PCOD Postgraduate MS 9.10.07

Polycystic Ovarian Syndrome
(PCOS)
By
Hisham Saleh, MD
Alexandria University.
Polycystic Ovarian Syndrome (PCOS)
Prevalence:
• Approximately 20% of women of reproductive age
demonstrate the ultrasound picture of polycystic
ovaries with half that number having clinical or
biochemical signs of anovulation or androgen
excess.
Definition:
• The patient must have ovulatory dysfunction and
evidence of hyperandrogenism clinically or by
laboratory means, but no other cause of
hyperandrogenism.
(From a 1990 National Institutes of Health/National Institute of
Child Health and Human Development (NIH/NICHHD)
conference).
Definition:
The 2003 Rotterdam consensus workshop
concluded that PCOS is a syndrome of ovarian
dysfunction along with the cardinal features of
hyperandrogenism and polycystic ovary (PCO)
morphology.
(The Rotterdam ESHRE/ASRM-Sponsored PCOS
Consensus Workshop Group).
Definition:
Diagnostic criteria of PCOS
1990 criteria (both 1 and 2)
1. Chronic anovulation
2. Clinical and/or biochemical signs of hyperandrogenism, and
exclusion of other aetiologies
Revised 2003 criteria (2 out of 3)
1. Oligo- and/or anovulation
2. Clinical and/or biochemical signs of hyperandrogenism
3. Polycystic ovaries
and exclusion of other aetiologies (congenital adrenal hyperplasias,
androgen-secreting tumours, Cushing's syndrome)
(The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus
AE-PCOS 2006 criteria
Clinical Features:
Menstrual symptoms: including amenorrhoea or
oligomenorrhoea (66%), less commonly polymenorrhoea,
menorrhagia, and dysfunctional uterine bleeding (4-14%).
Infertility
Hirsutism (70%), acne (25-35%), and less commonly
virilization (17%) (clitormegaly, voice changes, increased
muscle mass, and baldness in the frontal or crown areas)
Obesity (BMI >25) (35-50%).
Family history is important.
Biochemical description:
1. Hyperandrogenism:
Is central to the diagnosis of PCOS.
The ovaries are the primary source.
Disturbances in gonadotropins & reduced
insulin sensitivity contribute to
hyperandrogenism.
Free testosterone is most likely to increase in
PCOS.
Total testosterone may appear normal in some
patients. Similarly, differences in end-organ
sensitivities can prevent manifestations of
hyperandrogenism in some women. So, biochemical
hyperandrogenism will suggest PCOS in nonhirsute
women with ovulatory dysfunction, and conversely,
failure to detect hyperandrogenism in a hirsute woman
does not rule out PCOS.
A subset of women with PCOS also has adrenal
androgen excess, usually to a mild degree.
Androstenedione or DHEAS is elevated in 40% to
70% of women with PCOS.
Exclusion of other causes of hyperandrogenism is
critical for the diagnosis of PCOS.
2. Inappropriate gonadotropin secretion:
Hypersecretion of LH is frequently found (40-70%), and
can stimulate androgen secretion by theca cells in vitro.
LH pulse frequency is also increased.
FSH levels are normal.
LH/FSH ratio may be elevated.
Increased LH, and/or LH/FSH ratio are not essential for
the diagnosis of PCOS.
LH Androstendione Testosterone Atresia

LH Androstendione Testosterone
increases
increases increases
increases
+ increases
increases
Free
Free
Estrone
Estrone SHBG
SHBG testosterone
testosterone
increases
increases decreases
decreases increases
increases
Endometrial Free
Free Estradiol
Estradiol Hirsutism
cancer increases
increases
3. Hyperinsulinemia:
Hyperinsulinemia suggests a lack of insulin sensitivity
with respect to glucose metabolism.
Paradoxically, the ovary remains sensitive to insulin
effect for reasons that are not entirely clear.
Hyperinsulinism contributes to hyperandrogenism by
direct stimulation of ovarian androgen production and
suppression of SHBG, which creates a relative increase
in unbound testosterone.
4. Type II Diabetes or impaired glucose tolerance:
Identified in 39-45% of PCOS women.
The prevalence in non-obese PCOS women is 5-20%.
Risk factors for type II diabetes in PCOS are:
 Obesity especially if centripetal
 Insulin resistance
 Beta-cell dysfunction
 Family history of type II diabetes
 Dyslipidemia
 Age
Ovarian ultrasound in the diagnosis of PCOS:
Trasvaginal U/S is particularly useful.
Most investigators require a minimum of 12 echo-
free cysts, 2-9 mm in diameter in each ovary.
The ovarian volume is often increased (>10 mL),
averaging 1.5-3 times the normal.
Increased echo density of the ovarian stroma is
described, usually in a subjective fashion.
(However, this is omitted from the diagnosis)
Ovarian ultrasound in the diagnosis of PCOS:
Increased amount of ovarian stroma.
Doppler flow studies show increased blood flow to
PCO ovaries.
22% of the patients who have ultrasound picture of
"polycystic ovaries" do NOT have PCOS.
Other hyperandrogenic states eg CAH may have
typical PCO ovaries on U/S.
Role of exclusion in diagnosis:
(from other causes of hyperandrogenism and ovulatory
dysfunction)
Androgen-producing tumours of the ovary & hCG-producing
tumours outside the reproductive tract. (Clinical history of recent
onset, T > 250 ng/mL)
Adrenal hyperandrogenism:
 Non-classical congenital adrenal hyperplasia usually due to 21-hydroxylase
deficiency. (Increased levels of 17-hydroxyprogesterone (>4ng/mL), ACTH
stimulation test: 17-OHP >10ng/mL)
 Adrenal tumours that produce androgens (marked elevations of T &
DHEAS, dexamethasone suppression test, MRI)
Other types of ovulatory dysfunction:
 Hyperprolactinemia
 Hypothyroidism
Long-term risks of PCOS:

1. Type II diabetes
2. Cardiovascular risk
3. Risk on endometrial hyperplasia and
cancer
PCOS, Hyperandrogenism, and

Insulin Resistance
Insulin action
Insulin action:
S S Glu
S
Tyr GLUT-4
Tyr P Tyr
Tyr
Ser
Ser Ser
P Ser
(active)
(inactive)
(+) Phosphoglycan
mediators
Insulin receptor
TNF- substrate-1
(-)
Insulin resistance:
1. A biological response to insulin that is less
than normal is defined as insulin
resistance.
2. (The euglycemic hyperinsulinemic clamp
technique is the gold standard for
determining insulin resistance. A simple
technique is fasting insulin to fasting
glucose ratio.)
Types of insulin resistance:

1. Type A insulin resistance: Mutations in insulin
receptor gene are found. Severe insulin
resistance, hyperandrogenism, and acanthosis
nigricans results (HAIR-AN syndrome). This is
not present in PCOS.
2. Type B insulin resistance: Resistance to insulin
results from antibodies to insulin receptors. This
is not common in patients with PCOS.
Aetiology of insulin resistance in PCOS:

Remains undetermined.
Insulin resistance exists in many, but not all, women
with PCOS. It exists in both obese & lean PCOS
patients, although it is more common in the obese.
Decrease in insulin receptor number or affinity do
not exist in PCOS.
Aetiology of insulin resistance in PCOS:

A postreceptor defect in insulin action has been
suggested:
1. Increase in serine phosphorylation of insulin
receptor.
2. A defect in glucose transport as a result of
diminished production of GLUT-4 glucose
transporter.
Increased pancreatic insulin secretion resulting from
a genetic mutation. Because insulin itself may
downregulate its own receptor, excessive secretion
may theoretically result in insulin resistance.
Insulin
Insulin
Insulin receptor
Reduced
Reduced tyrosine
tyrosine autophosphorylation
autophosphorylation
Glucose
Glucose transport
transport decrease
decrease
Serine
Serine Phosphorylation
Phosphorylation
Glucose
Glucose transport
transport P450c17
P450c17 17,
17, 20
20 lyase
lyase
decreases
decreases activity
activity increases
increases
Ovarian
Adrenal androstene-
Hyper- DHA, DHAS dione,
insulinemia increase testosterone
increase
Hyperandrogenism & insulin resistance:

Insulin resistance causes hyperandrogenism, but
the reverse is not true.
Defects in insulin action (insulin resistance) may

be observed in only certain cell types (eg
muscles and adipose tissue), & not in other cell
types (eg the ovary) in the same individual.

Mechanisms are:
 Insulin acting via its own receptors or via IGF-1 receptors
stimulate ovarian androgen production (stimulation of 17α
hydroxylase, & 17-20 desmolase enzyme system (P450c17)
 Indirectly, insulin sensitizes the gonadotrope to GnRH.
 Insulin lowers SHBG levels by inhibiting its hepatic
production, thus increasing the levels of free androgens.
 Insulin inhibits the hepatic production of IGFBP-1 while
increasing ovarian IGF-1 binding. IGF-1 stimulates ovarian
androgen secretion while also amplifying the action of LH
on ovarian androgen production.

Not all patients with hyperinsulinemia are also
hyperandrogenic; e.g., many women with type II DM.
The cause is not known, but a logical speculation is
that an ovarian genetic susceptibility is required, or
that the existence of long-term anovulation must be
present & preceed hyperinsulinemia.
The problem of obesity:

Some authorities define obesity as BMI >25, while others use a
value of 27 or higher.
Obesity is associated with PCOS in 50% or higher.
Obesity independent of PCOS is a cause of insulin resistance.
PCOS women have android obesity (fat deposition in the
abdominal wall and visceral mesenteric locations). Android
obesity is diagnosed by a waist/hip ratio of > 0.85. Android
obesity is associated with hyperisulinism, impaired glucose
tolerance, DM, & hyperandrogenism. Android obesity is also
associated with cardiovascular risk factors, including
hypertension, and an unfavourable cholesterol-lipoprotein
profiles (lower HDL2).
The problem of obesity:

How obesity causes insulin resistance remains
unclear.
 TNF is produced in adipose tissues & exerts
inhibitory action within muscle and fat cells.
TNF inhibits peroxisome proliferators-activated
receptor gamma (PPAR-). (PPAR- activates
genes that code for proteins that lower insulin
resistance).
Summary of the pathophysiology of PCOS
Weight
Weight
increases
increases SHBG
SHBGdecreases
decreases
Inherited
Inherited
defects
defectsinin Insulin
Insulinincreases
increases IGFBP-1
IGFBP-1decreases
decreases Artesia
insulin action
insulin action
Insulin
Insulinreceptor
receptor
disorders
disorders
LH Theca Free
Free Free
Free
LHincreases
increases testosterone estradiol
FSH
FSHdeceases
deceases testosterone estradiol
(IGF-II, ?IGF-I) increases increases
increases increases
Androstenedione Testestosterone
Androstenedione
increases
increases + Testestosterone
increases
increases
Hirsutism
Endometrial
Estrone
Estroneincreases
increases cancer
Insulin lowering drugs in PCOS:

In the past, standard therapy for PCOS entailed the use
of oral contraceptive pills with or without androgen-
blocking agents such as spironolactone.
Today, data suggest that lowering insulin resistance
with the use of insulin-sensitizing drugs can ameliorate
menstrual cyclicity, improve ovulation, lower circulating
androgens, and improve the features of syndrome X
(insulin-resistant state characterized by hypertension,
low HDL cholesterol, and obesity). Syndrome X
increases the risk for cardiovascular disease.

Insulin-sensitizing durgs are:
 Metformin (dimethylbiguanide)
 Thiazolidionediones:
 Troglitazone
 Ciglitazone
 Pioglitazone
 Englitazone
 Rosiglitazone (Avandia)
 D-chiro-inositol

Metformin in PCOS:
Mechanism of action:
 It lowers insulin levels without producing
hypoglycemia.
 It inhibits gluconeogenesis thus reducing
excess hepatic glucose production.
 It may also increase peripheral insulin
sensitivity by an unknown mechanism.
The dose of metformin is 1500 mg/d

Metformin in PCOS:
 Metformin effects (obese & lean PCOS females):
 Decreased insulin levels
 Decreased serum free T
 Decreased basal GnRH-stimulated LH
 Increased serum SHBG
 Improved menstrual cyclicity
 Improved ovulation & improved response to CC

Metformin in PCOS:
 Metformin effects (obese & lean PCOS females):
 May reduce the risk of OHSS with hMG
 Pregnancies may occur
 No teratogenic effects in pregnancy
 If continued in pregnancy there is a marked reduction in
the inicidence of gestation diabetes
 Normalizes androgen levels during pregnancy and thus
lowers the risk of virilizing the female fetus
 May reduce the risk of early pregnancy loss attributable to
hyperinsulinemia (increased glycodelin & IGFBP-1)

Torglitazone in PCOS:
 Withdrawn from the market due to reported cases of
fatal liver toxicity
 The primary mechanism of action is via activation of
gamma peroxisome proliferation activator receptors
(PPAR). This induces complex binding to specific
response element that regulates the gene for
lipoprotein lipase or that have direct insulin mimetic
effects by activation of genes that encode for insulin
action, such as glucose transporters.

D-chiro-inositol in PCOS:
 It is a synthetic inositol phosphatidylglycan that
activates a nonclassical insulin signaling cascade.
 It produced effects similar to other insulin-sensitizing
drugs, but with no side effects.
Management of PCOS
I. Strategies for reduction of risk
1. Exercise and weight control
The impact of exercise and reduction in body
mass by hypocaloric dieting on ovarian
function in PCOS is well characterised.
Adoption of simple methods for reduction of
body fat and improvement in physical fitness
will result in resumption of ovulation and
increase in fertility in a high proportion of
anovulatory obese PCOS women.
Management of PCOS
The demonstration that improvement in
diet and exercise in obese young women
with PCOS is accompanied by a
normalisation in glucose metabolism
suggests that lifestyle alteration will
reduce the likelihood of developing type II
diabetes later in life.
Management of PCOS
There is no clear evidence of an effect of diet
or exercise on the long-term health of women
with PCOS who have normal body habitus,
although it seems prudent to advise such
patients to maintain their body weight within
the normal range.
Management of PCOS
2. Drug therapy
Insulin-sensitising agents: Evidence has
accumulated demonstrating both their safety and, in
some studies, efficacy in the management of short-
term complications of PCOS, particularly anovulation.
Long-term use of insulin-sensitising agents for
avoidance of metabolic complications of PCOS
cannot as yet be recommended.
Management of PCOS
3. Cyclic progestins or OCCP:
For patients with PCO who do not want to get
pregnant. OCCP are preferred if there is
hyperinsulinemia, or dyslipidemia.
Management of PCOS
4. Surgery:
A recent long-term cohort study up to 20 years after
laparoscopic ovarian electrocautery has shown
persistence of ovulation and normalisation of serum
androgens and SHBG over many years in over 60% of
subjects. However, at present, the risks of surgery do
not justify recommendation of this treatment purely in
an attempt to ameliorate the chances of developing
diabetes or coronary artery disease in later life.
Management of PCOS
5. Screening young PCOS patients for long-term
health risk
No clear consensus has yet emerged concerning
regular screening of women with PCOS for later
development of diabetes and dyslipidemia, but obese
women with a strong family history of cardiac disease
or diabetes should be assessed regularly in a general
practice or hospital outpatient setting. Local protocols
should be developed and adapted as new evidence
emerges.
Management of PCOS
II. Ovulation induction for patients wishing pregnancy:
Diagnostic workup before O/I
Semen analysis, HSG Exclude associated infertility factors

T Rule out ovarian androgen producing tumours
Baseline for evaluating response of
hyperandrogenism to weight loss, metformin etc.
DHEAS Rule out adrenal androgen-producing tumour,
asses value of adding corticosteroids to therapy
Management of PCOS
8am 17 OH-P Rule out nonclassical 21-

hydroxylase deficiency
Overnight dexamethasone Rule out Cushing's syndrome
suppression test
TSH, PRL (only in highly suspicious cases)
Management of PCOS
LH, FSH Low LH/FSH ratio may suggest low

likelihood of good response to CC
Unexpectedly high FSH means decreased
ovarian reserve
Fasting insulin/glucose ratio Assess for hyperinsulinism & value
of weight loss & metformin;
baseline for evaluation of response
to them. N fasting insulin is 10-20
U/mL, N I/G ratio is > 4.5
Management of PCOS
Endometrial biopsy In cases with thick endometrium to

rule out endometrial hyperplasia and
cancer
Treatment options
PCO
PCO
Obese
Obese Non-obese
Non-obese
Weight
Weight loss
loss CC
CC or
or other
other
±± metformin
metformin antiestrogens
antiestrogens ±±
dexamethasone
dexamethasone
CC
CC ifif they
they fail
fail
hMG/FSH
hMG/FSH ifif the
the
hMG/FSH
hMG/FSH ifif CC
CC fails
fails above
above fails
fails
Weight Loss
Striking improvement of ovulatory
dysfunction & hyperandrogenism due to
decrease in hyperinsulinism.
Successful pregnancies may result.
Long term metabolic complications are
decreased.
At least response to ovulation induction is
better .
Clomiphene Citrate: Indications
Initial agent of choice in lean PCO
patients
If weight loss and/or metformin fails
In combination with hMG/FSH

CC: Mechanism of action
Antiestrogenic effect on the hypothalamus
 Increase in GnRH release
 Increase in FSH & LH
Follicular growth
 E2 rises resulting in positive feedback
on the hypothalamic-pituitary unit
resulting in an LH surge & ovulation
It is a clomiphene “initiated” ovulation

CC: Dosage & monitoring
Starting dose is 50 mg daily for 5 days starting
on the 3rdrd-5thth MD after a spontaneous or
progestin-induced menses
If there is no ovulation, 50 mg increments in the
daily dose are added till ovulation is achieved or
the maximum of 200-250 mg/day is reached
without successful ovulation.
CC: Dosage & monitoring
Monitoring of the response is mandatory at
least in the initial cycle of stimulation. It
includes:
 Follicle
Follicle scanning
scanning by by TVS
TVS
 Measurement
Measurement of of endometrial
endometrial thickness
thickness on
on day
day of
of
maximum
maximum follicular
follicular development
development
 Monitoring
Monitoring ofof CM
CM atat the
the periovulatory
periovulatory period
period
 Mid-luteal
Mid-luteal PP measurement
measurement
If adequate ovulation is achieved, the same dose is
repeated in subsequent cycles for a maximum of 6
cycles.
CC is not initiated in subsequent cycles unless U/S
exclusion of cyst formation is done. If no pregnancy
occurs, CC is considered a failure and other
approaches are indicated to achieve pregnancy.
CC: Interventions to improve outcome
Dexamethasone (0.25 mg/d continuously or 0.5
mg/d discontinuously at bedtime) in cases with a
significant adrenal component (DHEAS > 200
µg/dL).
Metformin
Pretreatment with OCP for 1-2 months
CC: Interventions to improve outcome
hCG injection (5000-10000 IU IM) especially in
cases in which no LH surge is detected despite
adequate follicular growth.
Exogenous estrogen to antagonize the

antiestrogenic side effects of CC
Extended CC administration
Acetyl cysteine
Outcome of CC O/I
50% of patients ovulate on 50 mg/d dose
70-80% will ovulate when the maximum dose is
reached
50% have a significant adrenal component
Only 40-50% of those who ovulate with CC get
pregnant.
High abortion rates
Multiple gestation in the range of 5-10% including
1% high order multiple gestation.
N-Acetyl Cysteine
Recently, some reports discussed the
possible beneficial effects of NAC on
ovulation. Because it is an insulin
sensitizer, NAC was proposed as an
adjuvant to clomiphene citrate for
ovulation induction in patients with
polycystic ovary syndrome.
Metformin
Particularly indicated in PCO patients with
hyperinsulinemia
G/I side effects; gradual increase in dose
Dosage: 500 mg tid
Can be combined with CC if not effective alone
Should be stopped if pregnancy occurs
Other insulin lowering drugs include troglitazone,
rosiglitazone (Avandia), pioglitazone (Actos), and D-
chiro-inositol.
Gonadotropin Therapy
Preparations:
hMG
Purified FSH
Purified hMG
Recombinant FSH
There is little or no difference between the different
preparations as regards the clinical outcome.
Indications:
Clomiphene resistant cases
Obvious antiestrogenic side effects with

CC
Problems with gonadotropin O/I:
 High incidence of OHSS
 High incidence of multiple gestations
 Relatively high abortion rate
Treatment strategy:
The aim is to give the minimum amount of FSH
which will induce the development of a single
ovulatory follicle.
Protocols for ovulation induction with
gonadotropins:
1. Conventional "step up"
2. Down regulation with GnRHa followed by
"step up"
3. "Step down"
4. Down regulation with GnRHa followed by
"step down"
5. Low dose
In all regimens hCG (5000-10000 IU) is given to
induce ovulation when there is at least one follicle
≥18 mm.
HCG may be withheld if :

• More than 3 follicles ≥16 mm in diameter are
present
Or
• E2 is >1500 pg/mL.
"Step Up" Regimen
Higher incidence of OHSS
Lower pregnancy rate than HH
Premature luteinization and/or spontaneous
LH surge before there is at least one leading
follicle leading to cancellation of about 20%
of cycles
"GnRHa down regulation followed by "step up"
Supression of endogenous LH thus reducing the

incidence of premature luteinization
High incidence of multiple follicular development
High incidence of multiple gestation
Lower abortion rate
"Step down" protocol:

After an initial priming dose when a cohort
of follicles is selected the dose of FSH is
progressively reduced so that the
concentration falls below the threshold
necessary to activate additional follicles
"Step down" protocol:

Practically it is difficult to achieve this due to :
 FSH
FSH threshold
threshold varies
varies between
between women
women probably
probably due
due to
to
variations
variations inin the
the metabolism
metabolism ofof FSH
 Batch-to-batch
Batch-to-batch variations
variations
 The
The long
long half-life
half-life of
of FSH
FSH (almost
(almost 48 h) makes it very
difficult
difficult to reduce the level of
of FSH quickly so that the
'window"
'window" of of recruitment
recruitment remains
remains open
open for
for aa longer
period
period
"Step-down" protocols (with or without

GnRHa) have a lower multiple gestation and a
lower incidence of OHSS compared to the
"step-up" regimens.
Low-dose protocol :
The aim is to give the minimum dose of
gonadotropin necessary to induce normal
follicular development.
Injection of a small amount of FSH is often
sufficient to supplement endogenous FSH, so that
the concentration rises above the threshold.
Low-dose protocol :
Once so, growing follicle(s) secrete sufficient E2 &
inhibin to suppress the endogenous FSH so that
the overall level of FSH drops below the threshold
required to recruit additional follicles.
Low-dose protocol :
The
The starting dose dose is
is as
as low
low as
as 37.5
37.5 IU
IU for the first 14 days
increasing
increasing to to 75
75 IU
IU ifif there
there isis no
no sign
sign of
of follicular
follicular
development
development on on U/S.
U/S.
The
The dose is is increased again by by 37.5
37.5 IU
IU only
only if
if after a
further
further 7 days no no follicle
follicle >> 11
11 mmmm has
has developed.
developed.
The
The dose is is maintained at at this
this threshold dose until the the
follicle
follicle is
is >> 17-18
17-18 mm
mm when when 5000
5000 IU
IU of
of hCG
hCG is is given.
given.
Results of low dose protocol
High rate of monofollicular
monofollicular development
development (50-75%)
(50-75%)
10-20% are cancelled due to multifollicular
multifollicular development
development
or failure
failure to
to respond
respond
Low incidence of mild
mild OHSS
OHSS (8%)
(8%) that
that needs
needs no
no more
more
than conservative
conservative treatment
treatment
Low rate ofof multiple
multiple gestation
gestation (2%)
(2%)
Low pregnancy
pregnancy rate
rate (8
(8 to
to 12
12 %)
%)
High miscarriage rate
rate (20-30%)
In conclusion, the low dose protocol is the
protocol of choice for :
Patients starting their first cycle of
gonadotropin ovulation induction
or
for patients with previous multi-follicular
development with or without OHSS.
If pregnancy does not occur, repeat cycles of O/I

can start with the dose at which response occurred in
the previous low dose protocol cycle.
A slightly higher dose can be used instead to start

a step-down protocol.
Aromatase inhibitors
Aromatase inhibitors are agents that suppress the
biosynthesis of estrogen and, therefore, reduce the
negative feedback effect on the hypothalamic–
pituitary system. This results in increased secretion
of FSH that can lead to follicle selection and
maturation. The third generation compound,
letrozole, has been recently used for ovulation
induction in anovulatory PCOS women resistant to
clomiphene or with inadequate endometrial thickness
during clomiphene treatment. The daily dose is 2.5
mg from days 3 to 7 of the menstrual cycle.
Laparoscopic ovarian drilling
Surgical treatment of anovulation in PCOS patients by
wedge resection of the ovaries has been abandoned
due to serious adverse effects, such as adhesions and
substantial tissue loss. Advances in laparoscopic
techniques have rekindled interest in surgical
induction of ovulation. Laparoscopic ovarian drilling
(LOD) introduced by Gjönnaess (1984) restored
ovulation in 92% of patients with a pregnancy rate of
69%.
Laparoscopic ovarian drilling
Ovarian drilling is performed by using a pointed
monopolar or bipolar electrode or with laser energy,
although considerable variation exists in the
techniques used. ). The mechanism of action of LOD
is unclear, but it seems that destruction of the
androgenproducing ovarian stroma plays a key role.

PCOD Postgraduate MS 9.10.07

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Polycystic Ovarian Syndrome

LH Androstendione Testosterone Atresia

Long-term risks of PCOS:

PCOS, Hyperandrogenism, and

Types of insulin resistance:

Aetiology of insulin resistance in PCOS:

Aetiology of insulin resistance in PCOS:

Hyperandrogenism & insulin resistance:

Defects in insulin action (insulin resistance) may

Hyperandrogenism & insulin resistance:

Hyperandrogenism & insulin resistance:

The problem of obesity:

The problem of obesity:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Insulin lowering drugs in PCOS:

Semen analysis, HSG Exclude associated infertility factors

8am 17 OH-P Rule out nonclassical 21-

LH, FSH Low LH/FSH ratio may suggest low

Endometrial biopsy In cases with thick endometrium to

If weight loss and/or metformin fails

In combination with hMG/FSH

It is a clomiphene “initiated” ovulation

Exogenous estrogen to antagonize the

Obvious antiestrogenic side effects with

HCG may be withheld if :

Supression of endogenous LH thus reducing the

"Step down" protocol:

"Step down" protocol:

"Step-down" protocols (with or without

If pregnancy does not occur, repeat cycles of O/I

A slightly higher dose can be used instead to start

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