THE STUDY OF GDM AMONG PREGNANT WOMEN WITH AND WITHOUT PCOS
A COHORT STUDY
Dissertation submitted to
THE TAMILNADU Dr. M.G.R MEDICAL UNIVERSITY
In partial fulfilment of the requirement for the award of
M.S.DEGREE – BRANCH – II
OBSTETRICS AND GYNAECOLOGY
GOVT. KILPAUK MEDICAL COLLEGE KILPAUK, CHENNAI.
MAY 2018
This is to certify that this dissertation entitled “GDM AMONG PREGNANT WOMEN WITH AND WITHOUT PCOS” is the bonafide original work of Dr. OVIYA. C under the guidance of Dr. K.L. MALARVIZHI MD., DGO., Professor and Head of Department of obstetrics and Gynaecology, KMCH, Chennai in partial fulfilment of the requirements for MS Obstetrics and Gynaecology branch II examination of Tamil Nadu Dr.MGR Medical university to be held in May 2018.The period of Postgraduate study and training is from June 2015 to May 2018.
Prof. DR.K.L.MALARVIZHI, M.D, DGO., Professor and Head,
Department of Obstetrics and Gynaecology, Kilpauk Medical College and Hospital, Chennai- 600010.
Prof. Dr. P. VASANTHA MANI M.D, DGO, MNAMS, DCPSY, MBA.,
The DEAN,
Governmant Kilpauk Medical College and Hospital, Chennai-600010
I solemnly declare that this dissertation “GDM AMONG PREGNANT WOMEN WITH AND WITHOUT PCOS was prepared by me at Government Kilpauk Medical College and Hospital, Chennai, under the guidance and supervision of Dr.K.L.MALARVIZHI, MD., DGO. Professor, Department of Obstetrics and Gynaecology, Government Kilpauk Medical College and Hospital, Chennai. This dissertation is submitted to The Tamil Nadu Dr.M.G.R. Medical University, Chennai in partial fulfillment of the University regulations for the award of the degree of M.S. (Obstetrics and Gynaecology).
Place: Chennai Dr. C. OVIYA Date:
I start this thesis in the name of Almighty God, the most beneficent and forgiving. I thank God for giving me the privilege to learn from the able teachers in my department.
I express my sincere thanks to Prof. Dr. P. VASANTHAMANI M.D, DGO, MNAMS, DCPSY, MBA., Dean, Government Kilpauk Medical College for allowing me to conduct the study using the available facilities.
I convey my heartfelt gratitude and sincere thanks to our HOD and my guide Dr. K.L. MALARVIZHI M.D., DGO, Department of Obstetrics and Gynaecology, Kilpauk Medical College for her constant support and guidance throughout the course of my study and who with her exhaustive knowledge and Professional expertise has provided able guidance and constant encouragement throughout the preparation of this dissertation.
I am grateful to my Assistant Professors, colleagues and my friends for their advice and suggestions.
My heartful thanks to my family and friends, who have been a constant source of encouragement and immense help, for instilling in me a sense of commitment and for their belief in me.
Last but not the least I thank all my Patients, who formed the backbone of this study without whom this study would not have been possible. I thank them all and also pray for their good health.
(Dr. C.OVIYA)
GDM - Gestational diabetes Mellitus PCOS - Polycystic ovarian syndrome
ACOG - American college of Obstetrics and Gynaecology RCOG - Royal college of Obstetrics and Gynaecology BMI - Body mass index
GA - Gestational age
T2DM - Type 2 Diabetes mellitus RMP - Regular menstrual period TSH - Thyroid stimulating hormone WHO - World health Organisation ADA - American Diabetes association
IADPSG - International association of the Diabetes and Pregnancy study groups
FPG - Fasting plasma glucose PPPG - Postprandial Plasma glucose OGCT - Oral glucose challenge test OGTT - Oral glucose tolerance test MNT - Medical nutrition therapy
ASRM - American society of Reproductive medicine
ESHRE - European society of Human Reproduction and Embryology LH - Leutinising hormone
SHBG - Sex hormone binding globulin OR - Odds ratio
HTN - Hypertension
OI - Ovulation induction IUD - Intrauterine death
S.NO TITLE PAGE NO.
1. INTRODUCTION 1
2. AIM OF THE STUDY 6
3. REVIEW OF LITERATURE 41 4. MATERIALS AND METHODS 44
5. RESULTS 47
6. DISCUSSION 72
7. SUMMARY 77
BIBLIOGRAPHY 79
ANNEXURE
MASTER CHART PROFORMA
INTRODUCTION GESTATIONAL DIABETES MELLITUS:
Gestational diabetes mellitus is defined as carbohydrate intolerance of variable severity with its onset or first recognition during pregnancy [ACOG 2013]. It is one of the common complications during pregnancy which affects both mother and the foetus. As Indians are more prone for developing diabetes mellitus especially south Indian universal screening is recommended. Joslin described a case of diabetes in 1916, which presented in pregnancy and resolves after delivery [1].
The incidence of Diabetes complicating pregnancy increased approximately from 40 percent between 1989 and 2004 (Getahun, 2008).
Worldwide its prevalence differs according to age, ethnicity, race, body composition, screening and diagnostic criteria. As pregnancy advances insulin resistance increases due to hormones secreted by placenta which necessitate compensatory increase in insulin secretion. Women with GDM ultimately develop overt diabetes in the ensuing 20 years. Baby of GDM mothers are more prone to develop obesity and diabetes in their future. Thus it is a vicious cycle of tr ansmitting glucose intolerance from one generation to another.
Polycystic ovarian syndrome is a metabolic disorder first described by Leventhal in1935, also known as Stein-Leventhal syndrome. It is the most common cause of hyperandrogenism, hirsutism and anovulatory infertility in the developed countries of which insulin resistance plays a key role.Classically the disorder is lifelong characterized by abnormal menses from puberty with acne and hirsutism arising in the teens. Insulin resistance is a condition in which the body cells do not respond to insulin.
As a result the level of glucose in the blood increases. This may cause more insulin to be produced by the body which in turn leads to diabetes.
Hyperinsulinemia has shown to increase androgen production by the ovaries which in turn may play a central role in the pathogenesis of PCOS[2].
PCOS women have multiple pregnancy complications like pre- eclampsia, preterm, spontaneous abortion in addition to gestational diabetes mellitus[3]. It has a strong hereditary basis, if the mother is suffering from PCOS 20% of chance the children will get and if the sister is suffering 40 % of chance that she will get PCOS. This condition requires a multidisciplinary modality to treat.
POLYCYSTIC OVARIAN SYNDROME AND GESTATIONAL DIABETES MELLITU S:
Both pregnancy and PCOS increases insulin resistance which make the pregnant women more prone to develop GDM.GDM has shown to complicate PCOS pregnant women compared to normal pregnancy.
Women with PCOS have increased risk and earlier onset of glucose abnormalities (two to three fold increased risk of GDM and four to six fold increased risk of T2DM independent of BMI)[4].
A cross –sectional study analysis from the Australian Longitudinal Study on women’s health reported that PCOS was associated with a higher risk of GDM independent of BMI[5].
AIM OF THE STUDY
• To evaluate the risk of GDM in pregnant women with and without PCOS.
• To evaluate other risks associated with PCOS pregnant women.
EPIDEMIOLOGY:
However the prevalence of GDM differs according to race, age, ethnicity and by screening and diagnostic criteria. The prevalence of GDM in India ranging from 3.8 to 21%.As of 2010, there were an estimated 22 million women with diabetes between the age group of 20 and 39 and an additional 54 million women in this age group with impaired glucose tolerance or pre-diabetes with the potential to develop GDM if they become pregnant. GDM found to be more prevalent in urban areas than in rural areas.
CARBOHYDRATE METABOLISM IN PREGNANCY:
In early pregnancy, the level of basal glucose and insulin remain unchanged, and the glucose tolerance is normal or slightly improved in normal pregnant women. The fasting blood glucose levels gradually fall to reach the nadir at the end of the first trimester, when they are 10-15 mg/dl lower than the non-pregnant state. With advancing gestation, the basal as well as postprandial insulin secretion increases progressively to reach almost twice the non-pregnant levels by third trimester [6]. This is paralled by an increased insulin resistance which peaks around 34-36 weeks. Thus normal pregnancy is characterized by mild fasting hypoglycaemia, postprandial hyperglycaemia and hyperinsulinemia.
Progesterone and oestrogen may act, directly or indirectly, to mediate this sensitivity. Higher levels may increase lipolysis and liberation of free fatty acids. Plasma concentration of triglycerides, free fatty acids and cholesterol are higher. Freinkel and colleagues (1985) have referred this pregnancy induced switch in fuel from glucose to lipids as accelerated starvation.
In women with gestational diabetes, although the insulin secretion and the basal production of glucose is same as in non-diabetic women, insulin is less effective in supressing gluconeogenesis( unlike non-diabetic pregnancies) and there is a marked increase in peripheral
resistance to insulin. This results in increased glucose levels, which have been directly correlated with the fetal weight, and other fetal and neonatal complications.
FETAL GLUCOSE METABOLISM:
Glucose crosses the placenta by facilitated transport. Maternal insulin does not cross the placenta and the fetus produces its own insulin from late first trimester. Pederson proposed a theory of “hyperglycaemic hyperinsulinsm” [7]. According to this maternal hyperglycaemia leads to fetal hyperglycaemia,which in turn stimulates fetal pancreatic β-cells hypertrophy leading to hyperinsulinemia.This fetal hyperinsulinemia is responsible for increased fat deposition, macrosomia, increased erthyropoietin production and decreased surfactant production.
POLYHYDRAMNIOS:
Abnormally increased amniotic fluid volume is termed as polyhydramnios. Using single vertical pocket the criteria for mild is 8 to9.9 cm, moderate is 10 to 11.9cm and severe hydmanios ≥12 cm. The amniotic fluid concentration is higher in diabetes women than in those without diabetes and it may correlate with amniotic fluid glucose concentration. Maternal hyperglycaemia causes foetal hyperglycaemia
with resulting foetal osmotic diuresis into the amniotic fluid compartment. Most of the GDM mothers have mild hydramnios.
But at present scenario many of the GDM patients with associated pre-eclampsia develops oligohydramnios.
SCREENING AND DIAGNOSIS:
Universal screening for GDM detects more cases and improves maternal and neonatal outcomes. Women of Asian origin, especially Indians are in high risk, so universal screening method is recommended.
CARPENTER AND COUSTON
ACOG (2011)
WHO/NICE (2008)
IADPSG/ADA (2012) 75g
OGTT
100g OGTT
100g OGTT
75g OGTT 75g OGTT
Fasting >95 >95 >95 ≥126 >92
1-h >180 >180 >180 >180
2-h >155 >155 >155 ≥140 >153
3-h >140 >140
Tamil Nadu endorses universal screening of all pregnant women at 12-14 weeks gestation or at first antenatal visit. If the reports are normal next screening is done at 24-28 weeks gestation and later at 32-34 weeks.
Diabetes in pregnancy study group in India(DIPSI) endorse the single step test recommended by WHO for diagnosis of GDM using a
75gm OGTT irrespective of the last meal with a threshold value of 2 hour post glucose ≥140 mg/dl.
METHOD:
• Single step testing using 75gm oral glucose & measuring plasma glucose 2 hour after ingestion.
• 75 gram glucose is to given orally after dissolving it in 300 ml water .The intake of the solution has to be completed within 5minutes.
• If vomiting occurs within 30 minutes of oral glucose intake. The test has to be repeated the next day if vomiting occurs after 30mins the test continues.
• The threshold plasma glucose level of ≥140 mg/dl is taken as cut-off for diagnosis of GDM.
MATERNAL RISK:
• Polyhydramnios
• Pre-eclampsia
• Prolonged labour
• Obstructed labour
• Caesarean section
• Uterine atony
• Postpartum haemorrhage
• Infection
• Instrumental delivery
Glycaemic abnormalities during pregnancy are associated with adverse pregnancy outcomes including increased rates of pre-eclampsia, induction of labour, caesarean delivery, shoulder dystocia and neonatal hypoglycaemia [8].
FETAL RISK:
• Spontaneous abortion
• Intrauterine death
• Stillbirth
• Congenital malformation
• Shoulder dystocia
NEONATAL RISK:
• Neonatal hypoglycaemia
• Infant respiratory distress syndrome.
• Hypocalcemia
• Hyperbillirubinemia
• Hypothermia
• Polycythemia
PRINCIPLES OF MANAGEMENT:
• Glycaemic control
• Antenatal care
• Timing of delivery
• Neonatal care
• Postpartum follow up
Glycaemic control:
Desired plasma glucose levels:
FPG<90 mg/dl PPPG <140 mg/dl Guiding principles:
• All pregnant women who test positive for GDM for the first time should be started on Medical nutrition therapy (MNT) for 2 weeks.
• After 2 weeks of MNT a 2hrs PPPG (post meal) should be done.
• If 2hr PPPG <120mg/dl .repeat test every 2 weeks in second trimester and every week in third trimester.
• If 2hr PPPG≥120 mg/dl with medical management insulin to be started as per the guidelines.
ANTENATAL CARE:
• In cases diagnosed before 20 weeks of gestation, a fetal anatomical survey by USG should be performed at 18-20 weeks.
• A fetal growth scan should be performed at 28-30 weeks gestation and repeated at 34-36 weeks gestation. There should be 3 weeks gap between the 2 ultrasounds and it should include fetal biometry and amniotic fluid estimation.
• In pregnant women with well controlled glucose level and if there is no complication should go for routine antenatal check up.
• In pregnant women having uncontrolled glucose level or any other complication, the frequency of antenatal visits should be increased to every 2 weeks in second trimester and every week in third trimester.
• Monitor for abnormal fetal growth (Macrosomia) and polyhydramnios.
• Monitor for hypertension, proteinuria and other obstetric complication.
• In pregnant women with GDM between 24-36 weeks of gestation and requiring early delivery antenatal steroids should be given.
• Term pregnant women should be educated regarding fetal kick count monitoring at home.
MEDICAL NUTRITION THERAPY:
• The cornerstone for treatment of women with gestational diabetes mellitus is nutritional therapy. Caloric restriction reduces the insulin resistance and brings down the blood sugar levels as a result.
• ADA recommends individualised nutritional counselling based on height and weight.
• ACOG suggests that carbohydrate intake be limited to 40 percent of total calories, 20% as protein and 40% as fat.
• Obese women with BMI> 30 kg/𝑚𝑚2 may benefit from 30 percent caloric restriction, which approximates 25 kcal/kg/day.
• Langer et al (2012) found that insulin was necessary to reduce excess birthweight in offspring of obese women with gestational diabetes.
• Dietary intervention is usually prescribed for two weeks with regular blood sugar monitoring. If target blood sugar values are not achieved in two weeks insulin is added.
EXERCISE:
ACOG recommends (2013), a moderate exercise program as part of the treatment plan for women with gestational diabetes. It increases insulin resistance by increasing the glucose uptake by muscles.
FETAL SURVEILLANCE:
• Fetal heart rate should be monitored by auscultation on each antenatal visits.
• Ultrasound monitoring is required every trimester.
• A fetal Echo is must at 24 weeks, especially in prediabetes to rule out cardiac defects.
• She should be explained about daily fetal activity assessment.
• Cardiotograph is reqiured during active labour. In those women with high dose insulin therapy fetal heart rate should be monitored continuously by cardiotocograph during active labour.
TIMING OF DELIVERY:
• GDM pregnancies are associated with delay in lung maturity of the fetus so routine delivery prior to 39 weeks is not recommended.
• Pregnant women with controlled plasma glucose has not already delivered spontaneously, induction of labour should be scheduled at or after 39 weeks pregnancy.
• In pregnant women with poor glycaemic control or those with risk factors like hypertensive disorder of pregnancy, previous still birth and other complications should be delivered earlier.
• Vaginal delivery should be preferred and LSCS should be done for obstetric indications only.
• In case of estimated fetal weight >4kg consideration should be given for primary caesarean section at 39 weeks to avoid shoulder dystocia.
INSULIN THERAPY:
• Preferable to start with premix insulin 30/70 of any brand.
Starting dose : 4 units before breakfast .Every 4th day increase 2 units till 10 units.
• If FPG remains> 90 mg/dl advised 6 units before breakfast and 4 units before dinner.
• Total insulin dose per day can be divided as 2/3 in morning and 1/3 in the evening.
• Initially if post breakfast plasma glucose is high start premix 50/50.If GDM is diagnosed in the third trimester MNT is advisable for a week. Insulin is initiated if MNT fails.
• If 2 hour postprandial > 200mg/dl at diagnosis, a starting dose of 8 units of premixed insulin could be administered before breakfast and the dose has to be titrated before follow up.
INSULIN ANALOGS:
Insulin is the drug of choice for diabetes in pregnancy. Insulin is a polypeptide hormone, which is synthesised as a precursor (pro- insulin) that undergoes proteolytic cleavage to form insulin and c-peptide.
Measurement of c-peptide levels is a better index of insulin levels. Being
a large molecule it does not cross the placenta. It should be administered subcutaneously.
a) Rapid acting insulin analogues-Lispro and aspart have been found to be useful in achieving the targeted postprandial glucose value during pregnancy.
b) Short acting human insulin
c) Intermediate acting insulin-NPH (isophane) Action profiles of commonly used insulin
Insulin type Onset Peak(hr) Duration(hr) Short acting
Lispro < 15 min 0.5-1.5 3-4
Glulisine < 15 min 0.5-1.5 3-4
Aspart < 15 min 0.5-1.5 3-4
Regular 30-60 min 2-3 4-6
Insulin type Onset Peak(hr) Duration(hr) Long-acting
Detemir 1-4 hr Minimal Up to 24
Glargine 1-4 hr Minimal Up to 24
NPH 1-4 hr 6-10 10-16
GLYCAEMIC CONTROL DURING LABOUR:
During labour it is essential to maintain good glycaemic control to avoid hyperglycaemia and neonatal complications
PLASMA GLUCOSE AND INSULIN/ IV FLUIDS
PLASMA GLUCOSE At the time of onset of labour
INSULIN/IV FLUIDS
< 70 mg/dl 5% GNS-100ml/hr
90-120mg/dl NS- 100 ml/hr
120-140 mg/dl NS- 100 ml/hr plus
4 units of regular insulin added with IV fluids
140-180 mg/dl NS- 100 ml/hr plus
6 units of regular insulin added with IV fluids
>180 mg/dl NS- 100 ml/hr plus
8 units of regular insulin added with IV fluids
DRIP RATE: 16 to 20 drops per minute. Maternal capillary blood glucose to be checked by glucometer every 1 hour and drip rate adjusted.
NEONATAL CARE:
• Should receive early breastfeeding to prevent hypoglycaemia.
• Newborn should be monitored for hypoglycaemia (capillary blood glucose <44mg/dl) .Monitoring should be started at 1hour of delivery and continued every 4 hours (prior to next feed)
• Neonate should be evaluated for other neonatal complications like respiratory distress, convulsions and hyperbillirubinemia.
POSTPARTUM FOLLOW UP:
• Maternal blood glucose levels usually return to normal after delivery.FPG and PPPG is performed on the third day of delivery.
• Advise her to do 75g OGTT at 6 weeks postpartum.
• Counselling about lifestyle modification, weight monitoring and exercise.
CONTRACEPTION:
Low dose hormonal contraceptives may be used safely by women with recent gestational diabetes. Intrauterine device and barrier methods are good options.
RECURRENT GESTATIONAL DIABETES:
According to Holmes et al (2010) recurrence was documented in 40 percent of women with gestational diabetes. Obese women were more likely to have impaired glucose tolerance in subsequent pregnancies.
Ehrlich and colleagues (2011) found that loss of at least two BMI units was associated with a lower risk of gestational diabetes in women who were overweight or obese in the first pregnancy.
METABOLIC SYNDROME:
Women with a history of gestational diabetes are also at risk for cardiovascular complications associated with dyslipidemia, hypertension and abdominal obesity-The Metabolic syndrome. Akinci et al (2009) reported that a fasting glucose level ≥ 100 mg/dl in the index OGTT was an independent predictor of the metabolic syndrome.
ORAL HYPOGLYCAEMIC AGENTS:
Both metformin and glyburide are appropriate as first line glycaemic control in women with gestational diabetes.
METFORMIN:
A randamosied controlled study found that women with GDM, metformin supplementation was not associated with increased perinatal complications.
Metformin has been useful in women with PCOS who failed to conceive. Hameed et al (2011) showed that the rate of spontaneous miscarriage and GDM decreases with continuous use of metformin throughout pregnancy.
GLIBENCLAMIDE:
Limited trials have shown that glyburide therapy in pregnancy had maternal and neonatal outcomes that were comparable with metformin.
PRE-EXISTING DIABETES MELLITUS:
The risk of serious adverse pregnancy outcomes such as congenital malformations, stillbirth, or neonatal deaths are three to five times greater in women with pre-existing diabetes compared to normoglycaemic women [9].
It is therefore recommended that pre-pregnancy counselling should be offered to all diabetic women and that unplanned pregnancies must be
avoided. Pregnancy is contraindicated when HbA1c is >10%.Folic acid supplement should be commenced at a dose of 5mg/day.
CRITERIA FOR DIAGNOSIS OF DIABETES: (ADACRITERIA)
• HbA1c ≥ 6.5%
• FPG ≥ 126mg/dl (Fasting defined as no caloric intake for atleast 8 hrs)
• 2-hr plasma glucose ≥ 200mg//dl during 75g OGTT (WHO criteria)
• Random plasma glucose ≥ 200 mg/dl.
POLYCYSTIC OVARIAN SYNDROME
PCOS is the most common endocrine disorders in women of reproductive age group affecting 5 to 10 % worldwide. It is inherited as a complex genetic trait. Frequently associated with Insulin resistance and obesity. Obesity occurs in more than 50 % of patients with PCOS and there is an increased risk of Diabetes Mellitus and cardiovascular disease.
Clasically this disorder is lifelong, characterised by abnormal menses from puberty with acne and hirsutism arising in the teens. It may arise in adulthood, concomitant with the emergence of obesity, presumably because this is accompanied by the increasing hyperinsulinemia.
However lean women with PCOS also exhibits more insulin resistance than obese.
DIAGNOSTIC CRITERIA:
1. NATIONAL INSTITUTES OF HEALTH CRITERIA (1990):
This criteria was developed first for diagnosing PCOS. Must include all of the following:
• Hyperandrogenism
• Anovulation or oligo-ovulation
• Exclusion of possible related disorders.
Presence of polycystic ovaries is not necessary for diagnosing PCOS.
2. ESHRE/ASRM [ROTTERDAM CRITERIA]:2003
Presence of two of three criteria is sufficient to diagnosis PCOS.
• Menstrual cycle abnormalities (amemorrhea,oligomenorrhea)
• Clinical or biochemical hyperandrogenism.
Clinical hyperandrogenism includes hirsutism, male pattern alopecia and acne.
• Ultrasound appearance of polycystic ovaries after all other diagnosis are ruled out.(congenital adrenal hyperplasia, androgen secreting tumor, Cushing’s syndrome). The sonographic criteria for PCO requires the presence of 12 or more follicles in either ovary measuring 2 to 9 mm in diameter and/or increased ovarian volume (>10 ml)
3. ANDROGEN EXCESS AND PCOS SOCIETY (2006):
Requires all of the following:
• Hyperandrogenism
• Ovarian dysfunction
• Exclusion of possible related disorders.
This criteria emphasizes that PCOS diagnosis should not be made without the evidence of hyperandrogenism.
PATHOLOGY:
Macroscopically, ovaries in women with PCOS are two to five times the normal size. Cross section shows thickened cortex with multiple cysts,there is increase in the number of follicles with lutenized theca interna. Microscopically, the superficial cortex is fibrotic and hypocellular.
PATHOPHYS IOLOGY:
Abnormalities in four endocrinologically active compartments:
1. The Ovaries 2. The adrenal gland 3. The periphery (Fat)
4. The hypothalamus-pituitary compartment
Kim et al (2008) have focused genetic studies on androgenic factors in regard to possible PCOS etiology such as investigating polymorphism and CAG repeats in androgen receptors.
Insulin resistance results in a compensatory hyperinsulinemia, which in turn stimulates ovarian androgen production in an ovary which are genetically predisposed to PCOS .Arrest of follicular development (red
“X”) and anovulation could be caused by the abnormal secretion of gonadotrophins such as follicle stimulating hormone or leutinising hormone, intraovarian androgen excess, direct effects of insulin, or a combination of these factors. Insulin resistance, in concert with genetic factors, may also lead to hyperglycaemia and an adverse profile of cardiovascular factors.
Ovarian compartment:
Dysregulation of CYP17, the androgen forming enzyme in both the adrenals and the ovaries, may be one of the pathogenetic mechanisms underlying hyperandrogenism in PCOS. The increased testosterone level in patient with PCOS are considered ovarian in origin. Ovarian hyperandrogenism are contributed by ovarian stoma, theca, granulosa and are stimulated by LH. This hormones causes this by
• Total and free testosterone level correlates directly with LH levels.
• As a result of CYP17 dysregulation ovaries are more sensitive to gonadotrophic stimulation.
• Treatment with GnRH agonist effectively suppresses serum testosterone and androstenedione levels.
The peripheral compartment:
• Activity of 5 alpha reductase in skin determines the presence or absence of hirsutism.
• Peripheral aromatization is increased with increased body weight.
• Estrone levels are increased as a result of peripheral aromatisation of androstenedione.
The Hypothalamic pituitary compartment:
• Increase in LH pulse frequency
• Elevated LH and LH to FSH ratio
• FSH is not increased with LH
• Mildly elevated prolactin levels.
Genes involved in PCOS:
• Insulin resistance –related genes
• Genes that interfere with the biosynthesis and the action of androgens
• Genes that encode inflammatory cytokines
Characteristic features in PCOS women:
INSULIN RESISTANCE:
Patients with PCOS exhibit insulin resistance and hyperinsulinemia. Insulin resistance and hyperinsulinemia produces the ovarian steroidogenic dysfunction of PCOS. Insulin resistance may eventually lead to the development of hyperglycaemia and type 2diabetes mellitus .About one-third of obese PCOS patients have impaired glucose tolerance and 7.5% to 10% have type 2diabetes mellitus.
Insulin in collaboration with LH enhances the androgen production of theca cells, inhibits hepatic synthesis of SHBG, thus increasing the proportion of free testosterone, there by plays a role in the pathogenesis of hyperandrogenism.
Thus PCOS patients are already in a state of insulin resistance which makes them more prone for gestational diabetes mellitus comparing to a normal pregnant women.
The fasting glucose to insulin ratio is determined and value less than 4.5 indicate insulin resistance. Using the 2 hour GTT with insulin levels, 10 % of non obese and 40 % and to 50% of obese PCOS women have impaired glucose tolerance or overt type 2diabetes mellitus.
WHO CRITERIA:
TWO HOUR GLUCOSE TOLERANCE TEST NORMAL RANGES: (WHO CRITERIA, after 75 gm glucose load)
Fasting 64 to128 mg/dl
One hour 120 to 170 mg/dl
Two hour 70 to 140 mg/dl
TWO HOUR GLUCOSE VALUES FOR IMPAIREDGLUCOSE TOLERANCE AND TYPE 2 DIABETES (WHO CRITERIA, after 75 gm glucose load)
Normal <140 mg/dl
Impaired =140 to 199 mg/dl
Type 2 Diabetes mellitus ≥200mg/dl
The prevalence of IGT in the age group of 20-29 years and 30-39 years is 12.2% and 15.3 % as reported by our national survey [10].
Clinical Features that suggest insulin resistance:
• BMI > 27 kg/m²
• Waist to hip ratio > 0.85
• Waist > 100 cm
• Acanthosis nigricans
• Skin tags
ACANTHOSIS NIGRICANS:
Acanthosis nigricans is a reliable marker of insulin resistance in hirsute women. This thickened, pigmented, velvety skin lesion is most often found in the vulva and also in axilla, over the nape of the neck, below the breast and on the inner thigh. These patients often have fasting insulin levels of greater than 25µIU/ml (normal <20 to 24µIU/ml) and maximum serum insulin responses to glucose load (75gm) exceeding 300µIU/ml (normal at 160µIU/ml: at 2hours post glucose load)
HIRSUTISM:
It is defined as excessive growth of terminal hair in a male distribution. Most common cause of hyperandrogenism and hirsutism is polycystic ovarian syndrome.The severity of hirsutism is calculated by using Ferriman Gallway scoring system.
The prevalence of hirsutism was estimated to be 13%,acne 26%,menstrual disorder 28%,obesity19% and infertility 8% (Meta- analysis in Iranian women).
FERRIMAN-GALLWEY HIRSUTISM SCORING SYSTEM:
0- No score 4-Frankly virile
Hirsutism score Number
Non hirsute <8
Mild 8-16
Moderate 17-25
Severe >25
USG FINDINGS:
Typical USG finding is pearl necklace pattern. Points for diagnosis are
• Peripheral location of cysts
• Ovarian size (>10 cc)
• Follicles of similar size
• Hyper-echoic central stroma.
• ≥ 12 follicles of 2-9 mm in diameter in atleast one ovary.
WEIGHT REDUCTION:
It is the initial recommendation in patients with accompanying obesity as it reduces insulin, SHBG and androgen levels and may restore ovulation either alone or in combination with ovulation induction drugs.
Weight loss of even 5 to 7 % may decrease free testosterone level and restore ovulation and fertility in more than 75 % of women.
ORAL CONTRACEPTIVES:
OCPs decrease adrenal and ovarian production of androgen and reduce hair growth in nearly two thirds of hirsute people.
• Progestin component suppresses LH, thereby decreasing ovarian androgen production.
• Estrogen component increases hepatic production of SHBG, resulting in free testosterone concentration.
• Circulating androgen levels are reduced.
• Estrogen also decreases the conversion of testosterone to DHT in the skin by inhibiting 5 alpha - reductase.
METFORMIN:
It is an oral biguanide antihyperglycaemic drug used extensively for type 2 diabetes. It is a pregnancy category B drug. It lowers blood glucose mainly by inhibiting hepatic glucose production and by enhancing peripheral glucose uptake.
Used mainly to treat oligo-ovulatoryinfertility,hyperandrogenism and insulin resistance in PCOS patients. Used in combination with dietary restriction or either alone. The incidence of ovarian hyperstimulation is reduced with adjuvant metformin in PCOS at risk.
INFERTILITY:
It is defined as one year of unprotected intercourse without pregnancy. PCOS is the most common cause of anovulatory infertility.
One study states that prevalence of infertility was 72% in women with PCOS compared to 16% with women without PCOS [11].Tobias et al (2013) suggests that infertility associated with ovulatory disorder and tubal blockage increases the risk of GDM.
CLOMIPHENE CITRATE:
It is considered as a first line of treatment for anovulation infertility. Over a period of 6 months it results in 49 % ovulation, 23.9%
pregnancy and 22.5 % livebirth rates in women with anovulatory infertility [12].
Clomiphene citrate is a selective oestrogen receptor modulator that mimics the activity of oestrogen antagonist when given at typical pharmacological doses for the induction of ovulation. It binds and blocks oestrogen receptor in the hypothalamus for prolonged periods thereby decreases the normal ovarian –hypothalamic oestrogen feedback loop.
Given as a 50 mg tablet from day 2 to 6, 3 to 7, 5 to 9 of the menstrual cycle.
METABOLIC SYNDROME DIAGNOSTIC CRITERIA:
Female waist >35 inches
Triglycerides >150 mg/dl
HDL <50 mg/dl
Blood pressure >130/85 mm Hg
Fasting glucose 110-126 mg/dl
Two-hour glucose(75gm OGTT) 140-199 mg/dl
Long term risks:
• Hypertension
• Diabetes
• Cardiovascular disease
• Cancer
• Depression and mood disorder
Androgen excess and polycystic ovary syndrome (AE-PCOS) society recommends the following monitoring activities to assess cardiovascular risks and prevent disease in patients with PCOS.
• Waist circumference and BMI measurement at every visit, using the national health and nutrition examination survey method.
• A complete lipid profile using American heart association guidelines. If the fasting serum lipid profile is normal it should be reassessed every 2years or sooner if weight gain occurs
• A 2 hour post 75 –g oral glucose challenge measurement in PCOS women with a BMI greater than 30 kg/m² or alternatively in lean PCOS women with advance age ( 40 years),personal history of gestational diabetes or family history of type 2 diabetes.
• Blood pressure measurement at each visit. Ideal is 120/80 or lower.
• Regular assessment of depression, anxiety and quality of life.
REVIEW OF LITERATURE
In a field study in Tamil Nadu performed under Diabetes and pregnancy-Awareness and Prevention project, screened in urban, semi- urban, rural areas, the prevalence of GDM was found to be 17.8% in the Urban, 13.8% in the semi-urban and 9.9% in the rural areas. The incidence of GDM is expected to increase to 20% i.e. one in every 5 pregnant women is likely to have GDM.
The prevalence of GDM in PCOS in the literature varies between 0.15% to 12.3% .Women with PCOS also have increased risk of pregnancy complications like miscarriages, foetal anomalies and hypertension in pregnancy.
According to the previous studies, PCOS is associated with an OR of 2.32 (95% CI, 1.88-2.88) in GDM; OF 1.45(95% CI,1.24-1.69) in pre- eclampsia, and of 2.21(95% CI, 1.69-2.90) in preterm birth [13,14]
HAPO (Hyperglycaemia and adverse pregnancy outcomes) study is a cohort study which studied the association between non-diabetic maternal hyperglycaemia and adverse perinatal outcomes. This study shows that maternal hyperglycaemia is associated with increased birth weight and increased cord blood serum C-peptide. There is a significant but weaker association with hypoglycaemia, primary caesarean section,
preterm delivery, intensive neonatal care, hyperbillirubinemia, pre- eclampsia and shoulder dystocia and birth injury.[15]
S No Author, Journal
Objective Methodology Results 1 Biomed
research
international(20 13,China)Yunhu i
Wang,Xiaomiao Zhhao,Huidan Zhao,Hong Ding
To evaluate pregnancy outcomes and its determinants in women with polycystic ovary syndrome
220 pregnant PCOS and 594 healthy women were followed from early pregnancy.
Incidence of GDM was determined.
The incidence of GDM was notably higher among all PCOS
combined(54.9%:OR :2.9,95% CI:2.0-5.4) compared with controls(14.3%;
P<0.001) 2 Journal of
reproductive medicine(2013,I ndia)P.R.Jirgee, S.Chougule,S.K adam
To compare the occurrence of various
complications in women with PCOS and without PCOS conceived through ART.
69 pregnant women were followed up in a prospective observational study
The incidence of GDM was 27.5% in PCOS compared with non PCOS pregnant women (2.63%)
3 Human
reproduction(20 01,Finland)M.M ikola,V.Hiilesm aaM.Halttunen, L.Suhonen and A.Tiitinen
To evaluate the obstetric outcome in women with PCOS
99 pregnancies were
retrospectively evaluated in women with PCOS and the findings were compared with an unselected control population
GDM developed in 20% of PCOS patients and in 8.95 of controls.
4 Amita
Gupta,Kapila Raina,Taina Kalkkar,Yudhist er Veer,
International journal of scientific research, (2009,India)
To compare the pregnancy outcome, especially the prevalence of GDM in a group of patients with PCOS with a group of healthy weight matched women
56 pregnant women with PCOS compared with a group of age and weight matched controls.
Prevalence of GDM was 14.2% as compared with age and weight matched controls 3.5%
5. Dhananjayan R,Swaminathan S, International journal of scientific research 2016)India
To evaluate the effect of polycystic ovaries on GDM and infertility.
This review article in short highlights the research findings during the last decade on the prevalence, diagnosis, outcome measures linking PCOS,GDM and infertility
Pregnant women with a history of infertility and PCOS were at increased risk of developing GDM
6. Veltman- Verhulst,Van Haeften TW,De valk HW
To evaluate whether SHBG levels before conception are predictive of GDM in women with PCOS
A total of 50 pregnant women with PCOS were enrolled and followed up during pregnancy
of the 50women, 42%(21) were diagnosed with GDM
7. Saeeda Bibi,Uroo Saleem,Naheed mahsood (2015)JPMI
To find out the frequency of GDM and to explore associated risk factors
Cross sectional study conducted in women pregnant females coming for their routine check up after 24 weeks till 28 weeks
In this study half of the patients with GDM have history of Polycystic ovarian syndrome.
8. Toulis KA,Goulis DG,Papadimas Fertility and sterility (2008)
To evaluate the risk of GDM in women with PCOS
Systematic review and meta analysis of observational studies.721withh PCOS and 4572 controls without PCOS.
Women with PCOS demonstrated a significantly higher risk for the
development of GDM as compared with women without GDM
9. Prof CN Wijeyaratne,R Waduge, D Arandara, A Arasalingam, A Sivasuriam.
BJOG :An International journey of Obstetrics &
Gynaecology (2006)
To find out the risk of
metabolic syndrome and polycystic ovary
syndrome in a cohort of indigenous south asian women with a recent history of GDM
Case control study conducted in 274 indigenous Sri lankan women with previous GDM and 168 ethinically matched GDM
Women with
previous GDM were more likely to have hypertension (17.6
% versus 7.4%), hypertriglyceridaemi a (16.9 % versus 5.9%), larger mean interval waist circumference, 49%
had metabolic syndrome, 58 % had polycystic
ovaries.The prevalence of metabolic syndrome and PCOS is higher in those with previous GDM.
MATERIALS AND METHODS Type of study:
Cohort study Period of study:
January 2017 to August 2017 Place of study:
Antenatal outpatient department, antenatal ward, labour ward, Department of Obstetrics and Gynaecology,
Govt Kilpauk Medical College & Hospital,Chennai.
Sample size: 202
Ethical committee approval: Obtained Consent: Informed consent obtained.
Financial support: Nil Inclusion criteria:
Study group:
Pregnant women with PCOS aged 20-35 yrs registered /admitted before 20 weeks of gestation.
Healthy Pregnant women aged 20-35 yrs registered /admitted before 20 weeks of gestation.
Exclusion criteria:
1. Known diabetic women.
2. Women suffering from chronic illnesses 3. Twin pregnancy.
4. Women conceived after ART techniques.
Method of the study:
1. All pregnant patients attending Antenatal OPD and admitted in labour ward with PCOS who satisfy the eligibility criteria will be included till the sample size is reached and compared to equal number of healthy pregnant women without PCOS before 20 weeks of gestation and followed up till 38 weeks of gestation.
2. After getting consent from the patient 75 grams of glucose mixed with 300 ml of water is given to the patient and two of venous blood will be withdrawn after a period of two hours for blood sugar irrespective of the last meal or fasting status.
3. Detailed history regarding the symptoms of PCOS, when and how they got diagnosed will be elicited.
4. General examination including features of hyperandrogenism, insulin resistance will be elicited.
5. History regarding infertility, previous history of GDM, anomalous baby, recurrent abortion and history of LGA babies will be elicited.
6. Obstetrics examination will be performed.
7. Diabetology opinion will be obtained for the diagnosed cases and they will be treated according to their advice.
8. Phone number of the patients will be obtained.
Benefits of the study:
1) To find the risk of GDM in PCOS pregnant women.
2) To find out the other complications associated with GDM.
3) To find out other associated complications in PCOS pregnant women.
4) Creating awareness in non pregnant women wanting to become pregnant regarding earlier interventions to prevent or ameliorate GDM and in pregnant women with PCOS for earlier check up.
RESULTS Statistical methods:
What is the primary outcome variable:
Secondary outcome variable Primary explanatory variable Other explanatory variables
Descriptive analysis: Descriptive analysis was carried out by mean and standard deviation for quantitative variables, frequency and proportion for categorical variables. Data was also represented using appropriate diagrams like bar diagram, pie diagram and box plots.
Inferential statistics:
Quantitative outcome;
The association between categorical explanatory variables and quantitative outcome was assessed by comparing the mean values. The mean differences along with their 95% CI were presented. Independent sample t-test was used to assess statistical significance.
Categorical outcome:
The association between explanatory variables and categorical outcomes was assessed by cross tabulation and comparison of percentages.
Odds ratio along with 95% CI is presented. Chi square test was used to test statistical significance.
P value < 0.05 was considered statistically significant. IBM SPSS version 22 was used for statistical analysis.(1)
1. Machines IB. IBM SPSS Statistics for Windows, Version 22.0.
IBM Corp Armonk, NY; 2013.
Table 1.1: Association of Group with Demographic parameters of study population (N=198)
Demographic parameters
Group
Chi square P-value
Normal PCOS
Age group
Up to 24 48 (48.48%) 39 (39.39%)
1.661 0.436 25 to 29 40 (40.4%) 47 (47.47%)
30 and above 11 (11.11%) 13 (13.13%)
Out of 198 study population only 11 % of people belong to more than 30 years of age with mean age between 25 years of age in both normal pregnant women and PCOS pregnant women.
Table: 1.12 Association of GDM positive pregnant women with that of age
Age limit Normal PCOS
< 25 4(44 %) 7(36%)
≥ 25 5 (55%) 12(64%)
64%( 12) of PCOS pregnant women who developed GDM were more than 25 years of age while 55 %(5) of normal pregnant women who developed GDM were more than 25 years of age.
Table 1.13: Comparison of mean of age between the study population (N=198)
Parameter
Mean ±SD
P value Normal (N=99) PCOS (N=99)
Age 25.06 ± 3.61 25.58 ± 3.35 0.299 Table 1.2:
Education
Non educated 12 (12.12%) 13 (13.13%)
0.058 1.000 Primary 29 (29.29%) 28 (28.28%)
Secondary 36 (36.36%) 36 (36.36%) Higher
secondary 11 (11.11%) 11 (11.11%) Degree 11 (11.11%) 11 (11.11%)
Out of 198 study population 12 % of the population have no education and 11 % of the population have completed their degrees.
Table 1.3:
Socio Economic status
3rd class 8 (8.08%) 10 (10.1%)
3.166 0.205 4th class 81 (81.82%) 71 (71.72%)
5th class 10 (10.1%) 18 (18.18%)
Most of our study population belongs to socioeconomic class 4.
Table 2: Comparison of mean of BMI between the study population (N=198)
Parameter
Mean ±SD
P value Normal (N=99) PCOS (N=99)
BMI 25.36 ± 4 26.75 ± 4.55 0.024
Most of our study population belongs to a mean BMI of 25 kg/m²
Table 2.1: Association of GDM positive pregnant women with that of BMI
BMI Normal PCOS
≤ 25 4(44%) 8 ( 42%)
>25 5(55%) 11(58%)
58 % of PCOS pregnant women who developed GDM have BMI
>25 while 55 % of normal pregnant women who developed GDM have BMI > 25
Table 3: Association of Group with Obstetric parameters of study population (N=198)
Obstetric parameters
Group Chi
square P-value
Normal PCOS
Gravida
1 50 (50.51%) 72 (72.73%)
11.802 0.008 2 34 (34.34%) 22 (22.22%)
3 14 (14.14%) 5 (5.05%)
4 1 (1.01%) 0 (0%)
Para
0 54 (54.55%) 79 (79.8%)
15.929 <0.001 1 37 (37.37%) 19 (19.19%)
2 8 (8.08%) 1 (1.01%)
Number of living children
0 57 (57.58%) 81 (81.82%)
14.905a <0.001 1 35 (35.35%) 17 (17.17%)
2 7 (7.07%) 1 (1.01%)
Number of previous Abortion
0 86 (86.87%) 90 (90.91%)
1.620 0.655
1 10 (10.1%) 7 (7.07%)
2 2 (2.02%) 2 (2.02%)
3 1 (1.01%) 0 (0%)
Most of our PCOS pregnant women 72% are Primigravida comparing to normal pregnant women of these 50% primigravida.
History of previous abortion is almost same in both groups.
Table 4: Comparison of mean of GA in weeks between the study population (N=198)
Parameter
Mean ±SD
P value Normal (N=99) PCOS (N=99)
GA weeks 13.12 ± 4.44 12.11 ± 2.86 0.059
Our study population belongs to a mean GA of 12 to 13 weeks of amenorhea. Thus GA does not play any significant role in the development of GDM.
Table 5: Association of Group with GDM of the study population (N=198)
GDM ( any OGCT
positive)
Group
Chi square
P- value
Normal PCOS
Positive 9 (9.09%) 19 (19.19%)
4.160 0.041 Negative 90 (90.91%) 80 (80.81%)
9 % of normal pregnant women develop GDM and 19 % of PCOS pregnant women develop GDM.
This pie chart shows a twofold increased risk of GDM in PCOS pregnant women
0 10 20 30 40 50 60 70 80 90 100
NORMAL PCOS
GDM NO GDM
Table 5.1: Trimester wise OGCT level in diagnosed GDM of the study population (N=28)
OGCT 1 OGCT 2 OGCT 3 TOTAL
Normal 3(33.3%) 3(33.3%) 3(33.3%) 9 PCOS 3(15%) 6(31.5%) 10(52.6%) 19
In that 9 normal pregnant women who develop GDM 3 have increased OGCT in their first trimester, 3 in second trimester and 3 in third trimester.
In that 19 PCOS pregnant women who develop GDM 3 have increased OGCT in their first trimester, 6 in second trimester and 10 in third trimester. As insulin resistance increases the incidence of GDM in PCOS pregnant women also increases. In other words as pregnancy advances the incidence of GDM also increases.
Table 6: Association of Group with TSH of study population (N=198)
TSH Group Chi
square
P- value
Normal PCOS
Increased 5 (5.05%) 10 (10.1%)
1.803 0.179 Normal 94 (94.95%) 89 (89.9%)
10 % of PCOS pregnant women develop hypothyroidism while 5% of normal pregnant women develop hypothyroidism.
Table 6.1: Association of GDM with TSH of Normal (N=99)
TSH GDM Chi
square P-value Positive Negative
Increased 2 (22.22%) 3 (3.33%)
6.087 0.014 Normal 7 (77.78%) 87 (96.67%)
Out of 5 normal pregnant women who develop Hypothyroidism 2(22%) developed GDM also.
Table 6.2: Association of GDM with TSH of PCOS (N=99)
TSH
GDM Chi
square P-value Positive Negative
Increased 5 (26.32%) 5 (6.25%)
6.808 0.009 Normal 14 (73.68%) 75 (93.75%)
Out of 10 PCOS pregnant women who develop hypothyroidism 5(26%) have GDM.
Table 7: Association of Group with Mode of delivery of study population (N=198)
Mode of delivery
Group Chi
square
P- value
Normal PCOS
FORCEPS 0 (0%) 1 (1.01%)
15.654 0.001 LSCS 17 (17.17%) 6 (6.06%)
NIL 56 (56.57%) 80 (80.81%) NVD 26 (26.26%) 12 (12.12%)
Both LSCS and normal vaginal delivery rates were quite higher in normal pregnant women since most of our PCOS pregnant women are primigravidas as most of them suffered from primary infertility.
Table 8: Association of Group with PIH of study population (N=198)
PIH Group Chi
square
P- value
Normal PCOS
Yes 6 (6.06%) 14 (14.14%)
3.560 0.059 No 93 (93.94%) 85 (85.86%)
Out of the 198 study population 6% normal pregnant women develop PIH and 14% PCOS pregnant women develop PIH.
Table 8.1: Association of GDM with PIH of NORMAL (N=99)
PIH
GDM Chi
square P-value Positive Negative
Yes 1 (11.11%) 5 (5.56%)
0.444 0.505 No 8 (88.89%) 85 (94.44%)
Out of the 6 normal pregnant women who develop PIH only one person (11%) have GDM.
Table 8.2: Association of GDM with PIH of PCOS (N=99)
PIH
GDM Chi
square P-value Positive Negative
1 4 (21.05%) 10 (12.5%)
0.925 0.336 2 15 (78.95%) 70 (87.5%)
Out of 14 PCOS pregnant women who develop PIH 4 person (21 %) have GDM.
Table 9: Association of Group with RMP and with pain of study population (N=198)
Parameters Group Chi
square
P- value
Normal PCOS
RMP
Yes 91 (91.92%) 16 (16.16%)
114.383 <0.001
No 8 (8.08%) 83 (83.84%)
with pain
Yes 97 (97.98%) 15 (15.15%)
138.222 <0.001
No 2 (2.02%) 84 (84.85%)
91 % of normal pregnant women have h/o regular cycles while only 16 % of PCOS women have h/o regular cycles. 97 % of normal pregnant women have h/o dysmenorrhea while only 15% PCOS women have dysmenorrhea.
Table 10: Association of Group with acne and hirsutism of the study population (N=198)
Parameter Group Chi
square
P- value
Normal PCOS
Acne
Yes 4 (4.04%) 53 (53.54%)
59.151 <0.001
No 95 (95.96%) 46 (46.46%)
Hirsutism
Yes 1 (1.01%) 57 (57.58%)
76.469 <0.001
No 98 (98.99%) 42 (42.42%)
4 % normal pregnant women have h/o acne while 53 % of PCOS women have h/o acne. 1% normal pregnant women have hirsutism while 57 % PCOS women have hirsutism.
Table 11: Association of Group with DM and HTN in family history of study population (N=198)
Family history
Group Chi
square
P- value
Normal PCOS
Diabetes Mellitus
Yes 15 (15.15%) 36 (36.36%)
11.647 <0.001
No 84 (84.85%) 63 (63.64%)
Hypertension
Yes 12 (12.12%) 19 (19.19%)
1.874 0.171
No 87 (87.88%) 80 (80.81%)
15 % of normal pregnant women have h/o diabetes mellitus in family while 36% of PCOS pregnant women have h/o DM in family.
12 % of normal pregnant women have h/o hypertension in family while 19 % of PCOS pregnant women have h/o hypertension in family members.
Table 11.11: Association of GDM with DM in family history of NORMAL (N=99) DM in family
history
GDM Chi
square P-value Positive Negative
Yes 3 (33.33%) 12 (13.33%)
2.546 0.111 No 6 (66.67%) 78 (86.67%)
Out of 15 % normal pregnant women who have h/o diabetes mellitus only 3 person have GDM.
Table 11.12: Association of GDM with HTN in family history of NORMAL (N=99)
HTN in family history
GDM Chi
square P-value Positive Negative
Yes 2 (22.22%) 10 (11.11%)
0.948 0.330 No 7 (77.78%) 80 (88.89%)
Out of normal pregnant who have h/o hypertension 2 person develop GDM.
Table 11.21: Association of GDM with DM in family history of PCOS (N=99)
DM in family history
GDM Chi
square
P- value Positive Negative
Yes 16 (84.21%) 20 (25%)
23.261b <0.001 No 3 (15.79%) 60 (75%)
Out of 36 PCOS pregnant women who have h/o DM in family 16 person (44%) develop GDM.
Table11.22: Association of GDM with HT in family history of study population (N=99)
HT in family history
GDM Chi
square P-value Positive Negative
Yes 8 (42.11%) 11 (13.75%)
7.960 0.005 No 11 (57.89%) 69 (86.25%)
Out of 19 PCOS pregnant women who have h/o hypertension 8 person (42%) have GDM.
Table 12: Association of Group with OI of study population (N=198)
OI Group Chi
square
P- value
Normal PCOS
Yes 1 (1.01%) 44 (44.44%)
53.174 <0.001 No 98 (98.99%) 55 (55.56%)
1% of normal pregnant women had h/o ovulation induction while 44% PCOS population had h/o ovulation induction.
Table 13: Association of Group with OHA of study population (N=198)
OHA Group Chi
square
P- value
Normal PCOS
Yes 0 (0%) 37 (37.37%)
45.503 <0.001
No 99 (100%) 62 (62.63%)
None of the normal pregnant women had h/o oral hypoglycaemic agent intake while 37% of PCOS women had h/o OHA intake.
Table 14: Association of Group with Scan of study population (N=198)
Scan Group Chi
square
P- value
Normal PCOS
Yes 0 (0%) 84 (84.85%)
145.895 <0.001
No 99 (100%) 15 (15.15%)
84 % of PCOS pregnant women had scan findings suggestive of PCOS while none of normal pregnant women had so.
Table 15: Association of Group with Preterm of study population (N=198)
Preterm Group Chi
square
P- value
Normal PCOS
Yes 4 (4.04%) 6 (6.06%)
0.421 0.516 No 95 (95.96%) 93 (93.94%)
Both normal and PCOS pregnant women had 4 to 6% of preterm births.
Table 16: Association of Group with Polyhydramnios of study population (N=198)
Poly Group Chi
square
P- value
Normal PCOS
Yes 7 (7.07%) 23 (23.23%)
10.057 0.002 No 92 (92.93%) 76 (76.77%)
23 % of PCOS pregnant women have polyhydramnios while 7% of normal pregnant women have polyhydramnios.
Table 17: Association of Group with Weight reduced of study population (N=198)
Weight reduced
Group Chi
square
P- value
Normal PCOS
Yes 2 (2.02%) 26 (26.26%)
23.960 <0.001 No 97 (97.98%) 73 (73.74%)
26 % of PCOS pregnant women had h/o weight reduction preconceptionally while 2 % of normal pregnant women had so.
Table 18: Association of Group with Big baby of study population (N=198)
Big baby Group Chi
square
P- value
Normal PCOS
Yes 2 (2.02%) 3 (3.03%)
0.205 0.651 No 97 (97.98%) 96 (96.97%)
Both normal and PCOS pregnant women had similar rates of big baby.
