHBG
DHEAS if adrenal source is suspected

Use reliable assays. Biochemical testing can be inaccurate in patients using combined hormonal contraceptives because they elevate SHBG and reduce androgen production.

B. To exclude other causes

Condition to exclude	Suggested test
Pregnancy	Urine/serum beta-hCG
Thyroid disease	TSH
Hyperprolactinemia	Serum prolactin
Non-classic congenital adrenal hyperplasia	Early morning 17-hydroxyprogesterone
Cushing syndrome	Testing only if clinical suspicion
Androgen-secreting ovarian/adrenal tumor	Testosterone/DHEAS, imaging if markedly elevated or rapid virilization
Primary ovarian insufficiency	FSH, estradiol when indicated
Hypothalamic amenorrhea	History, FSH/LH/estradiol as clinically indicated

Mimics include thyroid disease, hyperprolactinemia, non-classical congenital adrenal hyperplasia, Cushing syndrome, and ovarian/adrenal androgen-secreting tumors.
Berek & Novak's Gynecology, p. 1919.

C. Metabolic evaluation

At diagnosis, assess:

Blood pressure
BMI and waist circumference
Lipid profile
Glycemic status

75-g oral glucose tolerance test (OGTT) is the most accurate assessment of glycemic status in PCOS. If unavailable, fasting glucose and/or HbA1c may be used, recognizing lower accuracy.

The international guideline advises a lipid profile at diagnosis regardless of age or BMI, with further testing based on risk. See the guideline summary.

D. Pelvic ultrasound

Used when needed to establish polycystic ovarian morphology or investigate other pelvic pathology.

Typical morphology in adults:

Increased follicle number per ovary and/or
Increased ovarian volume

Do not diagnose PCOS merely because the report says "polycystic ovaries." The clinical criteria and exclusion of mimics remain essential.

E. AMH

AMH may be used as an alternative to ultrasound for defining polycystic ovarian morphology in adults, but:

It should not be used as a single diagnostic test for PCOS.
It should not be used diagnostically in adolescents.

11. Long-term Complications

A. Endometrial hyperplasia and cancer

Chronic anovulation causes prolonged unopposed estrogen exposure, increasing the risk of:

Endometrial hyperplasia
Endometrial carcinoma

Risk is especially relevant in prolonged amenorrhea, obesity, diabetes, and persistent abnormal uterine bleeding.

Prevention: ensure regular withdrawal bleeding or continuous endometrial protection.

B. Metabolic complications

Impaired glucose tolerance
Type 2 diabetes mellitus
Dyslipidemia
Metabolic syndrome
Hypertension
Non-alcoholic fatty liver disease, where clinically suspected

C. Cardiovascular risk

PCOS is associated with increased cardiovascular risk factors. Absolute cardiovascular risk in young premenopausal women is low, but risk-factor screening and prevention are needed.

D. Sleep apnea

Consider screening for obstructive sleep apnea in women with PCOS who have:

Snoring
Unrefreshing sleep
Daytime somnolence/fatigue
Obesity

E. Mental-health issues

Screen for depression and anxiety, particularly at diagnosis and during major life stages.

12. Management

Principles

Management must be individualized according to the patient’s goals:

Menstrual regulation/endometrial protection
Hirsutism/acne/alopecia
Weight and metabolic health
Fertility
Psychological wellbeing
Prevention and management of long-term complications

A. Lifestyle Management

Recommended for all women with PCOS, irrespective of BMI.

Components:

Balanced, sustainable dietary pattern
Regular physical activity
Behavioural support
Sleep optimization
Reduction in sedentary time
Avoidance of weight stigma

Benefits

Improved metabolic parameters
Improved menstrual regularity and ovulation
Reduced androgen excess
Better quality of life
Improved fertility-treatment outcomes

There is no single "best PCOS diet." Choose an affordable, culturally appropriate, sustainable eating pattern.

Weight reduction

In women with overweight/obesity, even modest weight loss can improve:

Insulin resistance
Menstrual regularity
Ovulation
Fertility
Metabolic risk

Do not imply that weight loss is the only treatment. Lean women with PCOS also need metabolic and reproductive care.

B. Management of Menstrual Irregularity and Endometrial Protection

First-line: Combined oral contraceptive pill (COCP)

Useful for:

Irregular cycles
Acne
Hirsutism
Endometrial protection
Contraception

The international guideline recommends COCP as first-line pharmacological therapy for menstrual irregularity and hyperandrogenic symptoms.

Use the lowest effective estrogen dose consistent with individual contraceptive safety assessment.

If COCP is contraindicated or not acceptable

Options for endometrial protection include:

Cyclic oral progestogen
Progestogen-only pill
Levonorgestrel-releasing intrauterine system

A patient with prolonged amenorrhea should not remain without endometrial protection. Ensure withdrawal bleeding periodically or use continuous progestogen-based protection as clinically appropriate.

When to evaluate the endometrium

Assess for endometrial pathology when there is:

Persistent abnormal uterine bleeding
Prolonged amenorrhea with risk factors
Thickened endometrium on ultrasound where clinically relevant
Failed medical treatment

C. Management of Hirsutism and Acne

1. COCP

First-line drug treatment when contraception is also acceptable/needed.

Benefits:

Suppresses ovarian androgen production
Raises SHBG
Reduces free testosterone
Improves acne and hirsutism

Clinical benefit for hirsutism typically needs at least 6 months.

2. Cosmetic methods

Shaving
Waxing/threading
Depilatories
Bleaching
Laser/photoepilation
Electrolysis

These can be used with medical therapy.

3. Anti-androgens

Consider only if symptoms persist after at least 6 months of COCP and/or cosmetic therapy.

Examples:

Spironolactone
Cyproterone acetate in selected settings
Finasteride in selected cases

Important: Anti-androgens can harm a male fetus. Use only with effective contraception and specialist guidance.

4. Acne and alopecia

Standard dermatologic acne treatment may be used.
COCP may help acne.
Refer to dermatology for severe acne, scarring acne, or significant alopecia.

D. Metformin

Main role

Metformin is primarily used for metabolic indications, especially:

BMI ≥25 kg/m²
Insulin resistance
Impaired glucose tolerance
Type 2 diabetes
High metabolic risk

It may improve:

Insulin resistance
Glucose tolerance
Lipid profile
Cycle regularity in some patients

It is not the preferred first-line medicine for hirsutism if COCP can be used. COCP is more effective for irregular cycles and hirsutism, while metformin is preferred for metabolic indications according to the 2023 guideline.

Practical points

Start at a low dose and titrate gradually to reduce gastrointestinal adverse effects.
Common effects: nausea, abdominal discomfort, diarrhea.
Consider monitoring vitamin B12 in those with risk factors for deficiency or long-term use.
Metformin may be considered if COCP is contraindicated/not tolerated and cycles are irregular.

Inositol

Inositol may be used if a patient prefers it, but evidence for meaningful benefits in ovulation, hirsutism, or weight is limited compared with metformin. It should not replace evidence-based metabolic assessment and treatment.

E. Anti-obesity Medicines and Bariatric Surgery

For adults with PCOS and higher weight:

Consider anti-obesity drugs according to general obesity guidelines, alongside lifestyle intervention.
GLP-1 receptor agonists may be appropriate for selected patients after counseling about adverse effects, cost, need for contraception, and weight regain after cessation.
Bariatric/metabolic surgery may be considered according to general criteria.

These are not routine first-line PCOS therapies and require individualized medical evaluation.

13. Infertility Management in PCOS

A. Initial infertility evaluation

Before treating presumed anovulatory infertility, evaluate both partners.

Duration of infertility
Semen analysis
Assessment for ovulation
Tubal patency testing when indicated
Pelvic ultrasound
Assessment for additional female factors, including endometriosis or tubal disease
Preconception optimization:
- Folic acid
- Weight, glycemic control, blood pressure
- Smoking/alcohol/drug cessation
- Immunization review

B. First-line ovulation induction: Letrozole

Letrozole is first-line pharmacological therapy for anovulatory infertility in PCOS when no other infertility factor is present.

Compared with clomiphene citrate, it improves:

Ovulation rate
Clinical pregnancy rate
Live-birth rate

Use only after excluding pregnancy. It is off-label in some countries, so informed discussion is appropriate. The guideline supports letrozole over clomiphene for this indication, as summarized by ASRM.

C. Clomiphene citrate

Can be used where letrozole is not appropriate/available.
Risk of multiple pregnancy is higher than with natural conception.
Monitoring may be required.
Clomiphene plus metformin can be considered in selected women and improves outcomes over metformin alone.

D. Metformin for infertility

Metformin alone may improve ovulation and live birth compared with placebo, but it is generally less effective than letrozole or clomiphene-based ovulation induction.

Use especially when there are metabolic indications or as an adjunct in selected patients.

E. Second-line therapy

Gonadotropins

Consider after oral ovulation induction failure.
Effective but requires careful monitoring due to:
- Multiple pregnancy
- Ovarian hyperstimulation syndrome (OHSS)
- Cost and monitoring burden

Use a low-dose step-up protocol in specialist care.

Laparoscopic ovarian drilling (LOD)

Consider in selected clomiphene-resistant PCOS cases, especially when laparoscopy is otherwise indicated.

Advantages

May restore ovulation
Lower multiple pregnancy risk than gonadotropins

Disadvantages

Surgical/anesthetic risk
Adhesions
Potential reduction in ovarian reserve if excessive drilling is performed

F. Third-line therapy: IVF

IVF is considered if:

First- and second-line ovulation-induction treatments fail, or
There is another absolute indication, such as severe male factor or tubal factor infertility.

Use strategies to reduce OHSS risk, such as individualized stimulation, GnRH-antagonist protocols, agonist trigger where appropriate, and single embryo transfer.

14. PCOS and Pregnancy

Women with PCOS have increased risk of:

Gestational diabetes mellitus
Hypertensive disorders of pregnancy/preeclampsia
Miscarriage
Preterm birth
Higher risk of cesarean birth in some populations

Preconception care

Before conception:

Optimize weight and nutrition
Assess blood pressure
Evaluate glycemic status, preferably with OGTT
Treat diabetes/prediabetes where present
Start folic acid
Encourage smoking cessation
Address mental health and sleep disorders

During pregnancy

Early antenatal booking
Glycemic screening at booking or early pregnancy and repeat testing as indicated
Monitor blood pressure and fetal/maternal wellbeing according to obstetric risk
Do not use PCOS alone as a reason for unnecessary intervention

Use of metformin in pregnancy must be individualized. It is not automatically continued solely because a person has PCOS.

15. Short Exam Answer: PCOS Management

Management of PCOS is individualized based on symptoms and reproductive goals.

Lifestyle intervention for all
- Diet, exercise, behavioural support, weight management if relevant.
Menstrual irregularity/endometrial protection
- COCP first-line.
- Cyclic progestogen, progestogen-only method, or LNG-IUS if estrogen is unsuitable.
Hirsutism/acne
- COCP and cosmetic therapy.
- Add anti-androgen only with reliable contraception if inadequate response after 6 months.
Metabolic abnormalities
- Screen blood pressure, lipids, and glycemic status.
- Metformin for metabolic indications, particularly increased BMI or dysglycemia.
Infertility
- Letrozole first-line for anovulatory infertility.
- Clomiphene ± metformin, gonadotropins, ovarian drilling, then IVF depending on response.
Long-term follow-up
- Monitor diabetes risk, cardiovascular risk factors, endometrial protection, and mental health.

16. Viva Questions

What are the Rotterdam criteria?

Any two of:

Oligo/anovulation
Clinical or biochemical hyperandrogenism
Polycystic ovarian morphology
After excluding other etiologies.

Is raised LH:FSH ratio needed for diagnosis?

No. It may be seen but is not diagnostic.

Is obesity essential for PCOS?

No. PCOS can occur in lean women.

What is the most common cause of infertility in PCOS?

Chronic anovulation.

First-line drug for anovulatory infertility in PCOS?

Letrozole, when no other infertility factor exists.

First-line pharmacologic therapy for irregular periods and hirsutism in non-fertility management?

Combined oral contraceptive pill, if not contraindicated.

Why is progesterone important in PCOS with amenorrhea?

It prevents prolonged unopposed estrogen stimulation and reduces risk of endometrial hyperplasia.

What are important differentials for PCOS?

Pregnancy
Thyroid disorders
Hyperprolactinemia
Non-classic congenital adrenal hyperplasia
Cushing syndrome
Androgen-secreting ovarian/adrenal tumor
Hypothalamic amenorrhea
Primary ovarian insufficiency

When should an androgen-secreting tumor be suspected?

Rapidly progressive hirsutism or virilization, markedly elevated androgens, or onset over a short duration.

One-line summary

PCOS is a diagnosis of exclusion defined in adults by two of three features: hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology; management targets lifestyle, endometrial protection, metabolic risk, hyperandrogenic symptoms, and fertility goals.

Recent evidence check: the retrieved 2024-2025 systematic reviews did not identify a finding that changes these guideline-based core recommendations. The current primary reference remains the International Evidence-based PCOS Guideline.

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