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Polycystic Ovarian Syndrome (PCOS)

Polycystic Ovarian Syndrome (PCOS) Dr Michelle M Fynes MB BAO BCH (Hons) MD (Research) MRCOG DU

Dr Michelle M Fynes MB BAO BCH (Hons) MD (Research) MRCOG DU DipUS

Locum Consultant Reproductive Medicine Department of Obstetrics and Gynecology Cambridge University Hospitals NHS Foundation Trust 2018

Objectives • Introduce and overview the topic of PCOS • History of PCOS • What

Objectives

Introduce and overview the topic of PCOS

History of PCOS

What have we learnt about PCOS 1970-2018

Review the neuroendocrine control of adrenal and ovarian function

Review the functional anatomy of the ovary

Review the physiology of ovulation and the menstrual cycle

Summarize the pathophysiology of PCOS

Epidemiology of PCOS

Genetic basis of PCOS

Symptoms and signs of PCOS

Short, intermediate and long-term impact of untreated PCOS

Assessment and investigations for PCOS

Review best practice management of PCOS

Summary of topic

Provide references for further reading

MM Fynes 2018

Introduction to PCOS:

Introduction to PCOS: • This is the most common endocrine disorder diagnosed in females aged 18-44

This is the most common endocrine disorder diagnosed in females aged 18-44 years.

It affects 2-20% depending on how it is defined.

It is a disorder of the adrenal-ovarian endocrine axis.

Affected females may have elevated adrenal and or ovarian androgens.

It may present with a variety of symptoms that can remit or relapse over time.

These include; irregular or no menses, menorrhagia, excess facial and/or body hair, pelvic pain, subfertility/infertility, patches of thick darker velvety skin, truncal obesity, difficulty losing weight (due to insulin resistance).

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.

MM Fynes 2018

History of PCOS:

First published description 1721 in Italy.

Cyst-related ovarian changes described 1844.

Other names for PCOS; polycystic ovary disease, functional ovarian hyperandrogenism, ovarian hyperthecosis and SteinLeventhal syndrome.

The last option only used for subset with amenorrhea, infertility, hirsutism, enlarged PCO.

Most common name for the disorder PCOS is based on the finding at US of PCO. These ovaries have an abnormally large number of developing eggs arrested in development.

At US these cysts are usually peripheral and circumferentially arranged within the ovary and appear as a ‘string of pearls’.

Not all women with PCO will have PCOS and not all women with PCOS have PCO.

a ‘string of pearls’. • Not all women with PCO will have PCOS and not all

MM Fynes 2018

History of PCOS:

History of PCOS:

History of PCOS 1970-2018:

History of PCOS 1970-2018: What have we learned about PCOS over the last 50 years? •

What have we learned about PCOS over the last 50 years?

PCOS has no cure.

Treatment involves lifestyle changes such as weight loss and exercise.

The OCP may help improving the regularity of periods, excess hair growth, and acne.

Metformin and anti-androgens may also help.

Other typical acne treatments and hair removal techniques may be used.

Efforts to improve fertility include weight loss, ovulation induction (e.g. clomiphene), or metformin and IVF is used by some in whom other measures are not effective.

Laparoscopic ovarian drilling may be helpful in resistant cases or where hormonal therapy is contra-indicated or associated with severe side effects.

Fertility therapy with PCO is associated with an increased risk OHSS.

Untreated patients are at higher risk fo metabolic syndrome and cancer.

MM Fynes 2018

Understanding PCOS

Neuro-endocrinology:

Hypothalamic Pituitary Ovarian Axis (HPOA)

Neuro-endocrinology: Hypothalamic Pituitary Ovarian Axis (HPOA)

Regulation Adrenal Gland:

Regulation Adrenal Gland:

Adrenal androgenesis

Adrenal androgenesis

HPOA control of ovarian function:

HPOA control of ovarian function:

Normal HPOA neuro-endocrine-regulation

Normal HPOA neuro-endocrine-regulation

Menstrual cycle and ovarian function:

Menstrual cycle and ovarian function:

Anatomy of the normal ovary:

Anatomy of the normal ovary:
Anatomy of the normal ovary:

Normal ovary versus PCO

Normal ovary versus PCO

Overview of PCOS:

Overview of PCOS:

PCOS: Epidemiology

Prevalence of PCOS:

Prevalence of PCOS: • The prevalence of PCOS depends on the choice of diagnostic criteria. •

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.

Ultrasonographic findings of PCO are found in 825% of normal women.

14% women on oral contraceptives are found to have PCO.

PCO may also be found in women with levonorgestrel-releasing IUDs.

on oral contraceptives are found to have PCO. • PCO may also be found in women

Worldwide prevalence of PCOS

Worldwide prevalence of PCOS

PCOS: Genetics

Aetiology of PCOS:- Genetics

Aetiology of PCOS:- Genetics • PCOS is a heterogenous disorder of unknown aetiology. • Familial clustering

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.

The genetic variant(s) can be inherited from father or mother and passed along to both sons

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 from women with the allele.

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.

to the phenotype of PCOS. • Current understanding of the pathogenesis suggests it is a complex

PCOS Genetics

PCOS Genetics

Aetiology of PCOS: Obesity

Severity of PCOS symptoms appears largely determined by

factors such as obesity. PCOS has some aspects of a metabolic disorder since symptoms are partly reversible. Considered a gynecological problem, PCOS consists of 28

clinical symptoms.

PCOS suggests ovaries central to disease pathology but cysts are symptoms not cause. Some symptoms persist even with removal of the ovaries. PCOS can appear minus ovarian cysts.

Gynecologists see it as a gynecological wth ovaries being

the primary organ affected. However, research identifies a

multisystem disorder, the main issue is

hypothalamichormonal regulation, with the involvement of many organs.

PCOD is used when there is US evidence and the term PCOS where there is a wider spectrum of symptoms. Cysts are only seen in 15% PCOS cases.

PCOS may be related or worsened by exposure during the prenatal period, epigenetic or environmental factors

(especially industrial endocrine disruptors e.g. bisphenol

A) and certain drugs) as well as increasing rates of obesity.

IUGR increase risk of adult metabolic syndrome and PCOS

and certain drugs) as well as increasing rates of obesity. • IUGR increase risk of adult
and certain drugs) as well as increasing rates of obesity. • IUGR increase risk of adult

Fetal Growth Restriction and PCOS:

Fetal Growth Restriction and PCOS:

PCOS: Pathogenesis

Pathogenesis of PCOS: PCOS arises due to stimulation of genetically susceptible ovaries to produce excess

Pathogenesis of PCOS:

PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic hormones (e.g. testosterone) via one or more mechanisms including:

Excess release of LH from the anterior pituitary

High levels of blood insulin in women whose ovaries are sensitive to this stimulus

PCO (identified at TVUS), the sign being due to multiple immature ovarian follicles that develop from primordial follicles but whose development has been arrested at an early antral stage due to the disturbed ovarian function. These follicles oriented along the ovarian periphery may appear as a 'string of pearls' at US.

Women with PCOS experience increased frequency of hypothalamic GnRH pulses, resulting in an increase in the LH/FSH ratio.

Women with PCOS experience increased frequency of hypothalamic GnRH pulses, resulting in an increase in the

Pathogenesis of PCOS:

Pathogenesis of PCOS: PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic
Pathogenesis of PCOS: PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic

PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic hormones (e.g. testosterone) via one or more mechanisms including:

Most have insulin resistance and/or are obese. Elevated insulin levels contribute to

/cause abnormalities seen in the Hypothalamic-Pituitary-Ovarian Axis (HPOA) leading to PCOS. Hyperinsulinemia increases GnRH pulse frequency, LH over FSH dominance, increased ovarian androgen production, decreased follicular maturation, and decreased SHBG binding.

Excess insulin, acting through its cognate receptor in the presence of component cAMP signalling, upregulates 17 alpha-hydroxylase activity via P13K, 17α- hydroxylase activity being responsible for synthesising androgen precursors. The combined effects of hyperinsulinemia contribute to an increased risk of PCOS. Insulin resistance is a common finding among women with a normal weight as well as overweight women.

risk of PCOS. Insulin resistance is a common finding among women with a normal weight as

Pathogenesis of PCOS:

Pathogenesis of PCOS: PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic

PCOS arises due to stimulation of genetically susceptible ovaries to produce excess androgenic hormones (e.g. testosterone) via one or more mechanisms including:

Adipose tissue possesses aromatase converting androstenedione to oestrone and

testosterone to oestradiol. The excess of adipose tissue in obese women creates the paradox of having both excess androgens (causing hirsutism/virilization) and oestrogens (inhibit FSH via negative feedback).

PCOS may be associated with chronic inflammation and several researchers have linked inflammatory mediators with anovulation and other PCOS symptoms. Similarly, there seems to be a relation between PCOS and increased level of oxidative stress.

It has previously been suggested that the excessive androgen production in PCOS could be caused by a decreased serum level of IGFBP-1, in turn increasing the level of free IGF-1, which stimulates ovarian androgen production, but recent data

concludes this mechanism to be unlikely.

of free IGF-1, which stimulates ovarian androgen production, but recent data concludes this mechanism to be

Pathogenesis of PCOS:

PCOS arises due to stimulation of genetically susceptible ovaries to produce

excess androgenic hormones (e.g. testosterone) via one or more

mechanisms including:

PCOS has also been associated with a specific FMR-1 sub-genotype. The research suggests that women with heterozygous-normal/low FMR1 have polycystic-like symptoms of excessive follicle-activity and hyperactive ovarian function.

Transgender men may experience a higher than expected rate of PCOS due to

increased testosterone, if they choose to take hormone therapy as part of their

gender presentation.

Not everyone with PCOS has polycystic ovaries (PCO), nor does everyone with ovarian cysts have PCOS; although a TVUS is a major diagnostic tool, it is not the only one. The diagnosis is straightforward using the Rotterdam criteria, even when

the syndrome is associated with a wide range of symptoms.

is straightforward using the Rotterdam criteria, even when the syndrome is associated with a wide range

So what is PCOS?

So what is PCOS?

So what is PCOS? • PCOS is thus due to a combination of genetic/environmental factors. •

PCOS is thus due to a combination of genetic/environmental factors.

Risk factors include obesity, lack physical exercise, family history of someone with the condition.

Diagnosis is based on two of the following three findings: no ovulation, high androgen levels, and ovarian cysts. Cysts may be detectable by ultrasound.

Other conditions producing similar symptoms include; adrenal hyperplasia, hypothyroidism, high blood levels of prolactin.

MM Fynes 2018

PCOS- Definitions and diagnostic criteria

PCOS- Definitions and diagnostic criteria Two definitions are commonly used: • NIH: In 1990 a consensus

Two definitions are commonly used:

NIH: In 1990 a consensus workshop sponsored by the NIH/NICHD suggested that a person

has PCOS if they have all of the following: Oligoovulation, signs androgen excess (clinical or

biochemical), exclude disorders that result in menstrual irregularity and hyperandrogenism.

Rotterdam: 2003 consensus workshop ESHRE/ASRM in Rotterdam indicated PCOS to be

present if any 2 of 3 criteria are met, in the absence of other entities that might cause these findings; oligo-ovulation and/or anovulation, excess androgen activity, PCO at TVUS. This

definition is wider, including > women, the most notable being those without androgen

excess. Critics say findings obtained from the study of women with androgen excess cannot necessarily be extrapolated to women without androgen excess.

Androgen Excess PCOS Society: In 2006, the Androgen Excess PCOS Society suggested a tightening of the diagnostic criteria to all of the following: excess androgen activity,

oligoovulation/anovulation and/or PCO, exclusion of other entities causing excess androgen.

MM Fynes 2018

Features of PCOS: • Menstrual : PCOS mostly produces oligo-menorrhoea (fewer than nine menstrual periods

Features of PCOS:

Menstrual: PCOS mostly produces oligo-menorrhoea (fewer than nine menstrual periods in a year) or amenorrhoea (no menstrual periods for 3 or more consecutive months), but other types of menstrual disorders may also occur.

Infertility: Generally results directly from chronic anovulation (lack of ovulation).

Metabolic syndrome: This appears as a tendency towards central obesity and other symptoms associated with insulin resistance; Serum insulin, insulin resistance, and homocysteine levels are higher in women with PCOS.

High levels of masculinizing hormones: Known as hyperandrogenism, the most common

signs are acne and hirsutism (male pattern of hair growth, such as on the chin or chest), but it

may produce hypermenorrhoea (heavy and prolonged menstrual periods), androgenic alopecia (increased hair thinning or diffuse hair loss), or other symptoms.

Rate: Approximately three-quarters of women with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of hyperandrogenemia.

three-quarters of women with PCOS (by the diagnostic criteria of NIH/NICHD 1990) have evidence of hyperandrogenemia.
Long-term risks of untreated PCOS? • Endometrial hyperplasia and cancer • Type 2 DM even

Long-term risks of untreated PCOS?

Endometrial hyperplasia and cancer

Type 2 DM even controlling for BMI and also gestational DM.

Hypertension particularly if obese or during pregnancy

Depression and anxiety.

Disorders lipid metabolism: hypercholesterolaemia and triglyceridaemia. PCOS women decreased removal atherosclerosis inducing remnants, seemingly independent of insulin resistance/Type II diabetes.

Cardiovascular disease: two-fold risk of arterial disease for women with PCOS relative to women without PCOS, independent of BMI and stroke.

Weight gain and obesity.

Miscarriage.

Sleep apnoea.

Non-Alcoholic Steato-Hepatosis (NASH) particularly if obesity is present.

Acanthosis Nigrans (patches darkened skin under arms, groin area, on the back of the neck)

Autoimmune thyroiditis

The risk of ovarian and breast cancer is not significantly increased overall.

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Patient assessment and diagnosis

Patient assessment

History- Menstrual dysfunction, hirsutism, acne central obesity (sensitivity 77%/specificity 93%)

Examination- BP, BMI, skin changes, hirsutism

(Ferriman Galway score)

Targeted investigations Blood and US imaging

Provisional diagnosis

Patient counselling

Patient information leaflets

Information on support groups

Outline care plan for individual

Detailed discussion of risks versus benefits

Advice on long-term sequelae for untreated PCOS

Detailed discussion of risks versus benefits • Advice on long-term sequelae for untreated PCOS MM Fynes

MM Fynes 2018

Hirsutism: Ferriman Galway Score:

Hirsutism: Ferriman Galway Score: Score 1-4 for 9 body areas. Total score <8 is normal. Score
Hirsutism: Ferriman Galway Score: Score 1-4 for 9 body areas. Total score <8 is normal. Score
Hirsutism: Ferriman Galway Score: Score 1-4 for 9 body areas. Total score <8 is normal. Score
Hirsutism: Ferriman Galway Score: Score 1-4 for 9 body areas. Total score <8 is normal. Score
Hirsutism: Ferriman Galway Score: Score 1-4 for 9 body areas. Total score <8 is normal. Score

Score 1-4 for 9 body areas. Total score <8 is normal. Score 8-15 mild hirsutism and >15 indicates moderate or severe hirsutism. Score of 0 absence of terminal hair.

Diagnostic criteria

Rotterdam consensus criteria 2 out of 3 criteria must be met including;

PCO with >12 or more follicles or increased ovarian volume [> 10 cm3 ]. No single follicle should reach the pre-ovulatory size 16mm. At laparoscopy (not a diagnostic test) the ovaries would appear enlarged and have a sooth pearl like appearance.

Oligo-ovulation or anovulation

Clinical and/or biochemical signs of hyperandrogenism.

Exclusion other aetiologies for irregular cycles (e.g. thyroid dysfunction, acromegaly or hyperprolactinaemia, have been excluded if there is clinical suspicion.

Features of hyperandrogenism include hirsutism (excess facial, body and midline hair)

MM Fynes 2018

Differential diagnosis

If signs of virilisation (e.g. deep voice, reduced breast size, increased muscle bulk,

clitoral hypertrophy), rapidly progressing hirsutism (<1 year between hirsutism being

noticed and seeking medical advice), then exclude other diagnoses.

High total testosterone levels (> 5 nmol/l or >2 upper limit normal range) exclude androgen-secreting tumours and late-onset/non-classical Congenital Adrenal Hyperplasia (CAH).

17-OH Progesterone should be measured in follicular phase and will be raised in CAH.

It is possible to have CAH without testosterone >5 nmol/l, particularly if the woman is heterozygous for this condition. Hence measurement of 17-hydroxyprogesterone with high index of suspicion (e.g. Ashkenazi Jews, or family history of CAH).

Since management of CAH is different than that of PCOS if 17-OH Progesterone is borderline, it will have to be confirmed by an ACTH stimulation test to diagnose CAH.

If clinical suspicion of Cushing’s syndrome or acromegaly, this should be investigated as per local practice.

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Other diagnostic considerations

It should be noted that the diagnosis of PCOS can only be made when other

aetiologies for irregular cycles, such as thyroid dysfunction, acromegaly or

hyperprolactinaemia, have been excluded if there is clinical suspicion.

Women with non-Caucasian ethnicity might need different criteria to diagnose PCOS.

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PCOS treatment:

Treatment

Lifestyle measures; Weight loss

Exercise

Low CHO diet Homeopathy dietary supplements

Pharmacological therapies;

Combined Oral Contraceptive (COC)

Anti-Androgen (AA)

Metformin

Spironolactone

Flutamide

Inositol

Ovarian drilling

Hirsutism; LASER, Electrolysis, waxing, bleaching Acne; COC/AA, topical agents, oral antibiotics. Subfertility/infertility; Clomiphene; ovulation induction

MM Fynes 2018

Treatment PCOS:

Therapeutic approaches for adult patients not seeking fertility include combined oral contraceptives (COC), antiandrogens (AA) and/or insulin sensitizers, although these practices are supported by limited high-quality evidence.

Metanalysis published Human Reproduction 2017; COC versus AA versus Metformin alone of in combination for the treatment of PCOS. Outcome measures included hirsutism scores, IR, BMI, menses pattern, BP, lipid profile, GTT.

COC and AA are more effective than metformin for hyperandrogenic symptoms and

endometrial protection. Their combination with metformin adds a positive effect on BMI and

glucose tolerance.

Examples COC; Yasmin Microgynon etc

Examples COC +AA; Dianette (Cyproterone Acetate)

Examples AA; Cyproterone Acetate

Examples AA; Spironolactone or Flutamide

PCOS and Metformin:

Metformin was logically introduced to establish the extent to which

hyperinsulinaemia influences the pathogenesis of PCOS.

Early studies were very encouraging but RCTs and several meta-analyses have changed the picture.

In PCOS failure of the target cells to respond to normal or ordinary levels of insulin is regarded as insulin resistance (IR).

IR leads to a compensatory increased production of insulin by the pancreatic beta

cells to control the hyperglycaemia which ultimately fails leading to T2DM.

In PCOS, hyperinsulinaemia has been thought to increase hyperandrogenaemia via a central role or by decreasing the circulating levels of SHBG.

IR is not considered a diagnostic criterion in PCOS. However, it is recognized by many as a common feature in PCOS independent of obesity

PCOS and Metformin:

Metformin improves sensitivity of peripheral tissues to insulin reducing serum levels.

Metformin inhibits hepatic gluconeogenesis and it also increases the glucose uptake by

peripheral tissues and reduces fatty acid oxidation.

Metformin has a positive effect on the endothelium and adipose tissue independent of its action on insulin and glucose levels.

Main side effects are GI; nausea, diarrhoea, flatulence, bloating, anorexia, metallic taste and abdominal pain. These symptoms occur with variable degrees in patients and in most cases

resolve spontaneously.

Start dose of 500 mg daily during the main meal of the day for 12 weeks can lessen side effects and allow tolerance to develop. A weekly or biweekly increase by 500 mg a day can then be pursued up to maximum 25002550 mg/day.

Slow release metformin can be associated with fewer side effects. Metformin can also lead to

vitamin B12 malabsorption in the distal ileum in approximately 1030% of patients which is an

effect dependent on age, dose and duration of treatment.

Metformin in PCOS:

Metformin works by reducing the circulating insulin levels.

Conflicting evidence as to whether it can directly affect ovarian steroidogenesis.

May restore ovulation, reduce weight, reducing circulating androgen levels, reducing the risk

of miscarriage and reducing the risk of gestational diabetes mellitus (GDM).

Other studies have reported that the addition of metformin to the ovarian stimulation regime in in vitro fertilization (IVF) improves the pregnancy outcome.

The lack of an emphatic or overwhelming efficacy for Metformin in females with PCOS is

largely due to the patients' variability in phenotypes and their metabolic parameters. Some studies have tried to identify the patients that are most likely to benefit from metformin, yet

again the results have not been forthcoming.

Metformin does not replace the need for lifestyle modification among obese and overweight PCOS women. The evidence categorically does not encourage its use to help weight loss either although it may be useful in redistributing adiposity according to some evidence.

The long-term use of Metformin to prevent remote complications of PCOS is uncertain and a significant amount of work is needed before a decision can be made on this front. Stipulations from studies carried out on the general population is not the same and can be

misleading given the diversity of PCOS patients with regard to their metabolic comorbidities.

Laparoscopic ovarian drilling:

Laparoscopic drilling for PCOS was first used 1984 involving multiple micro-perforations of the ovarian surface via diathermy or LASER destroying ovarian stroma and peripheral follicles of PCOS.

Punctures ovarian cortex 410 mm deep/3 mm wide and number

of punctures related to subsequent ability to conceive. 5-10 punctures more likely to produce conception.

Use monopolar needle/hook and electrocoagulation at 40 W, (range from 30-400 W). Laparoscopic approach < morbidity then ovarian wedge resection.

Aims to reduce the amount of androgen producing tissue, may

reduce circulating E2 levels, LH level/pulsations, and inhibin B.

The most plausible theory is that reduction of these leads to an increase in the secretion of FSH and SHBG leading to effective follicular maturation and ovulation.

Low serum E2 associated with <aromatase activity. IGF-1 produced

with injury aids effects of FSH through greater blood flow GnRH

delivery. AMH levels fall after drilling

Goal of drilling treatment is induction of mono-ovulatory cycles.

AMH levels fall after drilling • Goal of drilling treatment is induction of mono-ovulatory cycles. MM
AMH levels fall after drilling • Goal of drilling treatment is induction of mono-ovulatory cycles. MM

MM Fynes 2018

Laparoscopic ovarian drilling:

Weight loss and Clomiphene Citrate (CC) first line therapy.

CC is a Selective Estrogen Receptor Modulator (SERM) with; 49% ovulation rate, 30% pregnancy rate, 23% live birth rate at 6 months, and 8% rate of multiple gestation.

Other non-surgical PCOS medical therapy options include; the SERM Tamoxifen or aromatase inhibitors, insulin sensitising drugs, and hormonal ovarian stimulation.

25% women are resistant to CC therapy

CC therapy is followed by GnRH therapy but >risk OHSS

Laparoscopic drilling may reduce the risk of OHSS

The effectiveness of the surgical procedure is similar to CC but results in fewer multiple pregnancies per ongoing pregnancy regardless if the technique is unilaterally or bilaterally performed

If patients do not become pregnant 6 months after ovulation is induced by ovarian drilling then GnRH therapy and IVF warranted

become pregnant 6 months after ovulation is induced by ovarian drilling then GnRH therapy and IVF
become pregnant 6 months after ovulation is induced by ovarian drilling then GnRH therapy and IVF

MM Fynes 2018

Summary and audit topics:

Summary of the metabolic consequences of PCOS and screening recommendations:

PCOS should be diagnosed according to the Rotterdam consensus criteria.

Women with PCOS should be informed of the possible long-term risks to health that are associated with their condition by their healthcare professional.

Clinicians may consider offering screening for gestational diabetes to women who

have been diagnosed as having PCOS before pregnancy.

During pregnancy a GTT may be performed at 2428 weeks of gestation, with referral to a specialist obstetric diabetic service if abnormalities are detected.

Women with PCOS and a BMI ≥ 25 kg/m2 ) and women with PCOS <a BMI<

25Kg/M2 who have added risks such as advanced age (> 40 years), personal

history of gestational diabetes, or family history of type II diabetes, should have a 2-hour post 75 g oral GTT test performed.

Those with impaired fasting glucose (6.1-6.9 mmol/l) or impaired GTT plasma glucose of 7.8 mmol/l or more but <11.1 mmol/l after a 2-hour oral GTT should undergo annual testing.

MM Fynes 2018

Summary of cancer and PCOS: What are the risks and how should these women be screened?

PCOS related oligo- or amenorrhoea may predispose to endometrial hyperplasia and later carcinoma.

It is good practice to recommend treatment with gestogens to induce a withdrawal

bleed at least every 3 to 4 months.

Transvaginal ultrasound should be considered in the absence of withdrawal bleeds or abnormal uterine bleeding.

In PCOS, an endometrial thickness of less than 7 mm is unlikely to be hyperplasia.

A thickened endometrium or an endometrial polyp should prompt consideration

of endometrial biopsy and/or hysteroscopy.

There does not appear to be an association with breast or ovarian cancer and no additional surveillance is required.

MM Fynes 2018

Clinical standards and auditable topics:

100% of women with PCOS should have;

An accurate diagnosis of PCOS made as defined by at least two out of three

Rotterdam criteria.

A GTT undertaken if overweight (BMI > 25), or where BMI <25 but other risks present (age > 40, previous gestational DM, family history type 2 DM).

BMI, waist circumference and BP checked at every visit.

Advice given on diet and lifestyle.

Psychological issues considered and addressed.

Any questions?

Any questions? MM Fynes 2018

MM Fynes 2018