Thesis Presentation

Dr Nidhi, DNB Resident ,1ST Year

Dept of Obstetrics & Gynaecology

Guide- Dr Madhu Roy , Senior Consultant,

Dept of Obstetrics & Gynaecology
Co-Guide- Dr Asim Siddiqui( Dept of Endocrinology)
Indraprasth Apollo Hospital , Sarita Vihar , New Delhi
Introduction

 PCOS is a hyper androgenic disorder associated with chronic

anovulation and polycystic ovarian morphology. It is often associated
with health implementation in later life.
 It can affect females throughout their lifetime from puberty to
menopause.

 It is not only a very prevalent cause of anovulatory infertility,

menstrual disturbances and hirsutism, but it is also a major risk
factor for the development of type 2 diabetes mellitus in later life.1
 The reproductive issues with PCOS are manifold starting with
anovulatory cycles leading to subfertility.
 Post conception, PCOS women are at increased risk for early
pregnancy loss (EPL).

 After having successfully passed the first trimester, they commonly

encounter later pregnancy complications like gestational diabetes
mellitus (GDM), pregnancy-induced hypertension (PIH),
preeclampsia, preterm delivery, and birth of small for gestational
age (SGA) infant
 The pathophysiology of PCOS is multifactorial, and it is believed that a
genetic predisposition exists that is exacerbated by excess adiposity. It is
thought that the pathophysiology of PCOS involves the interaction between
abnormal ovarian morphology, due to excess androgen production by the
PCO—hyperinsulinemia, and elevated luteinizing hormone (LH) levels.3

 The ‘Barker hypothesis’ of fetal programming in utero suggests that the

fetal nutrition and endocrine environment(e.g. hyperinsulinaemia) may
effect neuroendocrine systems regulating body weight, food intake and
metabolism, with consequences for long-term health in the offspring
NEED FOR THE STUDY

 While there have been several reports indicating that PCOS pregnancies
may be at increased risk of diabetic, hypertensive and other
complications, results of these studies have been often inconsistent.And
it is uncertain to what extent the medical condition itself influences
pregnancy and neonatal outcomes.

 To evaluate the risks for pregnancy outcomes in women with PCOS

versus controls, we planned to perform this type of study.
AIM AND OBJECTIVES

 To study the pregnancy outcome in the patients of PCOS and compare it

with controls.

 To study the incidence of pregnancy complications such as spontaneous

abortions, preterm labour, gestational diabetes, gestational hypertension,
preeclampsia, pregnancy and neonatal outcome in women with PCOS.
REVIEW OF LITERATURE

 In a developing country like ours, which is the diabetic capital of the

world, polycystic ovary syndrome (PCOS) is one of the top listed
endocrine disorders in women between 13 to 40 years of reproductive
age. Prevalence of the disease is between 5 to 10%.Stein and Levinthal
was the first to describe the condition.5

 Surendra et al (2017) in their study found that the maternal

complications in the form of spontaneous abortion, GDM, Gestational
hypertension, Pre-eclampsia in our study was higher than the normal
population which was found to be statistically significant
 Shivananjaiah C et al (2017) in their study found that Of the 100 women
who were diagnosed with PCOS, 62 had spontaneous conception, 32
conceived with ovulation induction, 4 with artificial insemination and 2
needed IVF for conception.
 18 women had spontaneous abortion, 58 were diagnosed with Gestational
diabetes mellitus (GDM) predominantly between 24 – 28 weeks’ period of
gestation, 16 women had hypertension complicating pregnancy.
 Fetal outcome in the form of preterm birth was noted in 14 patients, large
for gestation was noted in 11 new-borns, the rate of NICU admission was
significantly higher in the PCOS women’s infants constituting 33%.5
 Sterling L et al (2016) in their study found that Women with PCOS
demonstrated a higher risk of developing the following pregnancy
complications after adjusting for differences in age, parity, body mass
index, and time to conception: gestational diabetes (adjusted odds ratio
[AOR] 3.15, 95% confidence interval [CI] 1.35–7.33), hypertensive disorders
of pregnancy (AOR 4.25, 95% CI 1.94–9.32), preterm birth <37 weeks (AOR
2.30, 95% CI 1.07–4.97), and large for gestational age >90th percentile
(AOR 2.77, 95% CI 1.21–6.35).6
 Nivedhitha V. S. et al (2015) in their study found out that Out of 80
pregnancies with PCOS, 8 had spontaneous abortions, 11 Gestational
diabetes mellitus (GDM), 9 gestational hypertension, 5 preeclampsia and 3
had preterm labour.
 GDM is 3 times, Spontaneous Abortion is 4.33 times, gestational
hypertension is 3.25 times and neonatal intensive care unit (NICU)
admission is 3.25 times more in PCOD women.7

 Kamalanathan S et al (2013) in their study found that PCOS is associated

with increased risk of miscarriage, gestational diabetes mellitus, and
hypertensive disorders of pregnancy, preterm delivery, and birth of small
for gestational age infant.2
 Roos N et al (2011) in their study found that Polycystic ovary syndrome
was strongly associated with pre-eclampsia (adjusted odds ratio 1.45,
95% confidence interval 1.24 to 1.69) and very preterm birth (2.21, 1.69
to 2.90) and the risk of gestational diabetes was more than doubled
(2.32, 1.88 to 2.88).

 Infants born to mothers with polycystic ovary syndrome were more

prone to be large for gestational age (1.39, 1.19 to 1.62) and were at
increased risk of meconium aspiration (2.02, 1.13 to 3.61) and having a
low Apgar score (<7) at five minutes (1.41, 1.09 to 1.83).8
 Gupta A et al (2009) in their study found that Incidence of
Pregnancy induced hypertension in cases of PCOS was 14.2 % (8/56) ,
gestational diabetes was 14.2 % (8/56) IHCP 10.7% (6/56) as
compared of age and weight matched controls is with the incidence
of PIH was 7.10% (4/56), GDM 3.5% (2/56) IHCP 7% (4/56).The
differences in the incidence of GDM & PIH in two groups was not
significant.

 The outcome of pregnancy in controls & the test groups were not
significant, though numerically found to be higher.9
 Boomsma CM et al (2006) in their study found that Women with PCOS
demonstrated a significantly higher risk of developing gestational diabetes
[odds ratio (OR) 2.94; 95% confidence interval (CI): 1.70–5.08], pregnancy-
induced hypertension (OR 3.67; 95% CI: 1.98–6.81), pre-eclampsia (OR 3.47;
95% CI: 1.95–6.17) and preterm birth (OR 1.75; 95% CI: 1.16–2.62).

 Their babies had a significantly higher risk of admission to a neonatal

intensive care unit (OR 2.31; 95% CI: 1.25–4.26) and a higher perinatal
mortality (OR 3.07; 95% CI:1.03–9.21).4

 Haakova L et al (2003) in their study found that no any significant

differences in the prevalence of pregnancy complications such as
gestational diabetes mellitus, pregnancy-induced hypertension (PIH) and
premature deliveries between the group of PCOS patients and the
controls.10
 MATERIALS AND METHODS

 This study is a Descriptive Longitudinal type of study

 Study Area- Study will be carried out at Indraprastha Apollo Hospital New Delhi.
 Type of Study:- Descriptive Longitudinal study
Sample size
 Assuming that the spontaneous abortion as one of the important adverse
pregnancy outcome among patients with PCOS. As per the previous study the
incidence of spontaneous abortion in patient with PCOS was 6 out of 40, where
as in control group 2 out of 40 (based on study by Surendra et al1), at 2-sided
test with 95% confidence level (α=5%) and 80% power, expected sample size in
both group is 142 each, i.e total 284 sample size will be taken (142 with PCOS
and 142 control group)
Formula

 This calculator uses the following formulas to compute sample size

 N1= (Z1-α/2+ Z1-β)2 ഥ

𝑃𝑞ത (r+1)/r(p1-p2)2
Where,
 The notation for the formulae are: N1 = sample size of Group1 (With
PCOS).
 N2= sample size of Group2 (Control),
 Z1-α/2 =standard normal deviate for two-tailed test based on alpha
level (relates to the confidence interval level) two-sided Z value (e.g.
Z=1.96 for 95% confidence interval).
 Z1-β = power
 r = ratio of unexposed to exposed
 p1 = proportion of exposed with disease and q1 = 1-p1
 p2 = proportion of unexposed with disease and q2 = 1-p
Statistical Methods:

 Statistical analysis will be carried out with the help of Microsoft Excel
and Epi info 7.1 software. The description of the data will be done in
form of arithmetic mean +/- SD (or median) for quantitative data while
in the form of frequencies (%) for qualitative (categorical) data. P-
values of < 0.05 will be considered significant.

 For comparison of categorical variables (i.e. to examine the

associations between qualitative/quantitative variables), chi-square
test will be used if the number of elements in each cell are 5 or higher
and Fisher’s exact test, otherwise.
 Period of Study: - Aug 2019 to Aug 2021.
 Location: - Indraprastha Apollo Hospital, New

 INCLUSION CRITERIA
 1. Women with PCOS and
 2. Age ranging from 18 to 40 years
 EXCLUSION CRITERIA:
 1. Women with anovulation not due to PCOS
 2. Women with obesity not due to PCOS.
 3. Women with hirsutism due to adrenal or other causes and
 4. Women with other medical illness.
METHODOLOGY

 This study will be conducted in the department of Obstetrics and

Gynaecology, Indraprastha Apollo Hospital New Delhi in pregnant
women attending the antenatal clinic, satisfying the inclusion criteria.
It is a Descriptive Longitudinal study.

 We will study the outcome of pregnancy in the patients who are

diagnosed and having PCOS. The women should met the following
criteria for the diagnosis of PCOS.
 i) Oligomenorrhoea (menstrual cycle longer than 35 days)
 ii) Anovulatory infertility on follicular study
 iii) Typical morphology of polycystic ovaries on ultrasound scan.
 iv) Increase level of at least one androgen (reference values for normal
concentrations).
 Testoterose 0.5 -2.63 nmoll/l androstenediose 1.57 - 5.4 nmol/l,
dehydroepiandrostene 0.8 - 10.5 nmol/l & DHEA-S (2.4-14.5micromol/L)12.
All these women with their controls will be followed during pregnancy in
Indraprastha Apollo Hospital New Delhi.
 All patients will be interviewed personally to obtain the relevant
information about their medical and family history.
 The diagnosis of Gestational diabetes mellitus will be based on GTT
performed twice in the second and third trimester.(100gm of glucose and
cut off values in blood F105 mg%,1hr.190mg%,2hr.165mg %3hr145mg% ).11
 PIH is defined as Gestational hypertension (B.P >140/90 mg) without
proteinuria at 20wks of gestation on two or more occasions at least 6 hrs
apart and Preeclampsia (B.P > 140/90 mg) in combination with
proteinuria > 0.3 gm/24 hrs of urine after 20 weeks of gestation.)11
 In the family history we will consider first and second degree relatives i.e
parents, siblings and grandparents. family history of diabetes mellitus,
hypertension or ischaemic heart disease (myocardial infarction) will be
considered positive if one or more first degree relative having onset of
disease before the age of 45 yrs.

 Immediately after delivery, birth weight and APGAR scoring at 1 and 5

minutes will be recorded. If the birth weight is less than 2500 grams, it
will be classified as low birth weight and as macrosomy if more than 4000
grams, at more than 37 weeks.

 APGAR score of less than 7 at 5 minutes after birth will be considered as

the criterion for assessment of neonatal morbidity.
 A case matched control group based on age and weight will be obtained
from selection of women from our Antenatal OPD during this time period.

 Information regarding the course of their pregnancies will be obtained. The

controls will also be interviewed personally to obtain relevant information
in their medical & family histories.

 The outcome in term of PIH, GDM, IUGR, Abortion, Preterm labour will be
worked out and Compared among test and control arms.
 References

 1. Surendra , Choudhary V. A prospective control study evaluating pregnancy outcome in

PCOS patients: The bottom line truth of modern lifestyle. International Journal of
Surgery Science 2018; 2(1): 28-32.
 2. Kamalanathan S, Sahoo1 JP, Sathyapalan T. Pregnancy in polycystic ovary syndrome.
Indian Journal of Endocrinology and Metabolism.2013; 17 ( 1):1-7.
 3. McDonnell R, Hart RJ. Pregnancy-related outcomes for women with polycystic ovary
syndrome. Women’s Health.2017; 13(3):89–97
 4. Boomsma CM, Eijkemans MJC, Hughes EG, Visser GHA, Fauser BC and Macklon NS. A
meta-analysis of pregnancy outcomes in women with polycystic ovary syndrome Human
Reproduction Update.2006; 12(6): 673–683
 5. Shivananjaiah C, Kannan A, Devi M, Jayanthi, Satish D, Ramaiah R. Polycystic ovarian
syndrome and pregnancy outcome. Int J Reprod Contracept Obstet Gynecol
2017;6:3804-7.
 6. Sterling L, Liu J, Okun N, Sakhuja A, Sierra S. Pregnancy outcomes in women with
polycystic ovary syndrome undergoing in vitro fertilization. Fertility and Sterility.2016;
105( 3): 1-9
 7. Nivedhitha VS, Sankareswari R. Pregnancy outcome in women with polycystic ovary
syndrome. Int J Reprod Contracept Obstet Gynecol 2015;4:1169-75.
 8. Roos N, Kieler H, Sahlin L , Falconer H . Risk of adverse pregnancy outcomes in women
with polycystic ovary syndrome: population based cohort study. BMJ 2011;343:d6309.

 9. Gupta A, Raina K, Kalkkar T , Veer Y. Pregnancy Outcome In Women with the Polycystic
Ovarian Syndrome. JK SCIENCE.2009; 11( 2 ) :82-84.
 10. Haakova L, Cibula D, Rezabek K, Hill M, Fanta M and Zivny J. Pregnancy outcome in
women with PCOS and in controls matched by age and weight. Human Reproduction.2003
;18(7): 1438-1441.
 11.Cunningham FG, Macdonald P, Gant NF, Leveno KJ, Gilstrap LC. Hypertensive Disorders
in pregnancy Williams Obstetrics, 22nd edn; 2005:761-808
 12. Leon S ,Robert HG, Nathan GK. Chronic Anovulation & the Polycystic ovary . Clinical
Gynaecologic Endocrinology & Infertility, 6th edition. YEAR, pp.493-507

Thanks