Polycystic Ovarian Syndrome is a complex disease, with a constellation of etiology and symptoms. Much of the diagnosis is dependent on the laboratory tests of hormones. This presentation provides a concise and focused approach towards PCOS diagnosis and management.
2. Polycystic ovary syndrome is a clinical syndrome characterized by
mild obesity, irregular menses or amenorrhea, and signs of androgen
excess (eg, hirsutism, acne). 20-30% of patients have multiple cysts in
the ovaries. Diagnosis is by pregnancy testing, hormone
measurement, and imaging to exclude a virilizing tumor. Treatment
is symptomatic.
DEFINITION
3. IMPORTANT CONSIDERATIONS
PCOS is a complex, heterogenous disorder, which is largely caused by a disturbance in the metabolic pathways and
hyperandrogenism
It is also an endocrine disorder with Insulin Resistance, Sub-fertility, hyperandrogenism
PCOS is a cause of major concern as it is the most common endocrine disorder in women and is the leading cause of
Anovulatory subfertility
The presence of cysts in the ovary is not always required for a PCOS diagnosis (Rotterdam diagnostic Criteria will be
discussed later)
There is no known cause of the disease, although multiple theories exist on its etiology
DEFINING PCOS COMPREHENSIVELY
PCOS is a complex metabolic disorder that is characterized by chronic anovulation, increased
androgen production and associations with metabolic derangements such as insulin resistance,
hyperlipedemia and obesity. No exact cause is known for PCOS but evidence suggests that it is a
disease caused by the complex interaction of genetic and environmental factors
4. Diagnostics
There are two criteria that can be used for
diagnosing PCOS, however, the consensus is
on the Rotterdam criteria
ROTTERDAM CRITERIA
Two out of three factors required for diagnosis:
Anovulation or oligo-ovulation/amenorrhea or
oligomenorrhea
Clinical or Biochemical Hyperandrogenism
Ultrasound Evidence of multiple cysts
1.
2.
3.
ANDROGEN EXCESS AND PCOS SOCIETY
Evidence of hyperandrogenism and ovarian dysfunction
5. Exact etiology and pathogenesis is not known, however, LH
hypersecretion is observed and believed to cause
hyperandgrogenemia
Oversecretion of LH leads to increased Thecal Cell activity in the ovaries. This can
then lead to the secretion of DHEA and androgens.
However, lower FSH in comparison to LH, does not allow the conversion of
androgens to estrogens
Lower estrogen causes anovulation
These factors are combined with Insulin Resistance and lowered Sex Hormone
Binding Globulins
Further, this constellation causes the formation of Metabolic syndrome
1.
2.
3.
4.
5.
ETIOLOGY OF PCOS
9. DIAGNOSTIC EVALUATION
HISTORY
Menstruation
Adrenal enzyme deficiency
Hirsutism
Infertility
Metabolic Syndrome
Diabetes/Insulin Resistance
FAMILIAL IRREGULARITIES OF
PHYSICAL
LABORATORY
ANALYSIS
IMAGING
Insulin Resistance: Obesity and Acanthosis
Nigricans, Metabolic Syndrome
Hyperandrogenemia: Hirsutism, Acne, Alopecia
(Exclude Virlization)
Pregnancy
Hormone levels
Glucose
Lipid Panel
Transvaginal Ultrasound
MRI for Adrenal Glands
Diagnostic evaluation is largely meant to
exclude Virilization, Diabetes, Cushing's
Syndrome, Pituitary Tumours, Polycystic
Ovaries etc.
The differential Diagnosis of PCOS is vast.
10. Waist Circumference
Triglycerides
HDL
Blood Pressure
Fasting Glucose
Hypertension
Diabetes
Obesity
>88cm
Insulin Resistance in Women
LABORATORY ANALYSIS
Three or more of the following:
>150 mg/dL
<50 mg/dL
>130/85
>110 mg/dL
Metabolic Syndrome
11. 5-20 ng/ml
FSH
Elevated. If above 600ng/dL,
consider virilization
Testosterone
Lowered
SHBG
Elevated, indicative of Insulin
resistance and registers as
hyperinsulinemia
Insulin
Elevated
Estrogen
Lowered
Progesterone
To rule out hyperthyroidism
TSH
Elevated
Prolactin
Elevated
T4
Lowered
HDL
Elevated
LDL
Test for Pregnancy
hCG
5-20 ng/ml
Hormonal Profile
LABORATORY ANALYSIS
LH
LH:FSH ratio
2:1 (They might fall within
normal range individually, but
the ratio will be abnormal)
To rule out congenital adrenal
Hyperplasia
17-Hydroxyprogesterone
Elevated
DHEA