This document provides an overview of polycystic ovarian syndrome (PCOS), including its definition, pathophysiology, clinical features, diagnosis, and treatment. Some key points: - PCOS is a hormonal disorder affecting women in their reproductive years that causes irregular periods, excess androgen levels, and polycystic ovaries. It increases the risk of metabolic issues like diabetes. - The root causes involve excess LH stimulating the ovaries to produce androgens and insulin resistance driving higher androgen levels. This leads to problems like irregular periods and hirsutism. - Diagnosis is based on menstrual irregularity, clinical or biochemical signs of hyperandrogenism, and exclusion of other disorders

1. DR NISHMA BAJRACHARYA
FCPS 1ST YR RESIDENT
OBS/ GYNE

2. • PCOS is not merely a reproductive disorder but an
endocrinological disorder affecting women in their
reproductive years.
• Although hyperandrogenism and infertility that PCOS
causes are distressing to young women, its metabolic
sequelae eventually plague the individual in terms of
morbidity and mortality

3. PCOS AKAs
• Polycystic Ovarian Syndrome,
• Functional Ovarian Hyperandrogenism,
• Chronic Hyperandrogenic Anovulation,
• Ovarian Hyperandrogenic Dysfunction,
• Hirsutism-Anovulation Syndrome,
• Stein Leventhal Syndrome,
• PCO,
• PCOD,
• Polycystic Ovaries,
• Sclerocystic ovary,
• Stein’s Syndrome.

4. Historical Aspects of PCOS
• Vallisneri gave the first histological description of the
polycystic ovary, 1721
• Sclerocystic changes in the ovary described by Chereau,
1844
• Class description of a bearded women with DM,
Achard/Thiers 1921

5. • In 1935, Stein and Leventhal described 7 women with
bilateral enlarged PCO, amenorrhea or irregular
menses, infertility and masculinizing features.
• This seminal paper introduced clinicians to the
concept of reproductive endocrinopathies.

6. Definition of PCOS
1990 US NIH Consensus Conference:
2 minimal criteria
1. Menstrual Irregularity due to oligo- or
anovulation
2. Clinical or biochemical hyperandrogenism
a.Hirsutism,Acne,Male Pattern Baldness
b.Elevated Serum Androgen Levels
3. Above not attributable to other causes

7. 2003 ESHRE/ASRM (Rotterdam,Netherlands)
Consensus on the Dx of PCOS
• Requires the presence of two out of the following
three criteria:
1. Oligo- and/or Anovulation
2. Hyperandrogenism (clinical and/or biochemical)
3. Polycystic Ovaries, with the exclusion of other
etiologies

8. Task Force Appointed by the Androgen
Excess Society (AES) 2006
• Reviewed all available data and recommended a new evidence-based
definition.
The Task Force identified 4 key clinical features of PCOS:
1.Ovulatory and Menstrual Dysfunction
2.Hyperandrogenism
3.Hirsutism, Acne and Androgenic Alopecia
4.Polycystic Ovaries
Plus the exclusion of other disorders of androgen
(J Clin Endocrinol Metab.2006 Aug 29)

9. ►2012
Institutes of Health Evidence-based Methodology
Workshop on PCOS
Concluded 2003 Rotterdam criteria should be
adopted because most inclusive

10. PCOS-Epidemiology
• PCOS affects 6.5 to 8% (NIH 1990) of the female population of reproductive
age.
• It’s prevalence among infertile women is 15% to 20%.
• PCOS accounts for 95% of cases of hyperandrogenism
• PCOS is responsible for over 20% of all cases of amenorrhea
• PCOS is responsible for up to 75% of all cases of anovulatory infertility.

11. Pathophysiology
►Principal molecular defect that causes PCOS is unknown
►Interaction of multiple genetic variants and
environmental factors (diet, obesity)

12. evidences showed association between cytochrome P450
17-hydroxylase/17, 20-desmolase (CYP17) and PCOS.
Cytochrome P450 side-chain cleavage enzyme (CYP11A)
and PCOS.
Crosignani P, Nicolosi A. Polycystic ovarian disease: heritability and heterogeneity.
Human reproduction update. 2001;7(1):3-7.

13. Pathophysiology
►Principal genetic targets
• Gonadotropin secretion
• Insulin secretion
• Androgen biosynthesis
• Weight and energy regulation

14. Gonadotropin secretion

15. Pathophysiology
Gonadotropin secretion
► LH action enhanced at ovarian level
► LH receptor is overexpressed in theca cells
► LH increased relative to FSH levels
► Follicular arrest and increased androgen production in the ovarian
theca cells
► The most likely cause of anovulation is an FSH level too low to fully
mature the follicles
► FSH levels may be suppressed by negative feedback inhibition from
mid-follicular estradiol level
► Anovulation

16. Pathophysiology
Insulin secretion and action
►Insulin resistance (IR)
• Appears to be related to mutations in the insulin receptor gene
 altered function
►50 to 70% PCOS patients have IR

17. Pathophysiology
Insulin secretion and action
►IR leads to hyperandrogenism
• Hyperinsulinemia and LH synergistically stimulates theca cell
secretion of androgens
• Hyperinsulinemia inhibits hepatic sex-hormone binding
globulin (SHBG) production
►Resulting in an increase in free androgens

18. Pathophysiology
Androgen biosynthesis and action
►Produced by ovaries and adrenal glands
►Testosterone
►70% bound to SHBG
►20-30% bound to albumin
►1% free - - biologically active

21. Serum Androgens
►Testosterone (T)
• Majority made in ovary
• Most potent circulating androgen
• Biological activity determined by the amount of binding to sex
hormone binding globulin
• Free testosterone is active

22. Serum Androgens
►Androstenedione (A)
• Immediate precursor to testosterone
• Ovary and adrenal production
►Dehyrdoepiandrosterone sulfate (DHEA-S)
• Majority derived from adrenal glands
• Small percentage from ovary

23. Serum Androgens
►Dihydrotestosterone (DHT)
• Peripheral conversion in androgen responsive tissues
• Intracellular 5-alpha reductase converts T to DHT
• DHT binds to androgen receptor with affinity 10x greater than T
• Women with PCOS have increased 5-alpha reductase activity (converts T
to DHT)
• Resulting in increased activation of the pilosebaceous unit (hair growth,
sebum production) with increase in bioavailable testosterone

24. Ovarian Androgen Secretion
►Androgens produced in the theca cells which respond to LH
►Role of insulin
• Synergistic effect of LH and insulin to increase androgen secretion
►Theca cells synthesize mostly androstenedione and some
testosterone
►They diffuse across the basement membrane to the granulosa cells

25. Ovarian Androgen Secretion
(continued)
►The granulosa cells, in response to stimulation by FSH, produce
aromatase which converts androgen precursors to estrone and
estradiol (negative feedback to FSH)
►Impeded normal follicular growth, resulting in follicular arrest at
the 4-8mm diameter size
►A dominant follicle (18-25mm) does not develop therefore
ovulation does not occur

27. Ovarian Theca & Granulosa Cells

28. Adrenal Androgen Secretion
►Adrenal androgen secretion
• Under control of ACTH
• Over 50% of women with PCOS have evidence of
increased adrenal androgen secretion

30. Pathophysiology
Weight and energy regulation
►Obesity
►40-80% of PCOS are overweight or obese
• Presence of obesity results in:
►Insulin resistance  hyperinsulinemia
►Hyperinsulinemia  synergy with LH and drop in SHBG  Hyperandrogenism
 hirsuitism/acne
►Arrest of follicular development chronic anovulation
• PCOS patients
►31-35% have IGT (1.6% in non-PCOS)
►7.5-10% have DM (2.2% in non-PCOS)

31. Obesity and insulin resistance

33. Clinical Features
Adolescence
►No formal diagnostic criteria
• Obesity
• Irregular cycles
►50% of cycles are anovulatory in first 2 years after menarche
►More Concerning…
• Hyperandrogenism
• Peripubertal girls with pubarche before age of 8

34. Clinical Features
Reproductive age
►Anovulatory Symptoms
• 2/3 patients
• Erratic cycles with breakthrough bleeding
• Primary amenorrhea
• Oligomenorrhea
►Hirsutism
►Acne
►Male pattern hair loss
►Polycystic Ovary

35. Clinical Features
Reproductive age
►Obesity
40-80% have BMI > 30
►Insulin Resistance
majority of PCOS patients regardless of obesity
(30% lean and 70% obese)
►Diabetes (7.5 to 10% of PCOS
patients)
31-35 % of PCOS patients have glucose
intolerance
2-5 fold increase in developing DM
►Infertility
75% of infertility causes
Poor FSH stimulation and elevated LH levels
impair follicle maturation and ovulation
►Pregnancy
Spontaneous abortion rate 20-40% higher
Pregnancy complication rate (GDM 3.4x,
GHTN 3.4x, Pre E 2.2x, PTB 1.9x)

36. Clinical Features
Reproductive age
►Endometrial Hyperplasia/Cancer
• Chronic exposure to unopposed estrogens
►Dyslipidemia – low HDL, high triglycerides 70% of patients with PCOS
►Metabolic syndrome – 30 to 40%
►Nonalcoholic fatty liver disease – 30% in PCOS compared to 2% all women and
5% women with DM2
►Coronary heart disease
►Sleep apnea
►Depression/anxiety
►Eating disorders (binge eating)

37. Source of Image:http://fcionline.com/fertility/infertility-diagnosis-services/pcos

38. Differential
Diagnosis

39. Menstrual Dysfunction in PCOS
• Irregular Menses -less than 21 days or greater than 35 days.
• PCOS- typically have prolonged(>35 days) cycles.
• Menstrual disturbances in PCOS classically have a peripubertal
onset
• Both decreased menstrual cycle regularity and dysfunctional
uterine bleeding are clinical consequences of chronic
anovulation.
• Increased risk of endometrial hyperplasia/carcinoma
• Prolonged amenorrhea associated with endometrial atrophy

40. Ovulatory and Menstrual
Dysfunction per the Task Force of
the AES 2006
• 75% of patients have clinically evident menstrual
dysfunction, and 20% have a history of apparent
eumenorrhea.
• In women with hirsutism and eumenorrhea, anovulation
can be confirmed by measuring serum progesterone
during days 20 through 24 of the cycle.

41. Clinical Hyperandrogenism
• Hirsutism
• Acne 15% to 25%
• Male-pattern Balding
• Acanthosis Nigricans- Occurs in up to 5% of women
• - Mucocutaneous eruption characterized by hyperkeratosis,
papillomatosis and increased pigmentation.
• Occurs in the axillae, nape of neck, under the breast and the flexures.
• less common- Increased Muscle Mass, Deepening Voice, Clitoromegaly

43. Labs
►Goal is to exclude other etiologies
►Androgens
• Total Testosterone
►widely available
►mildly elevated in PCOS
►If >150 ng/dL (normal<70) consider androgen secreting tumor
• Free Testosterone
►more sensitive test
• DHEA-S
►marker for adrenal hyper androgenemia
►If >800 mcg/dL (normal <270) consider androgen secreting tumor
• SHBG ??

44. Labs
►LH – increased in PCOS, too variable to be useful
►FSH – Premature ovarian failure
PCOS
►FSH levels low
►LH levels high
►LH/FSH > 3
►PRL – hyperprolactinemia
►TSH – thyroid dysfunction

45. ►17-hydroxyprogesterone
• CAH
• Random < 4 ng/mL
• Morning fasting < 2 ng/mL
• High levels should prompt an adrenocorticotropic hormone (ACTH) stimulation
test
►Dexamethasone suppression test
• If suspicious of Cushing’s syndrome

46. Labs
►Fasting glucose
• Fasting plasma glucose
►<100 mg/dL normal
►100-125 mg/dL impaired fasting glucose/prediabetes
►>126 mg/dL DM
►2 hour glucose level after 75gm oral glucose load
• 140-199 mg/dL indicates impaired glucose tolerance
• Above 199 mg/dL is diagnostic for type diabetes
• Recheck every 2 years if IGT
Lipid Profile

47. Imaging
►Ultrasound is the imaging modality of choice
►Assessment of endometrial abnormalities
►Pelvic U/S to rule out ovarian mass
►PCOS ovaries are enlarged (>5cm)
• > 12 subcapsular follicles (2-9 mm) in one or both ovaries
• Ovarian volume >10mL
• Dense hyperechoic stroma
• “string-of-pearls” appearance

48. Ovarian Morphology on Pelvic Ultrasound
• Ovarian pattern is both insufficient and
unnecessary to make the diagnosis of PCOS
per NIH Conference on PCOS criteria of
l990
• However, it has been considered necessary
to redefine PCOS and include with it an
appropriate definition of the polycystic
ovary per 2003 ESHRE/ASRM criteria

49. Polycystic Ovaries per the Task Force by
AES 2006
• 75% of patients have polycystic ovaries detected by transvaginal
ultrasonography
• The Dx of polycystic ovaries should not be based merely on a
“polycystic” or “multicystic” appearance.
• At least 1 ovary should have a volume of >10cm3 (mL), or there
should be >= 12 follicles measuring 2 to 9 mm in diameter.

50. Additional Use for Pelvic Ultrasound
•To check the endometrium for
hyperplasia and carcinoma

51. Goals of Treatment
►Lifestyle changes
►Lower risk for DM and CV disease
►Avoid effects of hyperinsulinemia
►Reduce production and circulating levels of androgens
►Protect the endometrium against effects of unopposed
estrogen
►Induce ovulation to achieve pregnancy
►Contraception – return of ovulation with treatment

52. Treatment for those
NOT pursuing pregnancy
►Menstrual dysfunction and endometrial
protection
►OCPs – first line
• Cycle regulation – predictable/regular
withdrawal bleed
• Contraception
• Progestin antagonizes the proliferative
effect of estrogen and prevents
endometrial hyperplasia
• Progestin only
►Cyclical or continuous oral dosing
►Progestin IUD
►Progestin rod implant
• Metformin – second line
►Restoration of ovulatory cycles in
50% of women

53. Treatment for those
NOT pursuing pregnancy
►Androgen excess
• OCPs – first line
►Decreases LH secretion  decrease ovarian androgen production
►Increases hepatic production of SHBG  decrease in bioavailable
testosterone
►Decrease in adrenal androgen secretion

54. Treatment for those
NOT pursuing pregnancy
►Anti-androgen – added if suboptimal effects after 6 months * *
MUST use contraception
• Spironolactone – 50-100 mg BID
►Aldosterone antagonist diuretic
►Competitive androgen receptor antagonist
• Finasteride, flutamide, GnRH agonist
►Eflornithin HCl (Vaniqa) 13.9% cream BID
►Concomitant therapy (OC and anti-androgen)
• Cosmetic – mechanical (shaving, waxing, depilatories, electrolysis, laser

55. Treatment for those
NOT pursuing pregnancy
►Metabolic abnormalities
• Obesity – weight loss 5-10% to restart ovulatory patterns
(diet/exercise, pharmacotherapy, bariatric surgery)
►Caloric restriction is main factor
►No data supporting one diet over the other
• IR/risk of DM2 – metformin (first line)
►thiazolidinediones (wt gain, less studied in PCOS)
• Dyslipidemia – exercise/weight loss, pharmacotherapy if needed
• OSA – CPAP

56. Metformin
►Major effect is to decrease hepatic glucose production thus less need for
insulin secretion
►Target dose 1500-2000 mg/day (can use short acting or extended dosing)
►Side effects – diarrhea, nausea/vomiting, flatulence, indigestion, abdominal
discomfort
►Avoid if risk for lactic acidosis (renal insufficiency)
►“Off label” use – oligomenorrhea, hirsuitism, obesity, prevention of DM2

57. • A recent, uncontrolled, retrospective, observational study, showing that
long-term treatment with metformin delays or prevents the development
of impaired glucose tolerance and diabetes in women with PCOS, is
certainly in keeping with this concept.*
• Another study showed decreased weight and systolic blood pressure as
well as increased HDL in metformin-treated women with PCOS.* In this
study, metformin was also shown to increase insulin sensitivity and
lower testosterone in obese but not non obese PCOS women.
* Trolle B, Flyvbjerg A, Kesmodel U, Lauszus FF. Efficacy of metformin in obese and non-obese women with polycystic ovary
syndrome: a randomized, double-blinded, placebo-controlled, cross-over trial. Hum. Reprod. 22(11), 2967-2973 (2007)
* Sharma ST,Wickham III EP, Nestler JE. Changes in glucose tolerance with metformin treatment in polycystic ovary syndrome:
a retrospective analysis. Endo. Prac. 13(4), 373-379 (2007).

58. Dosing of Metformin
• “Start Low, Go Slow”
• Starting dose 500 mg daily with food/dinner x 1 wk
• 500 mg twice daily; breakfast, dinner x1 week
• 500 mg am, 1,000 mg pm x 1 week
• 1,000 mg BID; breakfast, dinner
• Increasing q 1- 2 weeks to max 2+ gms day
• Maximum 2250 mg total daily; 850 mg tid
• Garber et al. Am J Med 1997;103: Garber et al. Am J Med 1997;103: Ovulation improves w Single or Combination
therapy Ovulation improves w Single or Combination therapy NEW: NEW: Research supports benefits even if
NOT seeking pregnancy Research supports benefits even if NOT seeking pregnancy Secor 2011

59. Metformin and OCPs
►Metformin + OCPs
• Inadequate evidence to recommend routine addition of metformin as
unclear whether this combination has important cosmetic or metabolic
advantages over OCP monotherapy
►Metformin vs OCPs
• OCPs first line for oligomenorrhea and hyperandrogenism. OCPs less
beneficial for insulin sensitivity while metformin better at reducing fasting
insulin

61. Treatment for those
pursuing pregancy
►Weight loss – 5-10% loss yields resumption of ovulatory cycles
►Ovulation induction – be sure to do a semen analysis and HSG to
complete infertility
• Clomiphene
• Letrozole
• Metformin
• Gonadotropins

62. Treatment for those
pursuing pregancy
►Ovulation induction agents
• Clomiphene – first line
►Selective estrogen receptor modulator (SERM) – competitive inhibitor of
estrogen binding to receptors in hypothalamus (blocks the negative
feedback loop of estrogen) and results in increase in GnRH, FSH, and
LH and influence follicular development.
►It is an estrogen agonist enhancing FSH stimulation of LH receptors in
the granulosa cells
►50-150 mg per day orally 5 days: cycle days 3-7
►Ovulate approx 10 days after last dose, Monitor for LH surge
starting day 12
►80% will ovulate and 50% will conceive

63. Treatment for those
pursuing pregancy
►Ovulation induction agents
• Letrozole – aromatase inhibitor (off label use)
►Aromatase catalyzes the rate limiting step in production of estrogen
thus suppresses ovarian estradiol secretion and rise in FSH and follicle
production
►Also used as adjuvant endocrine therapy in postmenopausal breast
cancer
►5-7.5 mg po daily day 2-6 x 5 days
• Metformin – with or without clomiphene
• GnRH – higher risk for ovarian hyperstimulation syndrome

64. Treatment for those
pursuing pregancy
►Laparoscopic surgery
• Wedge resection – abandoned secondary to adhesion
formation, better results with clomiphene
• Ovarian drilling/diathermy
►In vitro fertilization (IVF)
►Intracytoplasmic sperm injection (ICSI)

65. Laparoscopic Surgery for Ovulation Induction in
PCOS
►Majority with anovulatory infertility will ovulate in
response to clomiphene, however up to 30% remain
anovulatory
• Of 70% who do ovulate, only 50% will conceive
• Addition of metformin can help ovulation %
• Those that are still unresponsive/resistant move to
gonadotropin therapy
►Issues: difficult to titrate the dose to achieve monofollicular ovulation,
30% risk of multiples, risk of ovarain hyperstimulation syndrome, cost,
SAB risk is higher

66. Laparoscopic Surgery for Ovulation Induction in
PCOS
►Dates to 1930’s – bilateral ovarian wedge resection
resulted in restoration of regular menses and pregnancy
• fell out of favor secondary to post-op adhesion formation and
the introduction of clomiphene
►Ovarian drilling/electrocautery – less adhesions, similar
pregnancy rates to gonadotropin with less multiple risk

67. Ovarian Drilling
►Create focal areas of damage to
the ovarian cortex and stroma
►Unipolar needle electrode
insulated down to 2 cm of
exposed probe. 4-6 punctures of
each ovary

68. Ovarian Drilling
►Laparoscopic candidates – PCOS patients who have failed
clomiphene and metformin, non-obese BMI <30, and no other fertility
factors
►Efficacy – similar conception rates to gonadotropin therapy
• Advantages – no cyclical monitoring, more cost effective, no increase risk of
multiple gestations or OHSS
• Disadvantages – anesthesia, surgical risk (bleeding, infection, damage to
surrounding tissues, adhesive disease)
• Other considerations – often unsuccessful in obese women, patients should have
no other infertility factors (tubal, endometriosis, male factor), IVF success

70. Long Term Issues
Associated with PCOS

71. Source of Image: Teede, Helena j. et al., Assessment and management of polycystic ovary syndrome: summary of an
evidence-based guideline, Med J Aust 2011; 195 (6): S69.

72. The Metabolic Syndrome and PCOS
• The prevalence of metabolic syndrome in women with PCOS is approximately 43-46%.*
WHO
• T2DM or IFG or IGT or insulin resistance plus ≥ 2 of the following:
• • BMI > 30 kg/m2
• • HDL < 1.0 mmol/L (< 40 mg/dL)
• • TG ≥ 1.7 mmol/L (150 mg/dL)
• • BP ≥ 140/90 mmHg or use of blood pressure medication
• • microalbuminuria > 20 pg/min
• • Alb/Crea ratio ≥ 30 mg/g
*Third report of the National Cholesterol Education Program. Expert panel on the detection, evaluation and
treatment of high blood cholesterol in adults. Final report. Circulation 106, 3143-3421 (2002).

73. • Insulin resistance is the major underlying pathophysiologic abnormality linking
the metabolic syndrome and PCOS.
• Weight loss with life-style modification is the safest and cheapest therapy that has
shown benefit both in MetS and PCOS

74. Polycystic Ovary Syndrome and Cardiovascular Disease: Premature Association?
Richard S. Legro
Endocrine Reviews June 1, 2003; 24 (3): 302-312
• Women with polycystic ovary syndrome (PCOS) are often assumed, a priori, to be at increased risk for
cardiovascular disease (CVD), given the high prevalence of the metabolic syndrome X among them.
• Long-term studies of well characterized women with PCOS are lacking, and the link to primary cardiovascular
events such as stroke or myocardial infarction remains more speculative than substantive.
• Epidemiological studies that have focused on isolated signs and stigmata of PCOS, such as polycystic ovaries,
hyperandrogenism, or chronic anovulation, have found mixed results.
• There are studies that suggest a slight increase in cardiovascular events in women with polycystic ovaries, with
perhaps stronger evidence between an increased risk of cardiovascular events in women with menstrual
irregularity.
• However, there is little evidence for an association between hyperandrogenism per se and cardiovascular events.
• Furthermore, there are less data to substantiate an increased risk of events in women with PCOS identified on
the basis of a combination of signs and symptoms, such as hyperandrogenic chronic anovulation.
• The existing data suggest that PCOS may adversely affect or accelerate the
development of an adverse cardiovascular risk profile, and even of subclinical signs of
atherosclerosis, but it does not appear to lower the age of clinical presentation to a
premenopausal age group.

75. Cardiovascular Risk in PCOS
• Several studies using intima media thickness as a
surrogate for cardiovascular risk evaluation have
shown potential increased cardiovascular risk in
women with PCOS.*
Talbot EO, Guzick DS, Sutton-Tyrrell K et al. Evidence for association between polycystic ovary syndrome and premature carotid
atherosclerosis in middle-aged women. Arterioscler. Thromb. Vasc. Biol. 20, 2414-2421 (2000).
* Vryonidou A, Papatheodorou A, Tauridou A et al. Association of hyperandrogenism and metabolic phenotype with carotid
intima-media thickness in young women with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 90, 2740-2746 (2005).
* Luque-Ramirez M, Mendieta-Azcona C, Alvarez-Blasco F, Escobar-Morreale HF. Androgen excess is associated with increased
carotid intima-media thickness observed in young women with polycystic ovary syndrome. Hum. Reprod. 22, 3197-3203 (2007).

76. Coronary Artery Calcification and PCOS
• A similar study using coronary artery calcification as
risk stratification has shown increased risk in patients
with PCOS.*
* Christian R, Dumesic DA, Behrenbeck T, Oberg AL, Sheedy PF, Fitzparick LA. Prevalence and predictors of
coronary artery calcification in women with polycystic ovary syndrome. J. Clin. Endocrinol. Metab. 88, 2562-2568
(2003).

77. Sleep Apnea and Other Sleep Disorders
• Multiple groups have documented an increased risk for
sleep apnea and other sleep disorders including increased
daytime somnolence, such as sleep disordered breathing
in women with PCOS.

78. Body Image and Quality of Life in PCOS
Patients
• There is little study of the psychopathology of women
defined as having PCOS in literature
• PCOS disease-specific questionnaire known as the PCOSQ has
been developed to study the above questions.
• Obesity and infertility cause the greatest degree of stress
• Both anorexia nervosa and bulimia have been linked with
PCOS(etiological link?)
• Many conditions co-exist with PCOS such as pelvic pain,
depression and altered mood but it is unclear where there is a
casual or causal association.

79. Poly cystic ovarian syndrome and cancers
• Endometrial carcinoma-
• The prevalence of endometrial hyperplasia with and without atypia in women with
PCOS varies from 1 to 48.8%
• chronic anovulation, which results in continuous estrogen stimulation of the
endometrium unopposed by progesterone
• Obesity, hyperinsulinemia, and hyperandrogenism state in PCOS, results in
increased bioavailability of unopposed estrogens by progesterone due to the
increased peripheral conversion of endogenous androgen into estrogen
• Hardiman P, Pillay OS, Atiomo W. Polycystic ovary syndrome and endometrial carcinoma.
• The lancet. 2003;361(9371):1810-2.

80. Ovarian cancer and breast cancer
• women with PCOS had a 2.5-fold increased risk of developing ovarian cancer,
• clomiphene citrate and gonadotropin therapy or ovulation induction was found to
increase the relative risk of ovarian tumors in women with PCOS around 4.1 x
• meta analysis about the association between PCOS and breast cancer showed that the
risk of breast cancer was not significantly increased overall
• However some studies showed that women with PCOS independently of age, age at
menarche or menopause, parity, using oral contraceptive pill, BMI and family history
of breast cancer, have 1.8 times as likely to report benign breast disease
Schildkraut JM, Schwingl PJ, Bastos E, Evanoff A, Hughes C. Epithelial ovarian cancer risk among women with
polycystic ovary syndrome. Obstetrics & Gynecology. 1996;88(4, Part 1):554-9.
Barry JA, Azizia MM, Hardiman PJ. Risk of endometrial, ovarian and breast cancer in women with polycystic ovary
syndrome: a systematic review and meta-analysis. Human reproduction update. 2014:dmu012.

81. •Polycystic ovary syndrome and
pregnancy

82. PCOS and abortion
• spontaneous Abortion occurs in 30 to 50% of PCOS women compared with 10 to 15%
of normal women
• a metaanalysis showed Treatment with ovulation-inducing agents is associated with a
higher incidence of abortion in PCOS women
• It is suggested that metformin therapies before and throughout pregnancy, could
decrease the risk of early abortion, but more studies are needed
Kjerulff LE, Sanchez-Ramos L, Duffy D. Pregnancy outcomes in women with polycystic
ovary syndrome: a metaanalysis. American journal of obstetrics and gynecology.
2011;204(6):558. e1-. e6.

83. PCOS and gestational diabetes mellitus
• affects 4–7% of pregnancies overall.
• There are 2.4-fold increased risks of GDM among PCOS women, independent
of age, race/ethnicity, and multiple gestations.
• GDM complicates 40 to 50% of PCOS pregnancies.
Lo JC, Feigenbaum SL, Escobar GJ, Yang J, Crites YM, Ferrara A. Increased Prevalence of
Gestational Diabetes Mellitus Among Women With Diagnosed Polycystic Ovary Syndrome A
population-based study. Diabetes care. 2006;29(8):1915-7.

84. PCOS and hypertensive disorders in pregnancy
• Hypertensive disorders occurs in 8% of PCOS pregnancies
• Increased levels of androgens in PCOS have been associated with
the development of preeclampsia
Roberts JM, Pearson G, Cutler J, Lindheimer M. Summary of the NHLBI working group on
research on hypertension during pregnancy. Hypertension. 2003;41(3):

85. PCOS-Key Points
• PCOS is one of the commonest reproductive endocrinopathies to affect
women (5-10%).
• PCOS is the most common cause of anovulatory infertility.
• PCOS probably represents a spectrum of disease with variable
presentations-
• Pathophysiology- Insulin resistance + androgen excess
• Diagnosis –Clinical +/- labs, USG
• Current treatment options- lifestyle, combination OCP +insulin
sensitizers
• Is important to diagnose PCOS because of the potential long-term
consequences.
• Further research is necessary in this syndrome.

86. Who Should Manage PCOS?
• PCOS has evolved out of the purview of the reproductive
specialist and gynecologist.
• PCOS is probably best managed by an internist, family
practitioner or endocrinologist with subspecialists
including gynecologists, fertility specialist, dermatologists
and in the long run, cardiologists and oncologists as
indicated.

87. References-
• Berek & Novak’s Gynecology
• Jeffcoate’s Principles of Gynecology
• Clinical gynecology Bieber, Joseph S. Sanfilippo, Ira R. Horowitz
• Uptodate.com
• Polycystic ovary syndrome : a guide to clinical management / Adam Balen ... [et al.]
• Polycystic ovary syndrome / edited by R. Jeffrey Chang, Jerrold J. Heindel, Andrea
Dunaif.
• ACOG practice bulletin, polycystic ovary syndrome
• Clinical gynecologic endocrinology and infertility / Leon Speroff, Marc A. Fritz

88. • Comprehensive Gynecology. 4th Edition. Stenchever, Droegemueller, Herbst,
Mishell.
• Clinical Gynecology. 1st Edition. Bieber, Sanfilippo, Horowitz.
• Polycystic Ovary Syndrome. ACOG Practice Bulletin. Number 108. October 2009.
Reaffirmed 2013
• A practical approach to the diagnosis of polycystic ovary syndrome. American
Journal of Obstetrics and Gynecology. Volume 191, Issue 3, Pages 713-717
(September 2004).
• Polycystic Ovarian Syndrome: 3 Key Challenges. Dale W. Stovall, MD
OBG Management · June 2003 · Vol. 15, No. 6
• Polycystic ovary syndrome: How are obesity and insulin resistance involved?. OBG
Management. October 2012 · Vol. 24, No. 10