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MODERN APPROACH TO PCOS. J. SERNA MD. PhD. IVI Madrid. Physiology and Diagnosis. What is PCOS? How to Diagnose it? How to Treat it?. High prevalent disease Multiorganic: ovaries, HH, adrenal, fat, skin, pancreas, etc... Different degrees of organ involvement

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modern approach to pcos

MODERN APPROACH TO PCOS

J. SERNA MD. PhD.

IVI Madrid

physiology and diagnosis
Physiology and Diagnosis
  • What is PCOS?
  • How to Diagnose it?
  • How to Treat it?
slide3
High prevalent disease
  • Multiorganic: ovaries, HH, adrenal, fat, skin, pancreas, etc...
  • Different degrees of organ involvement
  • Main feature: ovarian hyperandrogenism
  • Multiple phenotypes
slide4

Metabolic disorders

  • IR and Hyperinsulinism
  • Obesity (male pattern)
  • Impaired Glucose Tolerance and DM2
  • Hyperlypemia

PCOS: HETERGENEOUS

  • Reproductive disorders
  • Hyperandrogenism
  • Anovulation: Menstrual disorders, infertility
  • Polycystic ovaries
  • Miscarriage
  • General Health Disorders
  • Acantosis nigricans
  • Cardiovascular disease
  • Endometrial cancer
slide5

PCOSDg CRITERIA

  • Anovulation and/or dysovulation
  • Clinical and/or Biochemical Hyperandrogenism
  • Polycystics ovaries
  • and exclusion of other aetiologies (CAH,
  • tumours, HPRL, etc)
  • The Rotterdam ESHRE/ASRM sponsored PCOS consensus workshop group, 2003
slide6

Anovulation/dysovulation work-up

FSH,LH,PRL,TSH, 17 βE2

PRL

PRL N

FSH(N /  )

FSH

FSH/LH < 1

Estrogens N

FSH/LH > 1

Hypoestrogenism

Hypo-hypo Amenorrhea

WORK-UP

hyperPRL

PCOS

WORK-UP POF

Type IV

Type II

Type I

Type III

slide7

PCOS

  • Anovulation and/or dysovulation
  • Clinical and/or Biochemical Hyperandrogenism
  • Polycystics ovaries
  • and exclusion of other aetiologies (CAH, tumours, HPRL, etc)
  • The Rotterdam ESHRE/ASRM sponsored PCOS consensus workshop group, 2003
slide10

PCOS DIAGNOSIS

  • Biochemical hyperandrogenism
  • Normal boundaries established by laboratories RIA:
    • 95-97%
    • Control population?
  • High variability among normal population (absence of feed-back mechanism)
  • Diverse androgens: TT,ITL, 17OHP, DHA-S, A4, etc.
slide11

PCOS

  • Anovulation and/or dysovulation
  • Clinical and/or Biochemical Hyperandrogenism
  • Polycystics ovaries
  • and exclusion of other aetiologies (CAH, tumours, HPRL, etc)
  • The Rotterdam ESHRE/ASRM sponsored PCOS consensus workshop group, 2003
slide12

PCOS DIAGNOSIS

Polycystic ovary

Presence of 12 or more

follicles 2-9 mm 

and/or ovarian volume

higher than 10 mL

(one ovary is enough)

Non suitable to women on OCP or with a dominant follicle (>10 mm)

The Rotterdam ESHRE/ASRMsponsored PCOS consensus workshop group, Hum Reprod 2004,19:41-7

slide13

Polycystic ovaries. Pitfalls

False positives: 20% normal women

False negatives: 30% PCOS

US scan cannot make differential diagnosis between multycystic ovaries and polycystics ovaries

Time required for measurements

slide14

PCOS

  • Anovulation and/or dysovulation
  • Clinical and/or Biochemical Hyperandrogenism
  • Polycystics ovaries
  • and exclusion of other aetiologies (CAH, tumours, HPRL, etc)
  • The Rotterdam ESHRE/ASRM sponsored PCOS consensus workshop group, 2003
slide15

Dysovulation wo

?? hyperandrogenism

Normal cycle

and hyperandrogenism ??

PCOS DIAGNOSIS

Clinical and/or Biochemical Hyperandrogenism

Anov/dysovulation

HiperPRL, HA, POF, etc

Idiopathic Hirsutism

CAH, Tumors

  • Infertility and miscarriages

Exaggerated response to OI

  • Multiple pregnancy

PCO

The Rotterdam ESHRE/ASRMsponsored PCOS consensus workshop group, Hum Reprod 2004,19:41-7

slide17

Insulin-resistance in PCOS patients

75,3%(n=149)

N=198

HOMA (Homeostasis model assesment): Glucose x18,1/Insulin x0,139 (Insulin-resistance: Obese <5,09, Lean <5,48)

slide18

Prevalence of Impaired Glucose Tolerance and Diabetes in POCS in two American Studies (New York, Pensylvania y Chicago) and in a Spainish Survey

40

35

31,1

30

%

20

10

8,95

7,5

10

4,47

0

Legro, 1999

Ehrmann, 1999

HSPSC

Legro. J Clin Endocrinol Metab 1999. N=244.

Ehrmann. Diab Care 1999. N=122 (WHO, 1985)

HSPSC N=67 Criteria: WHO, 1999.

slide20

Methods for Insulin-Resistance work-up

      • Gold Standard test IR is euglucemic clamp
      • .
      • Due to its complexity, Oral Glucose Tolerance Test or Basal Glucose and Insulin measurements instead
      • .
      • OGTT is the main test in the diagnosis of Impaired Glucose Intolerance or Type II Diabetes
  • Other indexes are less used in clinical routine
slide21

IR

hyperinsulinism

¿?

Hyperandrogenic Anovulation

metabolic syndrome
Diabetes Mellitus

IGT

IFG or IR

And 2 of

≥ 140/90 mmHG

Dyslipidaemia

Central Obesity

Wais:hip ratio

BMI

Microalbuminuria

Central obesity (Waist)

Dyslipidaemia TG

Dyslipidaemia HDL-C

≥130/85

Fasting glucose >100 mg/dL

At least 3

Metabolic Syndrome

WHO

Adult Treatment Panel

slide26

Cardiovasculardisease in women

  • Near2,5 million women hospitalized each year due to CVD
  • 1st death cause in women (over the next 14 together)
  • Half of these deaths are from MCI
  • Annual cost estimated to be 28,65 billion dolars
  • Tsang y cols. Risk of caronary heart disease in women: current understanding. Mayo Found Med Educ Research, 2000
slide27

Clinical hyperandrogenism

  • Different prevalence among different populations: ethnicity
  • Absence of consensus on how to evaluate clinically the hyperandrogenism
  • Semiquantitative staging methods (Ferriman-Gallwey). Limitations:
    • Subjective: intra and inter-observer variability
    • Previous pharmacological or cosmetical treatments
    • Non validated
treat what33
TREAT WHAT?

Imparied

Treatment Options

Weight/Metabolic

Diet/lifestyle

Metformin

Dysfunctional bleeding

Cyclic progesterone

OCP

Infertility

Metformin

Clomiphene

Letrozole

Gonadotropins

Ovarian cautery

Skin

OCP + antiandrogen (spironolactone, flutamide, finasteride)

GnRH agonists

metabolic syndrome34
Metabolic Syndrome

Caloric restriction +/- weight loss ( 6-7 months )

Leptine

SHBG

IGFBP

Insulin Resistance

Ovulatory cycles

Improve Hirsutism

Acanthosis

Improvement in Gonadotropins metabolism

androgens

citochrome P450scc

17-αhidroxilase

slide36

Insulin-Sensitizing Agents

  • α-Glucosidasa Inhibitors
  • Sulfonilureas
  • Methiglinidas
  • Biguanides
  • Thiazolidindiones
treat what37
TREAT WHAT?

Imparied

Treatment Options

Weight/Metabolic

Diet/lifestyle

Metformin

Dysfunctional bleeding

Cyclic progesterone

OCP

Infertility

Metformin

Clomiphene

Letrozole

Gonadotropins

Ovarian cautery

Skin

OCP + antiandrogen (spironolactone, flutamide, finasteride)

GnRH agonists

treat what39
TREAT WHAT?

Imparied

Treatment Options

Weight/Metabolic

Diet/lifestyle

Metformin

Dysfunctional bleeding

Cyclic progesterone

OCP

Infertility

Metformin

Clomiphene

Letrozole

Gonadotropins

Ovarian cautery

Skin

OCP + antiandrogen (spironolactone, flutamide, finasteride)

GnRH agonists

slide40

Laparoscopic Electrocoagulation

Laparoscopic Ovarian Diathermy

Several energy sources:

Monopolar, LASER (CO2, Argon,

KTP, YAG)

Mechanism of action

  • Not well established
  • Removal of androgen-producing stroma
  • Total and free testosterone reduction to 40-50% basal levels
  • LH pulses amplitude decreases
  • Better prognosis for patients with LH > 10 UI/l before surgery
slide41

Year

Patients

Previous ttm

% Ovulation

% Spont preg

Gjonnaess

1985

58

----

72

41

Weise

1991

39

CC, HMG

---

59

Naether

1993

104

CC, HMG

55

34

29.1% had adherence at a 2nd laparoscopy

Saravelos

1996

21

CC

76

30

Merchan

1996

74

CC, HMG

88

57

Pelosi

1996

30

CC, HMG

83

70

Total

720

79.7

51.5

LAPAROSCOPIC ELECTORCAUTERY

Campo, S. Obst Gyn Surv 1998;53:297-308.

slide42

Year

Patients

Prevıous ttm

% Ovulatıon

% Spont Preg

Daniell (CO2)

1989

85

CC

71

41

Kojima (YAG)

1989

12

CC, HMG

83

58

Gurgan (YAG)

1992

40

CC

70

50

50% had adherence at a 2nd laparoscopy

Sinha (YAG)

1993

20

CC, HMG,FSH

100

40

Heylen Argon

1994

44

CC

80

55

Fukaya (YAG)

1995

26

CC, HMG

23

23

Total

322

71.5

43.7

LAPAROSCOPIC LASER VAPORIZATION

Campo, S. Obst Gyn Surv 1998;53:297-308.

treat what43
TREAT WHAT?

Imparied

Treatment Options

Weight/Metabolic

Diet/lifestyle

Metformin

Dysfunctional bleeding

Cyclic progesterone

OCP

Infertility

Metformin

Clomiphene

Letrozole

Gonadotropins

Ovarian cautery

Skin

OCP + antiandrogen (spironolactone, flutamide, finasteride)

GnRH agonists

slide44
Systemic

Antiandrogens

Spironolactone

Finasteride

Flutamide

OCP

GnRH analogs

Cutaneous

Eflornitine

Creams

Electrolysis

Laser

Skin