Polycystic ovarian syndrome (PCOS) is a condition
of unexplained hyperandrogenic chronic anovulation
that most likely represents a heterogenous disorder.
About 10% of women in the reproductive age group
suffer from this disorder.
3. 1. Introduction
• A syndrome of ovarian dysfunction
with
cardinal features of hyperandrogenism
polycystic ovary morphology
• Often complicated by chronic anovulatory infertility
• Clinical manifestations include oligomenorrhoea,
hirsutism and acne
4. • Many women are obese and have a higher
prevalence of
impaired glucose tolerance,
type 2 diabetes and
sleep apnoea
• They exhibit an adverse cardiovascular risk
profile.
5. • Cardiometabolic syndrome as suggested by a
higher reported incidence of ,
hypertension
dyslipidaemia
visceral obesity
insulin resistance
hyperinsulinaemia
6. • Prevalence - 5 – 10 % of women of
reproductive age
• The commonest cause for anovulation (80%)
• USS evidence of polycystic ovaries in 20-30 %
of women
• The most common endocrine disorder in
women
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8. High risk groups
• Women with oligo ovulatory infertility
• Obesity and/or insulin resistance
• Type 1 , type 2 or gestational diabetes mellitus
• A history of premature adrenarche
• First-degree relatives with PCOS
• Women using antiepileptic drugs (valproate)
9. 2. Aetiology
• Not fully known
• No gene or specific environmental substance
has been identified.
• Genetic studies showed a link between PCOS and
metabolic disturbances such as disordered
insulin metabolism.
• Hence it may be a manifestation of a complex
genetic disorder.
10. • Selective insulin resistance may be central to the
aetiology of PCOS.
• Compensatory hyperinsulinaemia
• Decreased levels of serum hormone binding
globulin (SHBG)
• Trophic stimulus to androgen production in the
adrenals and ovaries
• Direct effect on the hypothalamus causing
abnormally stimulated appetite and increased
gonadotropin secretion
11. • Hypersecretion of LH
Stimulation of androgen secretion from
ovarian thecal cells
• Elevated LH : FSH ratio
17. 4.Diagnosis
2 out of 3 features of Rotterdam criteria
• Amenorrhoea/oligomenorrhoea (cycle >42 days)
• Clinical or biochemical hyperandrogenism
( acne, hirsutism,alopecia )
• Polycystic ovaries on ultrasound
( 8 or more subcapsular follicular cysts <10mm in
diameter and increased ovarian stroma)
18. USS
• Bilateral enlargement of the ovaries > 8.0 cm.
Increased ovarian volume ( >10ml ).
• Thickened tunica albugenea
• Multiple small cysts (12 foliclles or lesser) of
0.2-0.9 cms in each ovary
• Absence of dominant follicle
• Thickened stroma (hyperthecosis)
• Resting or follicular endometrium
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20.
21. Laboratory investigations:
• Demonstration of biochemical hyperandrogenaemia.
– Total testosterone (>200ng/dL)/ Free testosterone
> 2.2pg/mL.
• S. Estradiol and FSH estimations.
– Exclude hypogonadotropic hypogonadism
( E2, FSH).
– Exclude premature ovarian failure
( E2, FSH).
22. • S. Dehydroepiandrosterone sulfate.
– Not of value if S. Testosterone is normal
– Values > 430μg/dL significant. It is indicative
of adrenal source of androgens.
– Levels > 700 μg/mL suggestive of androgen
producing adrenal tumour.
• 24 hours urinary cortisol
– Cortisil < 50 μg/24 hours
– Exclude Cushing’s syndrome if patient is
hypertensive.
23. Exclusion of other causes of
hyperandrogenism.
– Estimation of TSH to exclude thyroid dysfunction
– Estimation of serum prolactin to exclude
hyperprolactinemia
– Estimation of 17α hydroxyprogesterone.
Non classical congenital adrenal hyperplasia caused by
21-hydoxylase deficiency.
24. – Consider screening for Cushing’s syndrome,
and
– Rare conditions like acromegaly.
– Evaluation for metabolic syndrome X.
25. 5. Management
Treatment goals of polycystic ovary syndrome:
– Prevent endometrial hyperplasia, atypia/ cancer
– Restore normal ovulation / fertility
– Restore normal menstruation
– Correct hirsutism
27. 1.Lifestyle modification
• Weight reduction through exercise and diet – the
most important step in managing overweight
women.
• Even a modest weight loss (5%) can improve
symptoms.
• Effective in restoring ovulatory cycles and
achieving pregnancy.
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31. 2. Improving menstrual regularity
• Weight loss
• Combine oral contraceptive pills (COCP)
inhibits LH
Reduces circulating androgens
increases circulating SHBG
Low dose combination pill containing low dose
of synthetic estrogen in combination with a low-
androgenic progestin
32. • Metformin
Benificial in patients with hyperinsulinaemia
and CVS risk factors.
Improves peripheral insulin sensitivity;
improve ovulation rates
improve glucose tolerance
increased SHBG leading to reduced
bioavailability of androgens
33. 3. Controlling symptoms of
hyperandrogenism
• Mainly hirsutism
1st line treatment
Weight reduction
COCP
Medroxyprogesterone acetate
36. 4. Subfertility
• Weight loss
• Ovulation induction with antioestrogens or
gonadotrophins
Clomiphene citrate
Is a selective estrogen receptor modulator
1st line treatment in women with PCOS and
anovulatory infertility
Ovulation rate 70-80 %
Pregnancy rate 30-40 % over 6 cycles
38. • In vitro fertilization ( IVF )
when ovulation can’t be achieved; or doesn’t
succeed in pregnancy.
39.
40. 5. Insulin sensitizers
Metformin
• Metformin combined with clomiphene citrate
increases ovulation and pregnancy rates.
• No significant increase in birth rate.
• No significant improvement in acne or
hirsutism.
• Lowers androgen levels.
41. 6. Psychological issues
• Symptoms can be distressing and resulting
lower self esteem.
• Holistic approach
80 % from oxford hand book
Cardiometabolic syndrome (CMS) is a clustering of interrelated risk factors that promote the development of atherosclerotic vascular disease and type 2 diabetes mellitus.
Cardiometabolic syndrome (CMS) is a clustering of interrelated risk factors that promote the development of atherosclerotic vascular disease and type 2 diabetes mellitus
BMI >30 in 35-60% of women with PCOS
Obesity worsens insulin resistance.
(The best evidence comes from a meta-analysis of 11 studies demonstrating a twofold excess risk of developing PCOS in 556 women treated with valproate compared with 593 women treated with other antiepileptic drugs)
does not prevent insulin effect
on its receptors on the ovary, or
the effect on insulin SHBG and
the hepatic production of insulin growth factor-1 (IGF-1)
The main effect of insulin on the ovaries is not only to increase androgen production, but also to derange the regulation of androgen synthesis so as to prevent the down regulation of the LH receptors leading to increased production of androgens and estrone which coupled with insulin effect of lowering SHBG leads to hyperestrogenism and reduced FSH levels.
Estimation of 17α hydroxyprogesterone.
Random normal level < 4 ng/ml. Fasting < 2 ng/ml.
Improving insulin sensitivity is associated with improved ovulation rates, improved glucose tolerance and increased SHBG leading to reduced bioavailibility of androgens.
Sex hormone binding blobulin
Causes increasing cervical mucus thickening and also exhibits its anti-estrogenic effect on the endometrial lining; thereby negating any benefits of ovulation
should it occur..
generally started at a dose of 50 mg/day starting from day 2 - day 6 of the period.
If treated for more than 12months risk of endometrial CA