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Menopause	
  	
  and	
  Polycys/c	
  
Ovarian	
  Syndrome	
  
	
  
	
  
	
  
DR	
  KAWITA	
  	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  
RULES5
DR	
  KAWITA	
  BAPAT	
  
TREAT YOUR
AS
Patients
Queen
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DR	
  KAWITA	
  BAPAT	
  
SPREAD
IDEASANDMOVE
GYNAECOLOGIST
2
DR	
  KAWITA	
  BAPAT	
  
HELP
SEEWHAT YOU
SAYING
THEM
ARE
3
DR	
  KAWITA	
  BAPAT	
  
PRACTICE
DESIGNNOT DECORATION
4
DR	
  KAWITA	
  BAPAT	
  
History
•  Originally described
by Stein and
Leventhal in 1935,
first known as the
“Stein-Leventhal
syndrome”
DR	
  KAWITA	
  BAPAT	
  
Hyper
Andro
genism	
  
Menstrual
Irregularity
Polycystic
ovaries
Central
Adiposity
DR	
  KAWITA	
  BAPAT	
  
	
  
Classic syndrome
originally described
by
Stein and Levanthal
	
  
•  Syndrome, not a disease—multiple potential
etiologies with variable clinical expression
Diagnostic criteria
based on the modified consensus of
National Institutes of Health
Major
Chronic anovulation
Clinical signs of hyperandrogenism
Other etiologies excluded
•
•
–
DR	
  KAWITA	
  BAPAT	
  
Diagnostic criteria
based on the modified consensus of
National Institutes of Health	
  
Minor
Insulin resistance
Perimenarchal onset of hirsutism and obesity
Elevated LH : FSH ratio
Intermittent anovulation associated with
hyperandrogenemia (free testosterone, DHEAS).
DR	
  KAWITA	
  BAPAT	
  
Polycystic ovaries
(>12 peripheral
follicles
or increased
ovarian volume
>10cm3)
Oligo- or
anovulation
Clinical and/or
biochemical
signs of hyper
androgenism
And exclusion of other
etiologies such
1.  Hypothyroidism,
2.  Hyperprolactinemia
3.  Congenital Adrenal
Hyperplasia,
4.  Cushing Syndrome,
5.  Androgen Secreting
Tumors
•  1
Rotterdam criteria
• 2 • 3 • 4
AE-PCOS SOCIETY 2006
Hyperandrogenism-
hirsutism
and/
or
hyperandrogenemia	
  
Ovarian
dysfunction-
oligo-anovulation
and/ or
polycystic ovaries
Exclusion
of
other androgen
excess or
related disorders
DR	
  KAWITA	
  BAPAT	
  
Abnormal Pituitary Function— Altered Negative
Feedback Loop	
  
•  Increased GnRH from
hypothalamus
•  Excessive LH
secretion relative
to FSH by
pituitary gland
•  LH stimulates ovarian
thecal cells-- androgen
production
•  Ineffective suppression of
the LH pulse frequency
•  by estradiol and
progesterone	
  
•  Androgen excess
increases LH by
blocking the
hypothalamic inhibitory
feedback of
progesterone
DR	
  KAWITA	
  BAPAT	
  
Abnormal steroidogenenesis
•  Follicular maturation is inhibited
	
  
	
  
•  Excess androgen causes thecal
and stromal hyperplasia
	
  
	
  
•  Intraovarian androgen excess
results in excessive growth of
small ovarian follicles
	
  
	
  
DR	
  KAWITA	
  BAPAT	
  
HYPERANDROGENISM	
  
important	
  	
  
Hirsu/sm,	
  
acne,	
  male	
  
paAern	
  
balding,	
  	
  
alopecia	
  
Elevated	
  
Serum	
  	
  
Androgen	
  
Levels	
  
Free	
  
testosterone	
  
levels	
  most	
  
sensi/ve	
  
Increased	
  
Muscle	
  Mass,	
  
Deepening	
  	
  
Voice,	
  
Clitormegaly	
  	
  
Insulin resistance
•  Favors anovulation,
1.  androgen excess,
2.  reduced SHBG
•  Metabolic syndrome
•  Abdominal obesity
DR	
  KAWITA	
  BAPAT	
  
Insulin Resistance: Associated Conditions
Insulin Resistance
Type 2 diabetes
Hypertension
Impaired Glucose
tolerance
Obesity (central)
Polycystic ovary
diseaseHyperuricemia
Acanthosis
Nigricans
Decreased
Fibrinolytic
Activity
Dyslipidemia
Atherosclerosis
DR	
  KAWITA	
  BAPAT	
  
Clinical Presentation of Women with PCOS
Adolescent
Period
Reproductive
Period
Menopausal
♣ Menstrual
Irregularity
♣Cosmetic
concerns
♣ Acne
♣ Hirsutism
♣ Hair Loss
♣ Infertility
♣ Early Pregnancy loss
♣ During pregnancy
♣ PIH
♣ GDM
♣ Metabolic
Syndrome
♣ Ca Endometrium
ObesityDR	
  KAWITA	
  BAPAT	
  
MENSTRUAL
DYSFUNCTION	
  
Delayed
menarche
deficient
progesterone
secretion
Chronic
estrogen
stimulation 	
  
No Progesterone
For
Differentiation	
  
Intermittent
Breakthrough
Bleeding	
  
Dysfunctional
Uterine Bleeding	
  
Increased risk for
endometrial
hyperplasia 	
  Endometrial CA
DR	
  KAWITA	
  BAPAT	
  
•  Elevated	
  CRP	
  and	
  
heart	
  disease	
  
•  Advanced	
  
atherosclerosis	
  
4	
  
•  Metabolic	
  
syndrome—43%	
  
of	
  PCOS	
  	
  pa/ents	
  	
  
•  (2	
  fold	
  higher	
  
than	
  age-­‐matched	
  	
  
popula/on)	
  
3	
  
•  Sleep	
  apnea	
  
•  Nonalcoholic	
  
steatohepa//s	
  
2	
  
ASSOCIATED MEDICAL CONDITIONS	
  
•  Increased	
  risk	
  of	
  
developing	
  Type	
  2	
  	
  
Diabetes	
  	
  
•  Low	
  HDL	
  and	
  high	
  
triglycerides	
  
1	
  
DR	
  KAWITA	
  BAPAT	
  
PCOS & Metabolic Syndrome
Metabolic Syndrome:
•
•
Cluster of Cardiovascular risk factors related
to Insulin Resistance:
- Obesity
- Hyperinsulinemia
- Hypertension
- Atherogenic Dyslipidemia
- Atherosclerosis
- Hyperglycemia
Major Risk Factors:
- Physical inactivity
- Atherogenic diet
- Adiposity / abdominal obesity
DR	
  KAWITA	
  BAPAT	
  
Blood	
  pressure	
  	
  
130/	
  85	
  mm	
  Hg	
  
HDL cholesterol:
<50 mg/dL
Triglycerides
>150 mg/dL
.	
  
Waist
circumference
>88 cm (>35 inch)
.	
  
ATP	
  III	
  Clinical	
  Iden/fica/on	
  of	
  	
  the	
  Metabolic	
  Syndrome	
  
2	
  
3	
  
Fasting glucose
>110 mg/dL*New ADA guidelines
increases risk for Metabolic Syndrome
•Presence of any 2 of 5 criteria required
1	
  
4	
  
5	
  
DR	
  KAWITA	
  BAPAT	
  
Trouble	
  In	
  Diagnosis	
  	
  
•  With	
  PCOS	
  when	
  women	
  already	
  
reached	
  menopause	
  it	
  is	
  not	
  
possible	
  to	
  diagnose	
  Because	
  
•  The	
  Cardinal	
  Features	
  Disappear.	
  
•  Menses	
  Cease	
  
•  Testosterone	
  Levels	
  May	
  No	
  
Longer	
  Be	
  Higher	
  
DR	
  KAWITA	
  BAPAT	
  
Trouble	
  In	
  Diagnosis	
  	
  
•  Although	
  Less	
  Conven/onal	
  Measures	
  	
  
•  Androgen	
  Excess	
  	
  
•  Levels	
  Remain	
  Higher	
  	
  
1.  Free	
  Androgen	
  Index	
  	
  
2.  Human	
  Chorionic	
  Gonadotropin-­‐
s/mulated	
  Androstenedione	
  	
  
3.  17-­‐hydroxyprogesterone	
  
DR	
  KAWITA	
  BAPAT	
  
Trouble	
  In	
  Diagnosis	
  	
  
•  PCO	
  Morphology	
  Persists	
  Into	
  Menopause	
  
•  	
  Hypo	
  Echoic	
  Structures	
  On	
  Ultrasound	
  	
  
•  In	
  Postmenopausal	
  Women	
  With	
  PCOS	
  
Correspond	
  
1.  Inclusion	
  Cysts	
  
2.  Vascular	
  Structures	
  Rather	
  Than	
  Follicles	
  
Pathology	
  Studies	
  	
  
Do	
  Not	
  Demonstrate	
  Secondary	
  Follicles	
  In	
  
Postmenopausal	
  Ovaries	
  	
  
DR	
  KAWITA	
  BAPAT	
  
Trouble	
  in	
  diagnosis	
  	
  
•  	
  When	
  women	
  with	
  PCOS	
  had	
  reached	
  
menopause	
  	
  
•  no	
  difference	
  in	
  	
  
1.  fas/ng	
  insulin	
  levels	
  
2.  HOMA	
  of	
  insulin	
  resistance	
  	
  
3.  glucose	
  levels	
  	
  
•  prevalence	
  of	
  hypertension	
  higher	
  	
  
•  triglyceride	
  levels	
  increased	
  
DR	
  KAWITA	
  BAPAT	
  
MENOPAUSAL	
  TRANSITION	
  	
  
	
  
DYSLIPIDEMIA	
  
WITH	
  AGE	
  
SPECIFIC	
  
INCREASE	
  IN	
  
LDL	
  
01	
  
METABOLIC	
  
ABNORMALITIES	
  
IN	
  WOMEN	
  WITH	
  
PCOS	
  ALSO	
  
WORSEN	
  WITH	
  
AGE.	
  	
  
02	
  
•  WAIST	
  
CIRCUMFERENCE	
  
•  	
  CHOLESTEROL	
  
•  TRIGLYCERIDE	
  
LEVELS	
  INCREASE	
  
IN	
  	
  
•  AS	
  THEY	
  REACH	
  
40	
  TO	
  50	
  YEARS	
  	
  
03	
  
BMI	
  
INCREASED	
  IN	
  SOME	
  
04	
  
	
  All	
  women	
  experience	
  
	
  Increasing	
  insulin	
  resistance	
  	
  
Abdominal	
  adiposity	
  along	
  with	
  chronic	
  inflamma/on	
  	
  
PHENOTYPE	
  
	
  Recommenda/on	
  Of	
  The	
  	
  
Na/onal	
  Ins/tutes	
  Of	
  Health	
  (NIH)	
  	
  
Evidence-­‐based	
  Methodology	
  	
  
01	
   02	
   03	
   04	
  
(Phenotype	
  A)	
   ●	
  (Phenotype	
  B)	
  	
   ●(Phenotype	
  C)	
  	
   ●	
  (Phenotype	
  D)	
  	
  
Androgen	
  excess	
  +	
  
ovulatory	
  dysfunc/on	
  +	
  
polycys/c	
  ovarian	
  
morphology	
  
Androgen	
  excess	
  +	
  
ovulatory	
  dysfunc/on	
  	
  
Androgen	
  excess	
  +	
  polycys/c	
  
ovarian	
  morphology	
  	
  
Ovulatory	
  dysfunc/on	
  
+	
  polycys/c	
  ovarian	
  
morphology	
  	
  
	
  
in	
  menopausal	
  women	
  is	
  difficult	
  to	
  define.	
  	
  
DR	
  KAWITA	
  BAPAT	
  
Hyperandrogenism	
  
•  Persists	
  Ager	
  The	
  Menopausal	
  
Transi/on.	
  	
  
•  Con/nue	
  To	
  Manifest	
  The	
  Metabolic	
  
Altera/ons	
  Such	
  As	
  	
  
– Insulin	
  Resistance	
  	
  
– Which	
  Makes	
  Them	
  More	
  Suscep/ble	
  To	
  
Type	
  2	
  Diabetes	
  Mellitus.	
  	
  
DR	
  KAWITA	
  BAPAT	
  
Hirsutism
Regulation of
menses
Management
Immediate/Acute issues
	
  
01	
  
02	
  
Insulin
Resistance
Cardiovascular
Risk
Obstructive
Sleep Apnea
Malignancy
Risk
Management
Long-term Issues
01	
  
02	
  
03	
  
04	
  
Diet and Exercise
•  4-12 weeks of dietary restriction.
obese, endocrine-metabolic parameters
markedly improve
–  SHBG levels rise
•  Decrease
–  Serum insulin.
–  IGF-1 levels
–  free testosterone levels fall by 2-fold.
•
•
•
•
Moran LJ, Pasquali R, et all Treatment of obesity in polycystic ovary syndrome: a position statement of the Androgen Excess and Polycystic Ovary Syndrome
Society. Fertil Steril. Dec 3 2008;
DR	
  KAWITA	
  BAPAT	
  
Diet and Exercise
A moderate amount of daily exercise
1.  Increases of levels of IGF-1 binding protein
2.  Decreases IGF-1 levels by 20%.
lifestyle management as the primary
therapy in overweight and obese women
with PCOS for the treatment of
metabolic complications.
•
•
•
•
Moran LJ, Pasquali R, et all Treatment of obesity in polycystic ovary syndrome: a position statement of the Androgen Excess and Polycystic Ovary Syndrome
Society. Fertil Steril. Dec 3 2008;
DR	
  KAWITA	
  BAPAT	
  
Management:
Long-Term Issues
• Obstructive Sleep Apnea
–
–
–
•  30-fold increased risk of OSA,
not explained by obesity
alone.
•  Insulin resistance strongest
predictor of OSA (not BMI, age,
testosterone)
•  Consider polysomnography if at
risk
DR	
  KAWITA	
  BAPAT	
  
Management:
Long-Term Issues
• Risk for malignancy
–
–
–
•  3 fold increased risk
endometrial carcinoma in PCOS
•  Increased risk of ovarian and breast
cancer
•  Warrants regular screening, low threshold
for endometrial biopsy
DR	
  KAWITA	
  BAPAT	
  
Thank	
  you	
  
DR	
  KAWITA	
  BAPAT	
  
Thank	
  you	
  
DR	
  KAWITA	
  BAPAT	
  
DR	
  KAWITA	
  BAPAT	
  

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MENOPAUSE & PCO

  • 1.           Menopause    and  Polycys/c   Ovarian  Syndrome         DR  KAWITA    BAPAT   DR  KAWITA  BAPAT  
  • 9. TREAT YOUR AS Patients Queen The image cannot be displayed. Your computer may not have enough memory to open the image, or the image may have been corrupted. Restart your computer, and then open the file again. If the red x still appears, you may have to delete the image and then insert it again. DR  KAWITA  BAPAT  
  • 13. History •  Originally described by Stein and Leventhal in 1935, first known as the “Stein-Leventhal syndrome” DR  KAWITA  BAPAT  
  • 14. Hyper Andro genism   Menstrual Irregularity Polycystic ovaries Central Adiposity DR  KAWITA  BAPAT     Classic syndrome originally described by Stein and Levanthal   •  Syndrome, not a disease—multiple potential etiologies with variable clinical expression
  • 15. Diagnostic criteria based on the modified consensus of National Institutes of Health Major Chronic anovulation Clinical signs of hyperandrogenism Other etiologies excluded • • – DR  KAWITA  BAPAT  
  • 16. Diagnostic criteria based on the modified consensus of National Institutes of Health   Minor Insulin resistance Perimenarchal onset of hirsutism and obesity Elevated LH : FSH ratio Intermittent anovulation associated with hyperandrogenemia (free testosterone, DHEAS). DR  KAWITA  BAPAT  
  • 17. Polycystic ovaries (>12 peripheral follicles or increased ovarian volume >10cm3) Oligo- or anovulation Clinical and/or biochemical signs of hyper androgenism And exclusion of other etiologies such 1.  Hypothyroidism, 2.  Hyperprolactinemia 3.  Congenital Adrenal Hyperplasia, 4.  Cushing Syndrome, 5.  Androgen Secreting Tumors •  1 Rotterdam criteria • 2 • 3 • 4
  • 18. AE-PCOS SOCIETY 2006 Hyperandrogenism- hirsutism and/ or hyperandrogenemia   Ovarian dysfunction- oligo-anovulation and/ or polycystic ovaries Exclusion of other androgen excess or related disorders DR  KAWITA  BAPAT  
  • 19. Abnormal Pituitary Function— Altered Negative Feedback Loop   •  Increased GnRH from hypothalamus •  Excessive LH secretion relative to FSH by pituitary gland •  LH stimulates ovarian thecal cells-- androgen production •  Ineffective suppression of the LH pulse frequency •  by estradiol and progesterone   •  Androgen excess increases LH by blocking the hypothalamic inhibitory feedback of progesterone DR  KAWITA  BAPAT  
  • 20. Abnormal steroidogenenesis •  Follicular maturation is inhibited     •  Excess androgen causes thecal and stromal hyperplasia     •  Intraovarian androgen excess results in excessive growth of small ovarian follicles     DR  KAWITA  BAPAT  
  • 21. HYPERANDROGENISM   important     Hirsu/sm,   acne,  male   paAern   balding,     alopecia   Elevated   Serum     Androgen   Levels   Free   testosterone   levels  most   sensi/ve   Increased   Muscle  Mass,   Deepening     Voice,   Clitormegaly    
  • 22. Insulin resistance •  Favors anovulation, 1.  androgen excess, 2.  reduced SHBG •  Metabolic syndrome •  Abdominal obesity DR  KAWITA  BAPAT  
  • 23. Insulin Resistance: Associated Conditions Insulin Resistance Type 2 diabetes Hypertension Impaired Glucose tolerance Obesity (central) Polycystic ovary diseaseHyperuricemia Acanthosis Nigricans Decreased Fibrinolytic Activity Dyslipidemia Atherosclerosis DR  KAWITA  BAPAT  
  • 24. Clinical Presentation of Women with PCOS Adolescent Period Reproductive Period Menopausal ♣ Menstrual Irregularity ♣Cosmetic concerns ♣ Acne ♣ Hirsutism ♣ Hair Loss ♣ Infertility ♣ Early Pregnancy loss ♣ During pregnancy ♣ PIH ♣ GDM ♣ Metabolic Syndrome ♣ Ca Endometrium ObesityDR  KAWITA  BAPAT  
  • 25. MENSTRUAL DYSFUNCTION   Delayed menarche deficient progesterone secretion Chronic estrogen stimulation   No Progesterone For Differentiation   Intermittent Breakthrough Bleeding   Dysfunctional Uterine Bleeding   Increased risk for endometrial hyperplasia  Endometrial CA DR  KAWITA  BAPAT  
  • 26. •  Elevated  CRP  and   heart  disease   •  Advanced   atherosclerosis   4   •  Metabolic   syndrome—43%   of  PCOS    pa/ents     •  (2  fold  higher   than  age-­‐matched     popula/on)   3   •  Sleep  apnea   •  Nonalcoholic   steatohepa//s   2   ASSOCIATED MEDICAL CONDITIONS   •  Increased  risk  of   developing  Type  2     Diabetes     •  Low  HDL  and  high   triglycerides   1   DR  KAWITA  BAPAT  
  • 27. PCOS & Metabolic Syndrome Metabolic Syndrome: • • Cluster of Cardiovascular risk factors related to Insulin Resistance: - Obesity - Hyperinsulinemia - Hypertension - Atherogenic Dyslipidemia - Atherosclerosis - Hyperglycemia Major Risk Factors: - Physical inactivity - Atherogenic diet - Adiposity / abdominal obesity DR  KAWITA  BAPAT  
  • 28. Blood  pressure     130/  85  mm  Hg   HDL cholesterol: <50 mg/dL Triglycerides >150 mg/dL .   Waist circumference >88 cm (>35 inch) .   ATP  III  Clinical  Iden/fica/on  of    the  Metabolic  Syndrome   2   3   Fasting glucose >110 mg/dL*New ADA guidelines increases risk for Metabolic Syndrome •Presence of any 2 of 5 criteria required 1   4   5   DR  KAWITA  BAPAT  
  • 29. Trouble  In  Diagnosis     •  With  PCOS  when  women  already   reached  menopause  it  is  not   possible  to  diagnose  Because   •  The  Cardinal  Features  Disappear.   •  Menses  Cease   •  Testosterone  Levels  May  No   Longer  Be  Higher   DR  KAWITA  BAPAT  
  • 30. Trouble  In  Diagnosis     •  Although  Less  Conven/onal  Measures     •  Androgen  Excess     •  Levels  Remain  Higher     1.  Free  Androgen  Index     2.  Human  Chorionic  Gonadotropin-­‐ s/mulated  Androstenedione     3.  17-­‐hydroxyprogesterone   DR  KAWITA  BAPAT  
  • 31. Trouble  In  Diagnosis     •  PCO  Morphology  Persists  Into  Menopause   •   Hypo  Echoic  Structures  On  Ultrasound     •  In  Postmenopausal  Women  With  PCOS   Correspond   1.  Inclusion  Cysts   2.  Vascular  Structures  Rather  Than  Follicles   Pathology  Studies     Do  Not  Demonstrate  Secondary  Follicles  In   Postmenopausal  Ovaries     DR  KAWITA  BAPAT  
  • 32. Trouble  in  diagnosis     •   When  women  with  PCOS  had  reached   menopause     •  no  difference  in     1.  fas/ng  insulin  levels   2.  HOMA  of  insulin  resistance     3.  glucose  levels     •  prevalence  of  hypertension  higher     •  triglyceride  levels  increased   DR  KAWITA  BAPAT  
  • 33. MENOPAUSAL  TRANSITION       DYSLIPIDEMIA   WITH  AGE   SPECIFIC   INCREASE  IN   LDL   01   METABOLIC   ABNORMALITIES   IN  WOMEN  WITH   PCOS  ALSO   WORSEN  WITH   AGE.     02   •  WAIST   CIRCUMFERENCE   •   CHOLESTEROL   •  TRIGLYCERIDE   LEVELS  INCREASE   IN     •  AS  THEY  REACH   40  TO  50  YEARS     03   BMI   INCREASED  IN  SOME   04    All  women  experience    Increasing  insulin  resistance     Abdominal  adiposity  along  with  chronic  inflamma/on    
  • 34. PHENOTYPE    Recommenda/on  Of  The     Na/onal  Ins/tutes  Of  Health  (NIH)     Evidence-­‐based  Methodology     01   02   03   04   (Phenotype  A)   ●  (Phenotype  B)     ●(Phenotype  C)     ●  (Phenotype  D)     Androgen  excess  +   ovulatory  dysfunc/on  +   polycys/c  ovarian   morphology   Androgen  excess  +   ovulatory  dysfunc/on     Androgen  excess  +  polycys/c   ovarian  morphology     Ovulatory  dysfunc/on   +  polycys/c  ovarian   morphology       in  menopausal  women  is  difficult  to  define.     DR  KAWITA  BAPAT  
  • 35. Hyperandrogenism   •  Persists  Ager  The  Menopausal   Transi/on.     •  Con/nue  To  Manifest  The  Metabolic   Altera/ons  Such  As     – Insulin  Resistance     – Which  Makes  Them  More  Suscep/ble  To   Type  2  Diabetes  Mellitus.     DR  KAWITA  BAPAT  
  • 38. Diet and Exercise •  4-12 weeks of dietary restriction. obese, endocrine-metabolic parameters markedly improve –  SHBG levels rise •  Decrease –  Serum insulin. –  IGF-1 levels –  free testosterone levels fall by 2-fold. • • • • Moran LJ, Pasquali R, et all Treatment of obesity in polycystic ovary syndrome: a position statement of the Androgen Excess and Polycystic Ovary Syndrome Society. Fertil Steril. Dec 3 2008; DR  KAWITA  BAPAT  
  • 39. Diet and Exercise A moderate amount of daily exercise 1.  Increases of levels of IGF-1 binding protein 2.  Decreases IGF-1 levels by 20%. lifestyle management as the primary therapy in overweight and obese women with PCOS for the treatment of metabolic complications. • • • • Moran LJ, Pasquali R, et all Treatment of obesity in polycystic ovary syndrome: a position statement of the Androgen Excess and Polycystic Ovary Syndrome Society. Fertil Steril. Dec 3 2008; DR  KAWITA  BAPAT  
  • 40. Management: Long-Term Issues • Obstructive Sleep Apnea – – – •  30-fold increased risk of OSA, not explained by obesity alone. •  Insulin resistance strongest predictor of OSA (not BMI, age, testosterone) •  Consider polysomnography if at risk DR  KAWITA  BAPAT  
  • 41. Management: Long-Term Issues • Risk for malignancy – – – •  3 fold increased risk endometrial carcinoma in PCOS •  Increased risk of ovarian and breast cancer •  Warrants regular screening, low threshold for endometrial biopsy DR  KAWITA  BAPAT  
  • 42. Thank  you   DR  KAWITA  BAPAT  
  • 43. Thank  you   DR  KAWITA  BAPAT