Prof. Aboubakr Elnashar

1. OBESITY IN
GYNECOLOGICAL
PRACTICE
Prof. Aboubakr Elnashar
Benha university Hospital,
Egypt
ABOUBAKR ELNASHAR

2. Incidence of Obesity
https://www.google.com.eg/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&cad=rja&uact=8&ved=0ahUKEwje_93djLvSAhVHRhQKHUJSCfQQjRwIBw&url=https%3A%2F%2Fscconner.wordpress.com%2F2012%2F05%2F09%2Fegypt-independent-
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3. CONTENTS
I. EXAMINATION
II. REPRODUCTIVE MEDICINE
1. MENSTRUATION:
2. SEXUAL FUNCTION
3. FERTILITY: decrease
4. ART
5. CONTRACEPTION
III. BENIGN GYN PROBLEMS
IV. GYN MALIGNANCY
V. GYN SURGERY
VI. ANAETHESIA
ABOUBAKR ELNASHAR

4. II. REPRODUCTIVE HEALTH
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5. 1. MENSTRUATION.
 Childhood obesity:
1. Precocious menarche (<9 y).
2. Irregular cycles
3. Oligo/amenorrhoea
(van der Steeg et al., 2008; Brewer and Balen, 2010).
ABOUBAKR ELNASHAR

6.  Critical body weight hypothesis
(Frisch hypothesis).
 Menstruation is established once a threshold
 wt 48 kg or
 17% body fat composition (16% to 23.5%)
 Moderately obese: earlier menarche.
 Morbid obesity: delayed menarche
 Leptin:
 a peptide secreted by adipose tissues
 acts on CNS neurons, regulating eating behavior &
energy balance.
 Higher levels: earlier menarche.ABOUBAKR ELNASHAR

7.  Girls with an early onset of puberty are at increased
risk of
 ovarian hyperandrogenism
 PCOS
 CVD in later life
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8. 2. SEXUAL FUNCTION
 Obesity is associated with
 difficulties with sexual performance
 ±avoidance of sexual intercourse.
 Sexual quality of life is most impaired for
Class III obesity
(Kolotkin et al, 2005; Assimakopoulos et al, 2006)
ABOUBAKR ELNASHAR

9.  Female Sexual Function Index
strongly correlated with BMI
(Esposito et al, 2007).
 Desire and pain
did not correlate with BMI
 Arousal, lubrication, orgasm& satisfaction
did.
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10.  Obese Vs nonobese
 No significant differences in
arousal, orgasm, and desire
 Sexual satisfaction: significantly lower
 Preferred positions: rear entry in the obese and man on top in the lean.
 Three quarters of obese
 verbally abused by their husbands because of
their body shape.
 statistical correlation between weight loss and improvement in libido.
(Younis et al, 2013)
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11. 3. FERTILITY
 BMI >30kg/m2 :
Natural conception decrease by 4% per kg/m2
{Dutch national registery 2008}
 Obesity
Significant cause of infertility
(Norman and Clark,1998)
Poorer reproductive outcomes
regardless of the mode of conception
natural conception
ovulation induction
IVF
ICSI
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12. The rate of infertility
39,3
%*
60,7
%
8,7
%
91,3%
•- р<0,05 between I and II groups
•Artymuk., Krapivina ., 2005
obese non obese
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13. 1. Hyperinsulinaemia & hyperandrogenism
Simple obesity:
insulin resistance
In the ovary:
Insulin stimulates steroidogenesis:
increased androgens:
decreases liver synthesis of SHBG.
In adipose tissue:
excess sex steroids:
increased androgens.
ABOUBAKR ELNASHAR

14. 2. Anovulation
Obesity is commonly associated with anovulation
BMI: 24-31kg/m2
RR for anovulation 1.3 (95% CI=1.2-1.6)
BMI ≥ 32kg/m2
RR for anovulation 2.7 (95% CI=2-3.7)
Central obesity:
Higher risk of anovulation
Adipocytokines (Greek adipo-, fat; cytos-, cell; and -kinos, movement)
cytokines (cell signaling proteins) secreted by adipose tissue. leptin
and resistin
{have effects on hypothalamicpituitary signalling: inhibit
ovulation}
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15. 3. PCOS
Most women with PCOS are overweight
Obesity
may promote the development of the PCOS in
susceptible women
{Metabolic abnormalities induced by obesity
(insulin resistance)}: PCOS
 Increased phenotopic expression
Obesity in PCOS:
35% to 63%
 does not form part of the diagnostic criteria
(Balen et al. 1995, Azziz et al. 2004, Norman et al. 2007).
often the result of diet and not the endocrine disorder.
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16. р=0,001
Artymuk N., Krapivina N., 2005
52,5%*
8.7%
obese non obese
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17.  Effect of obesity on treatment of female
infertility
1. Poor response to ovulation induction
CC:
decreased response with
increased BMI or waist-to-hip ratio
FSH:
fewer mature follicles
decreased chance of ovulation
2. Higher doses of gonadotrophins
The most clinically useful predictors:
obesity & insulin resistance.
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18. 3. Increased risk of
OHSS
multiple pregnancies in PCOS obese
4. Decreased efficacy of fertility treatments:
Lower success rates with ART
5. DVT
{drugs
containing E
resulting in high levels of endogenous E
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19. 4. ART
SR: (Rittenberg et al, 2011)
33 studies including 47,967 tt cycles
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20.  OB (BMI:≥30) had significantly
lower CPR (RR = 0.90, P < 0.0001)
Lower LBR (RR = 0.84, P = 0.0002)
Higher miscarriage rate (RR = 1.31, P < 0.0001) compared
to women with a BMI< 25.
Longer duration of Gnt stimulation
(WMD 0.27, 95% CI 0.26–0.28, P < 0.00001).
Higher dose of Gnt stimulation
(WMD 406.77, 95% CI 169.26–644.2, P = 0.0008).
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21. Category 1: Safe
No restriction for use
Category 2: Usable
Advantages outweigh risks
careful follow-up
Category 3: Not recommended
Risks outweigh advantages
BM>30 COC
,P,R
POP injection implant LNG IUD Co IUD
>18Y 2 1 1 1 1 1
<18Y 2 1 1 2 1 1
Bariatric
Restrictive 1 1 1 1 1 1
Malabsorp COC:3
P/R:1
3 1 1 1
5. CONTRACEPTION
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22.  The preferred methods
 IUD (copper or levonorgestrel-releasing) or
 Implant (etonogestrel), over other methods
(Grade 2C).
1. have a very low rate of failure (compared with barrier
methods)
2. not associated with weight gain (compared with depot
medroxyprogesterone acetate [DMPA])
3. do not expose the woman to potential risks
associated with estrogen-containing
contraceptives.
ABOUBAKR ELNASHAR

23.  Efficacy:
 No strong evidence
that any method of contraception is ineffective in obese
women
 Concerns
 have been raised about the effectiveness of
 oral contraceptives
 patch and ring.
 Oral contraceptives
 generally effective at pregnancy prevention in obese women
 ±less forgiving of imperfect use because the pharmacokinetics of
steroid hormones appear to be altered in obese users compared
with normal-weight users.
 ovulation is still suppressed in most obese users.
 If contraceptive efficacy is reduced, the magnitude of effect is likely
to be small.
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24.  Weight gain:
 NO:
 combined hormonal contraceptives,
 progestin-only pills,
 intrauterine contraception
 contraceptive implants
 May be:
 DMPA
ABOUBAKR ELNASHAR

25.  Bariatric surgery procedures
 Malabsorptive:
 biliopancreatic diversion or
 jejunoileal bypass
 may interfere with the absorption of oral
contraceptives: reducing their effectiveness.
 If hormonal contraception is used: non-oral
hormonal contraceptives over oral hormonal
contraceptives (Grade 2C).
ABOUBAKR ELNASHAR

26. III. BENIGN GYNECOLOGICAL PROBLEMS
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27. 1. MENSTRUAL PROBLEMS
Abnormalities in
amount
duration,
length
regularity
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28. The rate of menstrual disorders
*Р<0,05 between I and II groups
Artymuk N., Krapivina N., 2005
67,7%*
17,4%
obese non obese
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29. 2. ENDOMETRIAL POLYPS
 BMI>30
 more likely to have endometrial polyps than
women with a BMI less than 30 (52 vs 15%).
(Onalan et al)
 an independent predictor for the development of endometrial polyps
[Onalan et al, 2009].
 positively correlated with their size and multiplicity.
 Pathogenesis
Hormonal factors related to estrogen excess, such
as obesity
[Onalan et al, 2009].
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30.  Types
 Most are benign
 Malignancy
 only 1.5% of cases
[Anastasiadis et al, 2000].
 risk factors for malignant transformation
 Postmenopausal status
 Hypertension
[Giordano et al, 2007].
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31. 3. FIBROIDS
 More likely
 Obese or severely obese (16 vs 7.2%) than a
general population of women
[Shikora et al, 1999].
 bodyweight of 70 kg or more in comparison with those who weigh
less than 50 kg
 {Relative hyperestrogenic state: encourages fibroid
growth}
[Okolo, 2008]
 Not all studies are in
accordance with this hypothesis
[Parazzini et al, 1988].
ABOUBAKR ELNASHAR

32. 4. URINARY INCONTINENCE
 increased especially stress
urinary incontinence (SUI)
[SR of 29 studies, 2008].
 Surgery for SUI in obese
women
 Safe
 less effective, than similar
surgery performed in
nonobese women
[Greer ; 2008, SR].
 {Raised intra-abdominal
pressure caused by central
obesity}
[Waetjen et al, 2007}.
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33. Frequency of urogenital disorders
*p<0,001
Artymuk N., Tachkova O., 2014
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34. 5. PELVIC ORGAN PROLAPSE
[Whitcomb et al, 2009].
 Obesity
 risk factor for lower urinary tract symptoms (LUTS)
 predictor of exacerbation of
 SUI
 overactive bladder (OAB).
BMI Pelvic floor dysfunction
>40 57%
>35 53%
>30 44%
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35. 6. MENOPAUSE
 Onset
 Raised BMI:
 early onset of menarche
 Late onset of menopause
(Akahoshi et al.2002)
 {increased levels of circulating estrogen,
secondary to peripheral aromatisation of
androstenidione secreted by the adrenal
glands and ovary}.
ABOUBAKR ELNASHAR

36. Symptoms: Relationship between obesity and hot flushing is
complex.
 Increase incidence of hot flushes
 {an insulating effect of the adipose tissue itself}
 This would explain why many obese men also
suffer from flushes and sweats.
(Thurston et al.2008)
 Decrease duration of hot flushes
(Freeman at al.2011)
 estrogen, produced by peripheral aromatisation
from androgen, plays a role in regulating
vasomotor changes
 hyperoestrogenic state of obesity may have a
‘protective role’.
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37. Kupperman index
*p<0,001
Artymuk N., Tachkova O., 2014
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38. ABOUBAKR ELNASHAR

39. Osteoporosis
 obesity
 ±protective
(Albala et al, 1996)
 increased androgen levels
 Increased estrogen levels
 detrimental to bone health.
 mechanical stress of excess weight on the
musculoskeletal system
 Fracture risk.
 Age of menopause:
more important than
BMI
(Zhao et al, 2oo7)
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40. ABOUBAKR ELNASHAR

41.  The severity of menopausal disorders
*p<0,05
Artymuk N., Tachkova O., 2014ABOUBAKR ELNASHAR

42. IV. GYNECOLOGICAL MALIGNANCY
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43. 1. ENDOMETRIAL CARCINOMA
 Obesity significantly increases the incidence of
endometrial cancer
(Modesitt , van Nagell , 2005)
 {prolonged exposure to unopposed estrogen and
hyperandrogenism
ABOUBAKR ELNASHAR

44. Endometrial Caner in Egypt
0
5
10
15
20
25
30
35
Overall ≥75 Years ≥60-74 Years ≥50-59 Years
Incidence/100,000 Women
Ibrahim AS et al. 2014
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45. OR of endometrial cancer in obese women
0.4
0.8 0.7
2.1
4.1
20-25 25-29.9 30-34.9 35-39.9 >40
BMI, kgm2
×1.9
×5.8
E. Ilenko, N. Artymuk, 2007
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46. 2. OVARIAN CANCER
 data are less convincing
 modestly increase the incidence of premenopausal
ovarian cancer
(Modesitt , van Nagell , 2005)
 Obesity per se
 not a risk factor for ovarian cancer
 may make the diagnosis more difficult.
 Most women with advanced ovarian cancer present with
abdominal distension. In obese women, they may not
have noticed distension, and thus present with more
advanced disease.
 Ultrasound may be more difficult to perform and
interpret
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47. ABOUBAKR ELNASHAR

48. 3. BREAST CANCER
 Postmenopausal:
 Increase oestrogen
receptor (ER)-
progesterone receptor
(PR)-positive breast
cancer
 {Obesity: insulin resistance:
increased levels of circulating
insulin: reduced hepatic
synthesis of SHBG
 increased peripheral
aromatisation of androgens:
increased levels of estrogens
(Key et al, 2003)}
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49.  Premenopausal:
 By contrast, an inverse correlation between BMI
and premenopausal breast cancer.
(Benedetto et al, 2015)
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50. 4. CERVICAL CANCER
 data are less convincing
 A modest positive association between BMI and
cervical cancer
 {impact on glandular cancers or decreased screening
compliance}.
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51. CONCLUSION
Impact of obesity on Gyn practice
 EXAMINATION: difficult
 REPRODUCTIVE MEDICINE
1. Menstruation: early onset. Irregular cycles
2. Sexual function: Dec sexual satisfaction
3. Fertility: Dec, inc PCOS, Dec response to tt
4. ART: Dec LBR, Inc miscarriage rate
5. Contraception: in morbid: estrogen containing
contraceptives: Inc DVT and failure rate
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52.  BENIGN GYN PROBLEMS:
1. Menstruation: Inc abnormalities
2. Polyp: Inc
3. Fibroid: uncertain
4. UI: Inc
5. POP: Inc
6. Menopause: Late onse, Inc hot flushes incidence
and dec duration
 GYN MALIGNANCY
I. Endometrial: Inc
II. Ovarian: In premenopausal
III. Breast: inc postmenopausal
IV. Cervical: uncertain
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53. You can get this lecture and 404
lecture from:
1.My scientific page on Face book:
Aboubakr Elnashar Lectures.
https://www.facebook.com/groups/2277
44884091351/
2.Slide share web site
3. elnashar53@hotmail.com
4.My clinic: Althwara st, Mansura, Egypt
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