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Polycystic ovary syndrome

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Prof. Yousef Gadmour Al- Fateh university Al- Jalla Maternity Hospital Tripoli - Libya Investigation 1. Check serum testosterone if – PowerPoint PPT presentation

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Title: Polycystic ovary syndrome


1
Polycystic ovarian syndrome
Prof. Yousef Gadmour Al- Fateh university Al-
Jalla Maternity Hospital Tripoli - Libya
2
Polycystic ovarian syndrome
  • Definition
  • It is a clinical syndrome characterized by
    presence of polycystic ovary and symptoms such as
  • 1. Infertility .
  • 2. Hirsutism.
  • 3. Oligo-amenorrhoea.
  • 4. Obesity.
  • 5. Dysfunctional uterine bleeding.
  • 6. Verilisation.
  • 7. Hyperprolactinaemia.

3
Incidence
  • - It is the Commonest endocrinal gynecologic
    disorder
  • - About 2 of general population.
  • - 4-10 based on clinical, biochemical and
    u/s criteria.
  • - 10-20 based on U/s only.
  • - 30 of infertility.
  • - 90 of Hirsutism with regular cycle.
  • - 87 of case of oligomenorrhea.
  • - 82 of cases with recurrent miscarriage.

4
Pathology
  • The ovaries are enlarged and show
  • Numerous small cystic follicles ( usually 2-8 mm
    in diameter and peripherally placed ) .
  • Thickened white ovarian capsule .
  • Theca cell hyperplasia ( due to increased LH ).
  • Granulosa cell atresia ( due to low FSH ) .
  • The cystic follicles and increased ovarian
    stroma can be demonstrated by ultrasound .

5
Endocrine abnormalities ( cont.)
  • Androgens ovarian androgens excretion
    (testosterone and
    androstenedione )is commonly increased but the
    adrenal (dehydroepiandrosterone-sulfate) is also
    involved in up to 40 of cases.
  • Sex hormone binding globulin (SHBG) levels are
    reduced This result in an increase in unbound
    (and therefore active ) androgen and oestradiol
    levels.
  • Insulin women with PCOS are hypre-insulinaemic
    but are insulin-resistant.
  • ( Hyper-insulinaemia levels of
    SHBG)
  • (? PC0S mechanism )

6
Pathogenesis
  • connective Tissue
  • Androstenedione
    Oestradiol
    Oestrone
  • ( ov. adrenal )
  • Obesity Insulin
    SHBG Free Oestradiol

  • DUB

  • FSH Granulosa cell
    atresia

  • LH No LH surge No
    ovulation


  • Theca cell hyperplasia

  • 5 a-reductase
  • Hirsutism DHT
    Androgens

Free Oestradiol
7
High Follicular phase LH concentrations have
been found to be associate with
  • Poor oocytes quality
  • Reduced rate of fertilization
  • Reduced pregnancy rate
  • Increase incidence of miscarriage

8
Diagnosis of PCOS
  • Oligoamenorrhea or amenorrhea and subfertility.
  • Symptoms of androgen excess.
  • U /S (Adams criteria) 1-Many follicles 8-10

  • 2-Follicles lt10mm diameter

  • 3-Thickened white capsule

  • 4-Hyperechogenic stroma
  • Biochemical ?LH in 40 of cases (LH/FSHgt2)
  • ?serum testosterone in
    30 of cases
  • serum prolactin in 40
    of cases

9
Management
  • Principals of management
  • Confirm diagnosis and identify category.
  • Identify and manage concurrent illness.
  • Identify and manage patient needs.
  • There are numerous options for successful PCO
    management medical / surgical

10
Preprocedural Considerations
  • Endometrial Neoplasia
  • Insulin Resistance
  • Metabolic Syndrome
  • Weight loss

11
Endometrial Neoplasia
  • Chronic anovulation associated with PCOS may lead
    to endometrial hyperplasia and sometimes to frank
    endometrial cancer (Meier and Schenker,1996).
  • Endometrial biopsy is indicated in all women with
    H/O long term unopposed estrogen exposure and in
    those where endometrial thickness is greater than
    12mm.

12
Insulin Resistance (IR)
  • IR is defined as reduced glucose response to a
    given amount of insulin.
  • It occurs in 80 of obese women and 30 to40 of
    women with normal wt. with PCOS .
  • Peripheral target tissue insulin resistance can
    be due to decreased no of peripheral insulin
    receptors, decreased insulin binding or a post
    receptor failure.
  • In PCOS it is caused by the post receptor defect
    due to excessive serine phosphorylation of beta
    chain of insulin receptor and of adrenal and
    ovarian cytochrome P450c enzyme . This enzyme is
    a rate limiting step in androgen biosynthesis
    thus leading to hyperandrogenemia .

13
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14
Diagnostic criteria for metabolic syndrome
  • Diagnosis is made when 3 or more of
  • these risk criteria are met
  • ? Glucose 6.1 mmol/l
  • Waist circumference 88 cm.
  • ? HDL-C 1.3 mmol/l
  • ?BP 130 / 85 mm Hg
  • ?TG 1.7 mmol/l
  • (Shroff et
    al.,2007)

15
Weight Loss
  • Weight loss has advantage of being effective and
    cheap with no side effects and should be the
    first line of treatment .
  • Weight loss improves endocrine profile and
    ovulation and subsequent healthy pregnancy
    (decreasing insulin and androgens and increasing
    SHBG ).
  • Weight loss has been shown to improve the outcome
    of all forms of infertility treatments, including
    IVF (Clark et al.,1998).

16
Various treatment modalities
  • Pharmacological Treatment
  • CC

  • Gonadotropin
    Hyperinsulinemia?
  • hMG
    Insulin sensitizer
  • uFSH GnRH-analogs
  • HP-FSH
  • rec-FSH

17
A. Medical Treatment
  • Infertility is treated by increasing the rate of
    ovulation, in part by reducing insulin drive
    through exercise and weight loss .
  • Ovarian stimulation is used for those patients
    who do not ovulate, despite loosing weight by
    different drugs and different protocols.

18
Medical Treatment (cont.)
  • Treat Hyperprolactinaemia with Bromocriptine.
  • Glucocorticoids for adrenal hyperplasia .
  • ( 0.25mg Dexamethasone at night )
  • COC pills or POP for dysfunctional uterine
    bleeding and to reduce the risk of endometrial
    carcinoma .

19
Insulin sensitizing drugs
  • Metformin
  • Action
  • -inhibit hepatic glucose production.
  • -enhance sensitivity of peripheral tissues to
    insulin
  • -? insulin secretion.
  • ? Ovarian hyperstimulation in gonadotrophin
    therapy
  • RCT- clomiphene -resistant pts., use of metformin
    CC produced significant improvement

20
B. Surgical treatment modalities
  • Surgical Treatment
  • Cauterization Wedge resection
  • ( laser, electric )

21
Methods of Ovarian Surgery For Ovulation
Induction In PCOS
  • Laparoscopic Techniques of Ovarian Surgery (LOS)
  • Laparoscopic Ovarian Drilling (LOD)
  • Diathermy / LASER.
  • Transvaginal Techniques of Ovarian Surgery (TVOS)
  • 1) Transvaginal mini-laparoscopy (Fertiloscopy)
  • 2) Transvaginal ultrasound (TVS)-guided ovarian
    drilling.

22
Indications
  • I. Ovulation induction in the following cases
  • a) C.C resistant PCO
  • Defined as failure to ovulate on a dose of 100
    mg, for 5 days (recently in 3 cycles, in contrast
    to 6 cycles in the past ) or
  • failure to ovulate on incremental doses of
    CC(50-150mg).
  • b) C.C failure PCO
  • Defined when pregnancy does not occur despite of
    regular ovulation on C.C for 6-9 cycles.
  • c) C.C pregnancy failure
  • Defined as failure to maintain pregnancy
    conceived with C.C.

23
Indications( cont.)
  • II. Other potential indications
  • 1. LH hypersecretion.
  • 2. Patient cannot follow treatment regularly.
  • Prevention of long term morbidity in PCOS



  • patient.
  • 4. Menstrual irregularity in PCOS patient.
  • 5. Acne and hirsutism resistant to treatment
    in
  • PCOS patient.

24
Mechanism of action Of LOS
  • 1. Drainage of atretic follicles with high
    (Androgen inhibin) content.
  • 2. Destruction of ovarian stroma that produce
    androgen.
  • 3.LOS ? Postoperative ? of FSH ??Intra-follicular
    aromatase activity
  • 1,2,3 ?
  • ?Intra-follicular androgenic environment ? remove
    intraovarian block to follicular maturation that
    precedes ovulation.

25
Mechanism of action Of LOS (CONT.)
  • 4.Surgical trauma to the ovary
  • Production of non steroidal factors ? Restore
    hypothalamo-pitutary-ovarian function.
  • Production of ovarian growth factorsIGF-1?
    Sensitize ovary to circulating FSH.

26
Risks
  • 1-Adhesion formation,
  • 2-Potential surgical risks (bleeding and
    infection)
  • 3-Anesthesia risks,
  • 4-Premature ovarian failure (theoretical
    complication)

27
Technique Of LOS
  • Utero-ovarian ligament
  • is grasped by atrumatic
  • forceps moving the ovary
  • (towards anterior
  • abdominal wall in
  • front of the uterus).

28
LASER versus electrocautery for LOS
  • Electrocautery IS superior why?
  • 1) Less coast easy application.
  • 2) Achieve higher ovulation and pregnancy rate.
  • 3) Less surface injury than CO2 LASER ? Surface
    adhesion.
  • 4 Effect of diathermy may last longer than the
    effect of LASER .

29
Results
  • Short term results
  • In responders ovulation occur within 2-4 wk,
    menstruation within 4-6 wks.
  • Ovulation rate 50-90.(Patient with high LH
    level respond better to LOS).
  • Cumulative Pregnancy Live birth rates76-64
    respectively.
  • Long term results
  • Improvement in reproductive performance is
    sustained for many years. (49 Of women conceived
    within the 1st year after LOS)

30
Conclusions
  • Obesity plays a central role in development of
    PCOS leading to Hyperinsulinemia in susceptible
    individuals.
  • This Hyperinsulinemia may alter androgen
    metabolism via a variety of mechanisms, the net
    result of which Hyperandrogenism.

31
Conclusions
  • The management of patients with PCOS depends upon
    the individual patients complaints.
  • Hyperandrogenism is optimally dealt with by
    reducing insulin drive to the ovary, such as
    exercise and reducing diet

32
Hirsutism
  • Definition
  • Excessive and inappropriate growth of facial and
    body hair .


33
Causes
  1. Endocrine- PCOS adrenal hyperplasia/Cushing's
    syndrome hypothyroidism acromegaly .
  2. Androgen-secreting tumours of adrenal or ovary .
  3. Drugs- phenytoin , diazoxide , danazol ,
    corticosteroids .
  4. Idiopathic .

34
Investigation
  • 1. Check serum testosterone if lt 5 nmol /l no
    further investigation .If gt 5 nmol/l repeat
    and check urinary steroids in 24
    hour sample.
  • 2. Check serum LH and FSH . An elevated LH
    suggests PCOS .
  • 3. Pelvic ultrasound will demonstrate polycystic
    ovaries.
  • 4. Check thyroid function .

35
  • 5. Measure serum 17-hydroxyprogesterone if
    congenital adrenal hyperplasia is suspected .
    If levels are high consider ACTH stimulation
    and dexamethasone suppression tests .
  • 6. If urinary cortisol is elevated investigate
    for Cushing's syndrome .
  • 7. If adrenal tumor is suspected carry out CT
    scans and consider direct catherisation of
    adrenal veins or surgical exploration .

36
Treatment
  • This will depend on the cause.
  • Sympathetic handling and reassurance are
    necessary at all times.

37
1. Polycystic ovary syndrome
  • Induce ovulation if infertility is also a
    problem.
  • combined oesrogen/progestogen pill to
    suppress androgen production. Response to
    treatment is slow at best. It may be 6 months to
    a year before any reduction in hirsutism is seen.
  • Cyproterone acetate is an anti-androgen
    with progestogenic activity.
  • Pregnancy must be avoided during its use.
  • It is therefore best used cyclically (day
    5-15) in combination with ethinyl Oestradiol
    (day 5-26) which not only helps to inhibit
    ovulation but also increases SHBG
    concentrations.
  • This lowers the levels of free androgens.

38
  • 2. Adrenal hyperplasia
  • This is the only situation in which
    corticosteroid treatment remove after
    localisation.
  • 3. Androgen producing tumours
  • Remove after localisation.
  • 4. Idiopathic hirsutism
  • This may be due to end organ
    hypersensitivity. There may be some
    response to the
    oesrogen/progestogen pill or spironolactone
    and electrolysis is useful cosmetically.

39
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