polycystic ovary syndrome
Senior lecturer Obstetrician and
Gynecology
[Link].B C.A.B.O.G
Ibn Sina University of Medical and
pharmaceutical sciences
Objectives
Define PCOS and recall its diagnostic criteria (Rotterdam).
Explain the hormonal imbalance and pathophysiology leading to
hyperandrogenism.
Apply appropriate investigations (hormone profile, ultrasound) in
patient assessment.
Design an individualized management plan including lifestyle
changes, hormonal therapy, and fertility options.
Definition: a
syndrome of
ovarian dysfunction
along with the
cardinal features of
hyperandrogenism
and polycystic
ovary
PREVALENCE:
PCOS is the most common endocrine
disorder in women, it affects around
10-15% of women of reproductive age.
The prevalence of PCO seen on U/S is
much higher-around 25%
Aetiology
The aetiology of PCOS is not completely clear
Although the frequent familial trend points to a
genetic cause.
It is a combination of genetic abnormality and
environmental factors(e.g., obesity, diet,
lifestyle)
Clinical manifestations:
• Oligomenorrhoea/amenorrhea in up
to 75% of patients, predominantly
related to chronic anovulation.
• Hirsutism ,acne .
• Subfertility
• Obesity in at least 40% of patients.
• Acanthosis nigricans (areas of
increased velvety skin pigmentation
occur in the axillae and other
flexures)
• May be asymptomatic
Diagnosis of PCOS:
Rotterdam criteria: Patients must have two of the
three features below:
Amenorrhea/oligomenorrhoea.
• Clinical or biochemical hyperandrogenism.
• Polycystic ovaries on ultrasound.
The ultrasound criteria for the diagnosis of a
polycystic ovary are eight or more subcapsular
follicular cysts <10 mm in diameter and increased
ovarian stroma.
Laboratory tests:
• Increase androgens
• Increase luteinizing hormone (LH)
• Normal follicle stimulating hormone (FSH)
• Increase fasting insulin
• Decrease sex hormone binding globulin
(SHBG),
• Increase estradiol
• Increase Anti-mullerian hormone (AMH)
Pathophysiology
The exact pathophysiology of PCOS is not fully
understood.
It is multifactorial, involving neuroendocrine, ovarian,
metabolic, and environmental mechanisms.
It can be discussed under five main components:
Gonadotrophins abnormality
Anovulation
Androgen excess
Insulin resistance
A. Gonadotropin Abnormalities
Altered GnRH pulsatility → preferential secretion of LH
over FSH.
LH:FSH ratio often > 2:1.
Leads to excess stimulation of theca cells → ↑
testosterone
B. Anovulation
High LH → theca cell hypertrophy and excessive
androgen production.(affect normal follicular
maturation)
Androgen Excess
• LH and insulin synergistically increase androgen
production by theca cells. Leads to elevated :
Testosterone
Androstenedione
• Free testosterone elevated in 70–80% of PCOS
women.
• Peripheral conversion of androstenedione → estrone
(E1) by aromatase contributes to estrogen dominance
and feedback disruption
• ↓ SHBG production in the liver ( lead to increase free
testosterone) due to:
Insulin Resistance
Seen in both lean and obese women with PCOS.
Defined as reduced tissue response to insulin
despite normal or elevated insulin levels.
Leads to compensatory hyperinsulinemia, which:
Stimulates ovarian theca cells to produce
androgens.
Suppresses hepatic SHBG synthesis,
increasing free testosterone.
Contributes to type 2 diabetes,
Management:
Lifestyle modification :
Weight loss
Dietary modifications
Exercise
Cessation of smoking recommended in
management of PCOS
Menstrual irregularities:
Combined oral contraceptive preparation. This
will result in an artificial cycle and regular
shedding of the endometrium.
Progestogen .cyclical to control bleeding every
1–3 months to induce a withdrawal bleed.
Continuous provision of progesterone into the
uterine cavity by LNG IUD (Mirena)
Subfertility:
•Clomiphene is the traditional first‐line therapy
and can be continued for 6–12 cycles of
treatment(oral antiestrogen) Women with PCOS
are also at increased risk of developing OHSS
(ovarian hyperstimulation syndrome)and
increase risk of multiple pregnancy.
Aromatase inhibitors such as
letrozole.(Inhibition of the
aromatase enzyme decreases
the aromatization of androgens
to estrogens )
Ovarian drilling, a laparoscopic
procedure to destroy some of
the ovarian stroma that may
prompt ovulatory cycles
Obesity
• Weight loss should be encouraged in
women with BMI>30%
• Drugs can be used for weight reduction
• Bariatric surgery can be effective
Hirsutism:
Eflornithine cream applied topically
Cyproterone acetate (an antiandrogen contained in the
Dianette contraceptive pill.)
Metformin: this is beneficial in a subset of patients with
PCOS, those with hyperinsulinemia. It improves
parameters of insulin resistance, hyperandrogenemia,
anovulation and acne in PCOS, and may aid weight loss.
GnRH analogues: this regime should be reserved for
women intolerant of other therapies
laser or electrolysis
Long term sequelae:
• Diabetes mellitus
• Hypertension, cardiovascular disease
• Endometrial carcinoma
Summary :
• PCOS is a common endocrine disorder (10–15%
prevalence) with genetic and environmental causes.
• Diagnosis requires 2 of 3: oligo/anovulation,
hyperandrogenism, and polycystic ovaries.
• Management includes lifestyle modification,
hormonal therapy for cycles, fertility drugs
(clomiphene, letrozole), and antiandrogens.
• Long-term risks include diabetes, hypertension, and
endometrial carcinoma.
References
• Gynaecology_by_Ten_Teachers_20th_Edition
• Dewhurst’s textbook of obstetrics and
gynaecology.– 7th ed. / edited by D. Keith
Edmonds.– 7th ed.
• [Link]
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