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Dr. Rafi Rozan
Consultant Specialist OBGYN
Associate Professor
Fellow REI
Obstetrician & Gynecologist (Masters)
Comprehensive Family Medicine (Masters)
Mastology & Cosmetic Gynecology.
Medical Technology
Polycystic Ovarian
Syndrome
Magic is believing in yourself,
if you can do that,
you can make anything happen.
Antonio Vallisneri
1721
Introduction
Irving Stein Michael Leventhal
1935
Introduction
Ovulatory
Disorder
Hyperandrogenism
PCOM
Definition of PCOS
Definition of PCOS
• Ovarian Hyperthecosis: Often considered a severe form of PCOS. It’s a
rare condition characterize by nest of lutheinized theca cells
distributed throughout the ovarian stroma. Affected women exibits
severe hyperandrogenism and greater degree of insulin resistance.
• HAIRAN Syndrome: is also an uncommon syndrome and consist of
marked hyperandrogenism, severe insulin resistance and acantosis
negricans.
• SAHA Syndrome: Seborrhea, acne, hirsutism, alopecia (tetrad).
Definition of PCOS
• PCOS is the most common
endocrine disorder of
reproductive age woman.
• It affects approximately 6 to 16%
of women globally.
• 1 in every 10 women is affected
with PCOS.
Incidence
September
Etiology
• The underlying cause of PCOS is unknown.
• A genetic basis that is both multifactorial and
polygenic is suspected as the syndrome aggregates
within families and first degree relatives.
• Some research suggested an autosomal dominant
inheritance with
expression in both male and females.
• Several risk loci have been identified by genome
wide association
studies in women with PCOS.
• Putative genes involved those involved in androgen
Synthesis,
obesity and insulin resistance.
Pathophysiology
Gonadotropin
Model for the initiation and
maintenance of PCOS).
Functional cysts of the ovary
Follicular cyst Corpus luteum Theca-lutein cyst
Pathophysiology
Insulin Resistance
Consequences of Polycystic Ovarian Syndrome
Menstrual Dysfunction
Clinical Manifestation
Clinical Manifestation Hyperandrogenism
Facial Hirsutism
Hirsutism
(coarse, dark, terminal hairs
distributed in a male pattern).
Male Pattern Escutcheon
Ferriman Gallwey score
Clinical Manifestation: Acne
The pathogenesis of acne vulgaris involves four factors:
1. Blockage of the follicular opening by hyperkeratosis,
2. Sebum overproduction,
3. Proliferation of commensal Propionibaterium
4. Inflammation
In the hair follicle, testosterone is converted within
sebauous glands to its more active metabolite DHT
by 5 alpha reductase.
Clinical Manifestation: Alopecia
Clinical Manifestation: Acanthosis Nigricans
Thick velvety, mossy plaques develops in the flexure areas such as the back of the neck, axilla, inframammary
creases, waist and groin.
Insulin resistance leads to hyperinsulinemia, which stimulate keratinocyte and dermal fibroblast growth,
producing the characteristic skin changes.
Dyslipidemia
The classic artherogenic lipoprotein profile
seen in PCOS shows:
• elevated total cholesterol
• elevated triglyceride levels
• increased low-density lipoprotein (LDL)
• Decrease high-density lipoprotein (HDL)
Obesity
• Women with PCOS are more likely to be obese,
as reflected by elevated BMI and waist: hip
ratio.
• This ratio reflects an android or central pattern of
obesity, which itself is an independent risk factor
for CVD and predicts insulin resistance.
• Insulin resistance is believed to play a large role in
the pathogenesis of PCOS and is often
exacerbated by obesity
• obesity can exacerbate hyperandrogenism by
lowering SHBG levels and thereby raise
bioavailable testosterone levels
• Thus, obesity can have a synergistic effect on
PCOS and can worsen ovulatory dysfunction,
hyperandrogenism, and acanthosis nigricans.
Obstructive Sleep Apnea (OSA)
• Obstructive sleep apnea is related to
central obesity
• 35% of PCOS women has obstructive
sleep apnea
Weight loss and exercise
Sleep position
Alcohol avoidance
Concomitant medications
Positive airway
pressure therapy. CPAP
Depression and
Anxiety
• Women with PCOS may present with various psychosocial problems
such as anxiety, depression, eating disorders, and negative body
image.
• Screening for depression and anxiety is recommended.
Non Alcoholic Fatty Liver Disease (NAFLD)
• NAFLD refers to the presence of hepatic steatosis when no other
causes for secondary hepatic fat accumulation are present.
• It may progress to cirrhosis and is likely an important cause of
inflammation, fibrosis and cryptogenic cirrhosis.
• Likely cause by insulin Resistance.
Nonalcoholic fatty
liver (NAFL)
Nonalcoholic
steatohepatitis (NASH)
Foie Gras
Infertility
Impaired Glucose Tolerance and Type 2 Diabetes Mellitus.
• Women with PCOS are at increased risk for impaired glucose
tolerance (IGT 30%) and type 2 DM (7%).
• Beta Cell dysfunction that is independent of obesity has been
reported in patients with PCOS.
Metabolic Syndrome and Cardiovascular Disease
• The metabolic syndrome is
characterized by insulin resistance,
obesity, atherogenic dyslipidemia,
and hypertension.
• It is associated with a greater risk
of CVD and type 2 DM.
• The prevalence of metabolic
syndrome approximates 45% in
women with PCOS.
• Relative risk of 7.4% for myocardial
infarction % in women with PCOS.
Endometrial
Neoplasia
• In women with PCOS, the risk of
endometrial cancer is increased
three to fourfold.
• Endometrial hyperplasia and
endometrial cancer are long-term
risks of chronic anovulation.
• Neoplastic changes in the
endometrium arise from chronic
unopposed estrogen.
• The effects of hyperandrogenism,
hyperinsulinemia, and obesity
lowers SHBG levels and raise
circulating estrogen levels which
add to this risk.
Complications in
Pregnancy
• PCOS who become pregnant
experience a higher rate of early
miscarriage (30 to 50 %)
• Higher risks of gestational diabetes,
• Higher risks of hypertension in
pregnancy
• Higher risks of preterm birth.
• Higher risk of multifetal gestations
(which are associated with elevated
rates of maternal and neonatal
complications).
Diagnosis
Clitoromegaly is assessed using the clitoral index
(clitoral length (mm) and width (mm) values).
Values greater than 35 mm2 are abnormal.
Anti Müllerian Hormone (AMH)
• The classic polycystic ovary contains two to
threefold more growing preantral and antral
follicles than normal ovaries.
• Within the granulosa cells of these
developing follicles, the dimeric
glycoprotein AMH is produced.
• Serum AMH levels correlate closely with the
number of preantral and antral follicles and
for this reason, AMH is viewed as a
potentially useful diagnostic marker for PCOS
Ultrasound
Histologically, a polycystic ovary displays a
greater number of ripening and atretic
follicles, cortical stromal thickness, and
number of hilar cell nests.
Many of these tissue changes can be seen
sonographically, and pelvic sonography is
commonly used to evaluate the ovaries in
women with suspected PCOS.
Ultrasound is particularly important for
women with PCOS seeking fertility and in
women with signs of virilization to exclude
an androgen-producing ovarian Tumor.
• Polycystic ovarian morphology (PCOM) is one criterion for PCOS
diagnosis.
• Earlier sonographic criteria for PCOM included >12 small cysts (2 to 9
mm in diameter or an increased ovarian volume (> 10 mL) or both
per ovary.
• More recently, follicle number per ovary (FNPO) threshold values
have been raised due to improved sonographic imaging resolution
• Notably, The criteria do not apply to women taking combination
oral contraceptive pills.
FNPO threshold of> 20 follicles and/or ovarian volume > 10
in either ovary has been adopted by ESHRE and ASRM.
Ultrasound
AEPCOS guidelines use the same ovarian volume value but
a higher FNPO threshold of >25 follicles.
PCOM often reflects normal adolescent
ovarian Physiology. Thus, sonography for
PCOS evaluation is not recommended
within 8 years of menarche.
Treatment : Diet
Vitamin D,
Vitamin B12
Cinnamon extract
Green tea
ω-3 fatty acid
Micronutrients
Treatment : Exercise
Treatment: combination oral contraceptive
pills
• COCs induce regular menstrual cycles, lower
androgen levels, and thin the endometrium.
• COCs suppress gonadotropin release, which
results in decreased ovarian androgen
production.
• the estrogen component raises levels of
SHBG, which binds free androgen.
• the progestin component antagonizes the
endometrial proliferative effect of
unopposed estrogen from PCOS, thus
reducing the endometrial hyperplasia risk.
Treatment : Insulin Sensitizers
• Metformin ( 1500mg to
2000mg)Pregnancy category B
• Thiazolidinediones : Pregnancy
category C
• Glucagon Like Peptide1 (GLP1)
• Sodium Glucose Cotransporter 2
(SGLT2): Empaglifozin
• Surgical treatment of infertile women with
PCOS was successfully revived by Halvard
Gjönnaess in 1984 in the form of
laparoscopic ovarian drilling (LOD) with
subsequent ovulation and pregnancy rates
of 92% and to 80%, respectively.
• Since that time, this minimally invasive and
less traumatic modern version of ovarian
wedge resection using either
electrocautery (diathermy) or laser has
continued to play an essential part in
management of infertile women with PCOS.
Surgical Therapy
Surgical Therapy: Ovarian Wedge Resection
The patient is placed in the supine position.
The bladder is emptied with a Foley catheter,
and a Pfannenstiel or lower midline incision is
made. The abdominal cavity is entered. The
uterus is retracted caudally against the pubic
symphysis. The polycystic ovary should be
large with a smooth oyster-like capsule.
A Babcock clamp is placed on the suspensory
ligament of the ovary. An additional Allis clamp may
be placed on the inferior pole of the ovary to stabilize
the structure so that adequate wedge resection can
be performed. A scalpel is used to incise the ovary
down to and including the hilum. Occasionally, a
small dermoid cyst may be located in the hilum. It is
also important to remove a portion of the hilum to
evaluate the possibility of a hilar cell tumor.
After an adequate wedge has been taken, the
ovary is closed in two layers. The first layer is
closed by a running lateral mattress suture that
enters the deep body of the ovary and exits
through the opposite side of the ovary. The
needle is reversed and reenters the body of the
ovary, exiting on the opposite side. In this
manner, the walls of the ovary are plicated in
the midline, and dead space is eliminated.
Surgical Therapy: Ovarian Wedge Resection
At the completion of the running mattress suture, the capsule of the ovary can be closed by
continuing the fine synthetic absorbable suture through the epithelium of the ovary. Care
should be taken to invert all raw edges to reduce the problem of postoperative adhesions
that could have an adverse effect on future fertility. Complete hemostasis is essential if
adhesions are to be avoided.
Surgical Therapy: Ovarian
Drilling
LOD is recommended as a second-line treatment in infertile
PCOS women who have CC resistance.
LOD has been also proposed as first-line approach for PCOS
related anovulation or as an adjuvant therapy before in vitro
fertilization (IVF) cycles
LOD seems to be as effective as gonadotrophin treatment
without an increased risk of multiple pregnancy or ovarian
hyperstimulation syndrome (OHSS).
Surgical Therapy: Ovarian
Drilling
LOD is most commonly performed using a monopolar
diathermy needle electrode.
LOD technique:
Ten or more punctures were performed in the two ovaries
together.
Each puncture having a diameter of ~3 mm
Depth of 2–4 mm
Power setting of 40 W
Duration for 2–4 s
640 Joules (J) per ovary (4 punctures × 4 s x 4 mm × 40 W) as
the lowest effective dose with an ovulation and pregnancy
rates of 86%.
Surgical Therapy: Ovarian
Drilling
Unilateral vs. Bilateral LOD
Fixed vs. Dose-Adjusted Energy
LOD as a 1st line therapy in PCOS may offer
several theoretical advantages:
LOD increase responsiveness of the ovary to oral
ovulation induction agents and gonadotrophins.
Resumption of mono-ovulatory cycles and avoiding of the
anti-oestrogenic effects of CC.
LOD might work as an adjuvant procedure before IVF.
Safety Concerns
The use of LOD did open an avenue for ovulation induction
but with inherent risks of general anaesthesia and surgical risks
of laparoscopy, e.g. visceral and vessel injuries, gas complications, etc.
The main shortcomings of LOD are the risk of postoperative adhesions and the
concern about a negative impact of the procedure on the ovarian reserve
secondary to excessive ovarian damage.
Post Surgical Adhesions
The incidence of perianexal adhesions after LOD does not represent a major constraint in its success story
References
Amer SA, Gopalan V, Li TC, et al: Long term follow·up of patients with poly. cystic ovarian syndrome after laparoscopic ovarian drilling: clinical outcome.
Hum Reprod 17:2035, 2002
American College of Obstetricians and Gynecologists: Diagnosis of abnormal uterine bleeding in reproductive-aged women. Practice Bulletin No. 128,
July 2012, Reaffirmed 2016
American College of Obstetricians and Gynecologists: Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Committee
Opinion No. 651, December 2015, Reaffirmed 2017
American College of Obstetricians and Gynecologists: Polycystic ovarian syn· drome. Practice Bulletin No. 194, June 2018
American Diabetes Association: 2. Classification and diagnosis of diabetes: stan·dards of medical care in diabetes---2019. Diabetes Care 42{1 suppl):Sl3, 2019
American Society for Reproductive Medicine: Current evaluation of amenorrhea. Fertil Steril 90(5 Suppl):S219, 2008
American Society for Reproductive Medicine: Role of metformin for ovulation induction in infertile patients with polycystic ovary syndrome {PCOS): a
guideline. Fenil Steril 108(3):426, 2017
Arroyo A, Laughlin GA, Morales AJ, et al: Inappropriate gonadotropin secre·tion in polycystic ovary syndrome: influence of adiposity. J Oin Endocrinol
Metab 82:3728, 1997
Azziz R: lhe evaluation and management of hirsutism. Obstet Gynecol 101 :995, 2003
Axziz R, Carmina E, Dewailly D, et al: Position statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an
Androgen Excess Society guideline. J Clin Endocrinol Metab 91:4237, 2006
Bahri Khomami M, Joham AE, Boyle JA, et al: Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of
obesity-a systematic review, meta-analysis, and meta·regression. Obes Rev 20(5):659, 2019
Banaszewska B, Duleba A, Spaczynski R: Lipids in polycystic ovary syndrome: role of hyperinsulinemia and effects of metformin. Am J Obstet Gynecol 194:1266, 2006
Polycystic Ovarian Syndrome.pptx

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Polycystic Ovarian Syndrome.pptx

  • 1. Dr. Rafi Rozan Consultant Specialist OBGYN Associate Professor Fellow REI Obstetrician & Gynecologist (Masters) Comprehensive Family Medicine (Masters) Mastology & Cosmetic Gynecology. Medical Technology Polycystic Ovarian Syndrome
  • 2. Magic is believing in yourself, if you can do that, you can make anything happen.
  • 7. • Ovarian Hyperthecosis: Often considered a severe form of PCOS. It’s a rare condition characterize by nest of lutheinized theca cells distributed throughout the ovarian stroma. Affected women exibits severe hyperandrogenism and greater degree of insulin resistance. • HAIRAN Syndrome: is also an uncommon syndrome and consist of marked hyperandrogenism, severe insulin resistance and acantosis negricans. • SAHA Syndrome: Seborrhea, acne, hirsutism, alopecia (tetrad). Definition of PCOS
  • 8. • PCOS is the most common endocrine disorder of reproductive age woman. • It affects approximately 6 to 16% of women globally. • 1 in every 10 women is affected with PCOS. Incidence September
  • 9. Etiology • The underlying cause of PCOS is unknown. • A genetic basis that is both multifactorial and polygenic is suspected as the syndrome aggregates within families and first degree relatives. • Some research suggested an autosomal dominant inheritance with expression in both male and females. • Several risk loci have been identified by genome wide association studies in women with PCOS. • Putative genes involved those involved in androgen Synthesis, obesity and insulin resistance.
  • 10.
  • 12. Model for the initiation and maintenance of PCOS).
  • 13. Functional cysts of the ovary Follicular cyst Corpus luteum Theca-lutein cyst
  • 14.
  • 16. Consequences of Polycystic Ovarian Syndrome
  • 18. Clinical Manifestation Hyperandrogenism Facial Hirsutism Hirsutism (coarse, dark, terminal hairs distributed in a male pattern). Male Pattern Escutcheon
  • 20. Clinical Manifestation: Acne The pathogenesis of acne vulgaris involves four factors: 1. Blockage of the follicular opening by hyperkeratosis, 2. Sebum overproduction, 3. Proliferation of commensal Propionibaterium 4. Inflammation In the hair follicle, testosterone is converted within sebauous glands to its more active metabolite DHT by 5 alpha reductase.
  • 22. Clinical Manifestation: Acanthosis Nigricans Thick velvety, mossy plaques develops in the flexure areas such as the back of the neck, axilla, inframammary creases, waist and groin. Insulin resistance leads to hyperinsulinemia, which stimulate keratinocyte and dermal fibroblast growth, producing the characteristic skin changes.
  • 23. Dyslipidemia The classic artherogenic lipoprotein profile seen in PCOS shows: • elevated total cholesterol • elevated triglyceride levels • increased low-density lipoprotein (LDL) • Decrease high-density lipoprotein (HDL)
  • 24. Obesity • Women with PCOS are more likely to be obese, as reflected by elevated BMI and waist: hip ratio. • This ratio reflects an android or central pattern of obesity, which itself is an independent risk factor for CVD and predicts insulin resistance. • Insulin resistance is believed to play a large role in the pathogenesis of PCOS and is often exacerbated by obesity • obesity can exacerbate hyperandrogenism by lowering SHBG levels and thereby raise bioavailable testosterone levels • Thus, obesity can have a synergistic effect on PCOS and can worsen ovulatory dysfunction, hyperandrogenism, and acanthosis nigricans.
  • 25. Obstructive Sleep Apnea (OSA) • Obstructive sleep apnea is related to central obesity • 35% of PCOS women has obstructive sleep apnea Weight loss and exercise Sleep position Alcohol avoidance Concomitant medications Positive airway pressure therapy. CPAP
  • 26. Depression and Anxiety • Women with PCOS may present with various psychosocial problems such as anxiety, depression, eating disorders, and negative body image. • Screening for depression and anxiety is recommended.
  • 27. Non Alcoholic Fatty Liver Disease (NAFLD) • NAFLD refers to the presence of hepatic steatosis when no other causes for secondary hepatic fat accumulation are present. • It may progress to cirrhosis and is likely an important cause of inflammation, fibrosis and cryptogenic cirrhosis. • Likely cause by insulin Resistance. Nonalcoholic fatty liver (NAFL) Nonalcoholic steatohepatitis (NASH)
  • 30. Impaired Glucose Tolerance and Type 2 Diabetes Mellitus. • Women with PCOS are at increased risk for impaired glucose tolerance (IGT 30%) and type 2 DM (7%). • Beta Cell dysfunction that is independent of obesity has been reported in patients with PCOS.
  • 31. Metabolic Syndrome and Cardiovascular Disease • The metabolic syndrome is characterized by insulin resistance, obesity, atherogenic dyslipidemia, and hypertension. • It is associated with a greater risk of CVD and type 2 DM. • The prevalence of metabolic syndrome approximates 45% in women with PCOS. • Relative risk of 7.4% for myocardial infarction % in women with PCOS.
  • 32. Endometrial Neoplasia • In women with PCOS, the risk of endometrial cancer is increased three to fourfold. • Endometrial hyperplasia and endometrial cancer are long-term risks of chronic anovulation. • Neoplastic changes in the endometrium arise from chronic unopposed estrogen. • The effects of hyperandrogenism, hyperinsulinemia, and obesity lowers SHBG levels and raise circulating estrogen levels which add to this risk.
  • 33. Complications in Pregnancy • PCOS who become pregnant experience a higher rate of early miscarriage (30 to 50 %) • Higher risks of gestational diabetes, • Higher risks of hypertension in pregnancy • Higher risks of preterm birth. • Higher risk of multifetal gestations (which are associated with elevated rates of maternal and neonatal complications).
  • 35. Clitoromegaly is assessed using the clitoral index (clitoral length (mm) and width (mm) values). Values greater than 35 mm2 are abnormal.
  • 36. Anti Müllerian Hormone (AMH) • The classic polycystic ovary contains two to threefold more growing preantral and antral follicles than normal ovaries. • Within the granulosa cells of these developing follicles, the dimeric glycoprotein AMH is produced. • Serum AMH levels correlate closely with the number of preantral and antral follicles and for this reason, AMH is viewed as a potentially useful diagnostic marker for PCOS
  • 37. Ultrasound Histologically, a polycystic ovary displays a greater number of ripening and atretic follicles, cortical stromal thickness, and number of hilar cell nests. Many of these tissue changes can be seen sonographically, and pelvic sonography is commonly used to evaluate the ovaries in women with suspected PCOS. Ultrasound is particularly important for women with PCOS seeking fertility and in women with signs of virilization to exclude an androgen-producing ovarian Tumor.
  • 38. • Polycystic ovarian morphology (PCOM) is one criterion for PCOS diagnosis. • Earlier sonographic criteria for PCOM included >12 small cysts (2 to 9 mm in diameter or an increased ovarian volume (> 10 mL) or both per ovary. • More recently, follicle number per ovary (FNPO) threshold values have been raised due to improved sonographic imaging resolution • Notably, The criteria do not apply to women taking combination oral contraceptive pills. FNPO threshold of> 20 follicles and/or ovarian volume > 10 in either ovary has been adopted by ESHRE and ASRM. Ultrasound
  • 39. AEPCOS guidelines use the same ovarian volume value but a higher FNPO threshold of >25 follicles.
  • 40. PCOM often reflects normal adolescent ovarian Physiology. Thus, sonography for PCOS evaluation is not recommended within 8 years of menarche.
  • 42. Vitamin D, Vitamin B12 Cinnamon extract Green tea ω-3 fatty acid Micronutrients
  • 44. Treatment: combination oral contraceptive pills • COCs induce regular menstrual cycles, lower androgen levels, and thin the endometrium. • COCs suppress gonadotropin release, which results in decreased ovarian androgen production. • the estrogen component raises levels of SHBG, which binds free androgen. • the progestin component antagonizes the endometrial proliferative effect of unopposed estrogen from PCOS, thus reducing the endometrial hyperplasia risk.
  • 45. Treatment : Insulin Sensitizers • Metformin ( 1500mg to 2000mg)Pregnancy category B • Thiazolidinediones : Pregnancy category C • Glucagon Like Peptide1 (GLP1) • Sodium Glucose Cotransporter 2 (SGLT2): Empaglifozin
  • 46. • Surgical treatment of infertile women with PCOS was successfully revived by Halvard Gjönnaess in 1984 in the form of laparoscopic ovarian drilling (LOD) with subsequent ovulation and pregnancy rates of 92% and to 80%, respectively. • Since that time, this minimally invasive and less traumatic modern version of ovarian wedge resection using either electrocautery (diathermy) or laser has continued to play an essential part in management of infertile women with PCOS. Surgical Therapy
  • 47. Surgical Therapy: Ovarian Wedge Resection The patient is placed in the supine position. The bladder is emptied with a Foley catheter, and a Pfannenstiel or lower midline incision is made. The abdominal cavity is entered. The uterus is retracted caudally against the pubic symphysis. The polycystic ovary should be large with a smooth oyster-like capsule. A Babcock clamp is placed on the suspensory ligament of the ovary. An additional Allis clamp may be placed on the inferior pole of the ovary to stabilize the structure so that adequate wedge resection can be performed. A scalpel is used to incise the ovary down to and including the hilum. Occasionally, a small dermoid cyst may be located in the hilum. It is also important to remove a portion of the hilum to evaluate the possibility of a hilar cell tumor. After an adequate wedge has been taken, the ovary is closed in two layers. The first layer is closed by a running lateral mattress suture that enters the deep body of the ovary and exits through the opposite side of the ovary. The needle is reversed and reenters the body of the ovary, exiting on the opposite side. In this manner, the walls of the ovary are plicated in the midline, and dead space is eliminated.
  • 48. Surgical Therapy: Ovarian Wedge Resection At the completion of the running mattress suture, the capsule of the ovary can be closed by continuing the fine synthetic absorbable suture through the epithelium of the ovary. Care should be taken to invert all raw edges to reduce the problem of postoperative adhesions that could have an adverse effect on future fertility. Complete hemostasis is essential if adhesions are to be avoided.
  • 49. Surgical Therapy: Ovarian Drilling LOD is recommended as a second-line treatment in infertile PCOS women who have CC resistance. LOD has been also proposed as first-line approach for PCOS related anovulation or as an adjuvant therapy before in vitro fertilization (IVF) cycles LOD seems to be as effective as gonadotrophin treatment without an increased risk of multiple pregnancy or ovarian hyperstimulation syndrome (OHSS).
  • 50. Surgical Therapy: Ovarian Drilling LOD is most commonly performed using a monopolar diathermy needle electrode. LOD technique: Ten or more punctures were performed in the two ovaries together. Each puncture having a diameter of ~3 mm Depth of 2–4 mm Power setting of 40 W Duration for 2–4 s 640 Joules (J) per ovary (4 punctures × 4 s x 4 mm × 40 W) as the lowest effective dose with an ovulation and pregnancy rates of 86%.
  • 51. Surgical Therapy: Ovarian Drilling Unilateral vs. Bilateral LOD Fixed vs. Dose-Adjusted Energy LOD as a 1st line therapy in PCOS may offer several theoretical advantages: LOD increase responsiveness of the ovary to oral ovulation induction agents and gonadotrophins. Resumption of mono-ovulatory cycles and avoiding of the anti-oestrogenic effects of CC. LOD might work as an adjuvant procedure before IVF.
  • 52. Safety Concerns The use of LOD did open an avenue for ovulation induction but with inherent risks of general anaesthesia and surgical risks of laparoscopy, e.g. visceral and vessel injuries, gas complications, etc. The main shortcomings of LOD are the risk of postoperative adhesions and the concern about a negative impact of the procedure on the ovarian reserve secondary to excessive ovarian damage.
  • 53. Post Surgical Adhesions The incidence of perianexal adhesions after LOD does not represent a major constraint in its success story
  • 54. References Amer SA, Gopalan V, Li TC, et al: Long term follow·up of patients with poly. cystic ovarian syndrome after laparoscopic ovarian drilling: clinical outcome. Hum Reprod 17:2035, 2002 American College of Obstetricians and Gynecologists: Diagnosis of abnormal uterine bleeding in reproductive-aged women. Practice Bulletin No. 128, July 2012, Reaffirmed 2016 American College of Obstetricians and Gynecologists: Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Committee Opinion No. 651, December 2015, Reaffirmed 2017 American College of Obstetricians and Gynecologists: Polycystic ovarian syn· drome. Practice Bulletin No. 194, June 2018 American Diabetes Association: 2. Classification and diagnosis of diabetes: stan·dards of medical care in diabetes---2019. Diabetes Care 42{1 suppl):Sl3, 2019 American Society for Reproductive Medicine: Current evaluation of amenorrhea. Fertil Steril 90(5 Suppl):S219, 2008 American Society for Reproductive Medicine: Role of metformin for ovulation induction in infertile patients with polycystic ovary syndrome {PCOS): a guideline. Fenil Steril 108(3):426, 2017 Arroyo A, Laughlin GA, Morales AJ, et al: Inappropriate gonadotropin secre·tion in polycystic ovary syndrome: influence of adiposity. J Oin Endocrinol Metab 82:3728, 1997 Azziz R: lhe evaluation and management of hirsutism. Obstet Gynecol 101 :995, 2003 Axziz R, Carmina E, Dewailly D, et al: Position statement: criteria for defining polycystic ovary syndrome as a predominantly hyperandrogenic syndrome: an Androgen Excess Society guideline. J Clin Endocrinol Metab 91:4237, 2006 Bahri Khomami M, Joham AE, Boyle JA, et al: Increased maternal pregnancy complications in polycystic ovary syndrome appear to be independent of obesity-a systematic review, meta-analysis, and meta·regression. Obes Rev 20(5):659, 2019 Banaszewska B, Duleba A, Spaczynski R: Lipids in polycystic ovary syndrome: role of hyperinsulinemia and effects of metformin. Am J Obstet Gynecol 194:1266, 2006

Editor's Notes

  1. Vallisneri was a Italian Medical Scientist and naturalist who pioneer the Diagnosis of PCOS in 1721. He stated that scientific knowledge is best acquired through experience and reasoning. Stein Leventhal both American Gynecologist in 1935 describe a triad of amenorrhea, Obesity and hirsutism as one of the most common endocrine disorder in women.
  2. Science, practice and evidence are dynamic processes. This is typically vivid when it relates to Polycystic Ovarian Syndrome. PCOS is a heterogenous, metabolic endocrinopathy. It is the commonest hyperandrogenic disorder in women and one of the most common causes of ovulatory infertility. It is a disorder characterized by Ovulatory disorder, hyperandrogenism and/or PCOM.
  3. Subsequently an NIH workshop in 2012 emphasized the variable phenotypes presentations of PCOS. The consensus recommended the 2003 Rotterdam criteria to be used to assign one of the 4 specific patients phenotypes. Importantly, the same criterias are not appropriate for adolescents.
  4. Fraenkel gave the name hyperthecosis to this histopathological finding. These conditions are exaggerated PCOS phynotypes
  5. The epigenetic modification of genetic susceptibility within the maternal fetal environment may influence adult PCOS Development.
  6. Genetic evidence suggests men can develop PCOS-like condition | Endocrine Society
  7. Anovulation in women with PCOS is characterized by inappropriate production of gonadotropin secretion. Specifically, altered GnRH pulsatility leads to preferential Production of LH compared to FSH. It is currently unknown whether hypothalamic dysfunction is a primary cause of PCOS or secondary to abnormal steroid Feedback. LH FSH ratios are elevated and rise above 2: I approximately 60% of patients.
  8. Both Insulin and LH stimulates androgen production by the ovarian theca Cells and as a result the affected ovaries secrete Elevated levels of testosterone and androstenedione, free testosterone and DHEAS. SHBG are decreased in PCOS, and is linked to impaired Glucose and DM2.
  9. Follicular cyst (the most common functional ovarian cyst) 8cm Corpus luteum cyst (most commonly ruptured and causing hemoperitoneum) 3-11cm unilateral. EP, hemoperitoneum, Halban syndrome Theca-lutein cyst (events of increase HCG: molar pregnancy, multiple gestation., rh isoimmunization, ovulation induction with clomid hmg,fsh. 30cm, multicystic
  10. The four most common ovulatory disorders include polycystic ovary syndrome (PCOS), hypogonadotropic hypogonadism (HA), primary ovarian insufficiency (POI), and hyperprolactinemia
  11. Insulin Resistance is define as a reduce glucose uptake response to a given amount of insulin. This lower insulin sensitivity appears to stem from a post binding abnormality in insulin receptor-mediated signal transduction. Both lean and obese women with PCOS are found to have insulin resistance. insulin resistance is associated with several disorders including HTN, DM2, dyslipidemia and CVD. As such PCOS is not simply a disorder of Short term consequences but one of potential long term consequences. hyperinsulinaemia inhibits hepatic sex hormone-binding globulin (SHBG) production in women with PCOS [6], resulting in a marked increase in circulating free testosterone levels. hyperinsulinaemia may alter physiologic gonadotrophin secretory dynamics, increasing luteinising hormone (LH) levels, which then act in concert with insulin to augment ovarian androgen production
  12. menstrual dysfunction usually begins with menarche and may range fiom amcnorrbca to oligomenonhca to episodic heavy menstrual bleeding with associated iron-deficiency anemia. In most cases, amcnorrhea and oligomcnorrhca result fiom anovulation. Namely, without ovulation and endogenous progesterone production fiom the coipus lutcum, a normal menstrual period is not triggered. Instead, chronic cstrogcn exposure results and produces constant mitogenic stimulation of the endomctrium. The instability of the thickened endometrium leads to unpredictable bleeding.
  13. the most common areas affected with excess hair growth include the upper lip, chin, sideburns, chest, and linea alba of the lower abdomen. Escutcheon is the term used to describe the hair pattern of the lower abdomen, triangular shape in unaffected women and Diamond in affected. In the hair follicles the enzyme 5 alpha reductase converts testosterone in diydrotestosterone.
  14. To quantify the degree of hirsutism for research purposes, it was developed in 1961 and later modified in 1981. Abnormal hair distributionis assessed in 9 body areas and scored from 1 to 4. Hirsutism is greater that 4, Modified is greater and igual to 4. Some specialist choose to classlify as Mild, moderate or severe.
  15. Female androgenic alopecia is a less common finding in women with PCOS.
  16. Topical retinoids are first line adjunct option.
  17. These changes may raise the cardiovascular disease risk in women with PCOS. The prevalence of dyslipidemia in PCOS approaches 70 %
  18. Males<0.9 Females<0.85
  19. Obstructive sleep apnea (OSA) is a disorder that is characterized by obstructive apneas and hypopneas due to repetitive collapse of the upper airway during sleep. Untreated OSA has many potential consequences and adverse clinical associations, including excessive daytime sleepiness, impaired daytime function, metabolic dysfunction and an increased risk of cardiovascular disease and mortality. The goals of OSA therapy are to resolve signs and symptoms, improve sleep quality, and normalize the apnea-hypopnea index (AHI) and oxyhemoglobin saturation levels. OSA should be approached as a chronic disease that requires long-term, multidisciplinary management.
  20. Nonalcoholic fatty liver (NAFL): without evidence of significant inflammation Nonalcoholic steatohepatitis (NASH): inflammation Ultrasonography often reveals a hyperechoic texture or a bright liver because of diffuse fatty infiltration.
  21.  In French law, foie gras is defined as the liver of a duck or goose fattened by gavage (force feeding). Foie gras is a popular and well-known delicacy in French cuisine.  Its flavour is described as rich, buttery, and delicate.
  22. For anovulatory infertility, ESRE/ASRM guidelines recommend first line treatment with letrozole or clomiphene citrate in women with PCOS Metformin is a second line agent. Gonadothrophins Menopur.
  23. ACOG recommends Endometrial assessment in ay women older than 45 years with AUB
  24. baseline rate of Miscarriage in General population is approximately 15 %
  25. Free testosterone levels are more sensitive than total testosterone levels as an indicator of hyperandrogenism. However, current free testosterone assays lack a uniform laboratory standard. For this reason, total testosterone levels remain the best approach for identifying a possible Tumor. Threshold values >200 ng/dL of total testosterone warrant evaluation for an ovarian lesion. DHEAS is essentially produced exclusively by the adrenal gland. Therefore, serum DHEAS levels > 700 µg/dL are highly suggestive of an adrenal neoplasm, and adrenal imaging with abdominal CT or MR imaging is warranted. Serum LH levels are affected by sample timing within a menstrual cycle, use of oral contraceptive pills, and BMI. CAHIS is a complete or partial deficiency of 11 and 21Hydroxylase. It can be in neonates with ambiguous genitelia and life threatening Hypotension. In the late onset CAH, it leads to cortisol deficiency and inn response ACTH rise to normalise cortisol production and this results in adrenal hyperplasia and androgens rise And result in precursor C19 accumulation witch is converted into DHEAS, androstendione and testosterone. Late onset CAH leads is generally from 21 hydroxylase deficiency which leads to 17 alpha hydroxyprogesterone which when >200ng/dlshould prompt an ACTH stimulation test250ug IV and then erume17 alpha is checked in 1 hour. If >1000ng/dl then its indicative of late onset CAH.
  26. In patients who are not candidates for COCs progesterone withdrawal is recommended every 1 to 3 months. Examples of regimens used include: medroxyprogesterone acetate (MPA), 5 to 10 mg orally daily day for 12 days, or micronized progesterone, 200 mg orally each evening for 12 days.
  27. Atlas of Pelvic Surgery website
  28. Amer et al An ovulation and pregnancy rates of 67% were reported using four punctures to deliver 600 J per ovary (4 punctures × 5 s × 30 W = 600 J)
  29. Endocrine.org | Endocrine Society Homepage | Figo Figo.org