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 Journal of Reproduction & Contraception  doi: 10.7669/j.issn.1001-7844.2014.03.0133

2014 Sep.; 25(3):133-145 E-mail: randc_journal@163.com

Study on the Clinical and Endocrine Characteristics of Poly-

cystic Ovary Syndrome with Different Ovarian Morphology

Zhi-ping HU, Tian-shu PANG, Ying WANG, Jie QIAO, Mei-zhi LI

 Reproductive Medical Center, Peking University Third Hospital, Beijing 100191, China

Objective  To evaluate the differences of the clinical manifestation and endocrine

 situation in patients with different ovarian morphology of polycystic ovary syndrome

(PCOS).

 Methods   A total of 234 PCOS patients were enrolled according to the ovary

morphology and divided into three groups: 112 patients with B-polycystic ovary mor-

 phology ( both two ovaries were PCOM, B- PCOM), 50 with U-PCOM (only one ovary was

 PCOM) and 72 with N-PCOM (none was PCOM). There were 39 inferti le women

without PCOS as control group. Data were analyzed by using SPSS 15.0 software.

 Results  There was no statistical difference in body mass index (BMI) among the three

 groups of PCOS. The endometrial thickness increased in patients with B-PCOM and decreased with N-PCOM. The levels of testosterone, androstenedione and luteinizing 

hormone increased in PCOS groups, especially in N-PCOM patients. HOMA-IR

increased, HOMA- β  , disposition index (DI) and ∆ I 60 / ∆G60 decreased in patients with N-

 PCOM compared with in B-PCOM and U-PCOM groups. Higher level of total choles-

terol (TC) and lower level of high-density lipoprotein (HDL)-C existed in PCOS patients,

especially in N-PCOM. There were positive correlations between oligo-anovulation,

endometrial thickness, LH/FSH ratio, fasting insulin (FINS), the area under curve of 

 glucose(AUC GLU  ) and PCOM, while there was a negative correlation between HOMA-

 IR and PCOM.Conclusion  There are relationships among hyperandrogenism, hyperinsulinemia,

insulin resistance (IR) and ovary morphology in PCOS patients. PCOS patients with-

out PCOM have more serious IR and hyperandrogenism.

Key words: polycystic ovary syndrome (PCOS); polycystic ovary morphology (PCOM);

  hyperandrogenism (HA); insulin resistance (IR)

Corresponding author: Ying WANG; Tel: +86-13911688652; E-mail: wangying02114@bjmu.edu.cn

 ORIGINAL PAPER  

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Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders,

which affects 6%-10% of reproductive-aged women[1]. This syndrome is not a well-defined

entity and shows the great variation and heterogeneity in clinic, menstrual disorders, infertility,

acne, obesity and polycystic ovary morphology (PCOM) are typical clinical manifestations.

Further more, insulin resistance (IR), hyperinsulinemia and hyperlipidemia increase with age.

Anovulation and hyperandrogenism (HA) are the main manifestations of PCOS. There

is still a controversy on the diagnosis criteria so far. In the year of 1992[2], National Institutes

of Health/National Institute of Child Health and Human Development (NIH/NICHD) drew

up the first diagnostic criteria which was widely recognized, including oligoanovulation, HA

and/or clinical manifestations of HA. Then European Society of Human Reproduction and

Embryology/American Society For Reproductive Medicine (ESHRE/ASRM) revised this

criteria in 2003 as Rotterdam Criteria[3], meeting at least 2 of the following 3 standards:

menstrual disorder (menstrual cycle >35 d and/or

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sity Third Hospital from Jan. 1, 2005 to Apr. 1, 2008 as PCOS group. The patients with

PCOS were divided into three groups according to the ovary morphology: B-PCOM group

(both two ovaries were PCOM), U-PCOM (only one ovary was PCOM) and N-PCOM

(none was PCOM). The diagnosis criteria of PCOS was according to the 2003 Rotterdam

Criteria[3]. This study was approved by the Ethics Committee of Peking University.

The diagnosis criteria of PCOM included 12 follicles or more in the both or one ovary

under B ultrasound screen, and the diameter was 2-9 mm, and / or ovary volume increases

(each ovary >10 ml, ovary volume = 0.15 multiplied by length, width and thickness of ovary

respectively).

Infertile women were recruited who were treated in Reproductive Medical Center of 

Peking University Third Hospital for IVF-ET treatment with simple tubal factor as control

group. All patients in the control expressed normal menstruation or BBT biphasic and basic

endocrine determination without the organic disease in uterus and ovary.

All subjects did not have any hormone therapy or medicine treatment which could

affect endocrinology status. There was no statistical difference in age between the PCOS

groups and control group.

Obesity and overweight were determined according to Asia standard, the BMI of 

obesity stage II, obesity stage I, overweight and normal weight is more than 30 kg/m2, 25.0-

30.0 kg/m2, 23.1-24.9 kg/m2 and 18.5-23.0 kg/m2, respectively.

The diagnosis criteria of the metabolic syndrome was according to the China Diabetes

Association criteria[5] , there were more than three items as follows: overweight and/or 

obesity (BMI>25 kg/m2); higher glucose [fasting blood glucose (FBG)≥6.1 mmol/L and/or 

2 h post glucose≥ 7.8 mmol/L and/or diabetes mellitus which has been diagnosed]; hyper-

tension (systolic/diastolic blood pressure≥140/90 mmHg and / or hypertension disease which

has been diagnosed); dyslipidemia [Triglyceride (TG)≥ 17 mmol/L and/or high-density

lipoprotein (HDL)-C100 mIU/L].

Clinical data collection

We collected detail data as follows: chief complaint, history of present illness, menstrual

history, obstetrical history, disease history, family disease history; height, weight, calculating

BMI, breast development, lactation, hirsutism, acne and pelvic examination; hormone level

determination, including estradiol (E2), luteinizing hormone (LH), follicle-stimulating hormone

(FSH), testosterone (T), androstenedione (A), FBG, FINS, tota l cholesterol (TC), TG,

low-density lipoprotein (LDL-C) and HDL-C; oral glucose tolerance test and insulin releasing

test; transvaginal ultrasound inspection, including ovary form and volume, number of follicles

in both ovary and endometrial thickness.

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Oral glucose tolerance test and insulin releasing test

An oral glucose tolerance test (OGTT) was performed in the usual manner: blood

samples was drawn before the patients took 75 g of glucose in 250 ml water, and 2 more

samples were taken 60 min (G60) and 120 min (G120) later. Then the serum levels of glucose

and insulin were examed at each time point respectively.

Statistical analysis

Data were analyzed using SPSS software for Windows, version 15.0 (SPSS, Chicago,

Illinois, USA). Data were expressed as mean± standard deviation ( x-± s) and compared

 by using analysis of Variance, Chi-square test and Logisitic regression. P 0.05).

Baseline characteristics comparison between PCOS group and control group

Patients in B-PCOM group had higher BMI, longer menstrual cycle and thicker 

endometrium than those in control group ( P 

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Table 3 Explain method to assess IR degree

  Item Calculation methods Significance

HOMA-IR 

HOMA-β

∆I60/∆G60

ISI

AUCGLU

AUCINS

DI

FBG× FINS/22.5

20× FINS/(FBG-3.5)

I60-FINS/G60-FBG

ISI=1/(FBG× FINS)

(FBG+G120)/2+G60

(FINS+I120)/2+I60

(∆I60∆G60)/HOMA-IR 

Assess IR degree

Assess Islet β-cell function

The early secretion index of Islet, assess Islet β-cell function and potential

Fasting insulin sensitivity index, said body insulin sensitivity

Glucose disposition index

Table 1 Baseline characteristics of the 234 subjects enrolled for analysis ( x   s)

Indicator 

  PCOS group (n=234)

Control (n=39)  B-PCOM (n=112) U-PCOM (n=50) N-PCOM (n=72)

Age (year)

BMI (kg/m2)

Menstrual cycle (d)

Endometrial thickness (cm)

*: P 

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three PCOS subgroups than in the control, HOMA-β and DI decreased significantly

(both P 

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PCOM group was higher than that in control group ( P 

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Correlation analysis of glucose and lipid metabolism level with PCOM 

FINS, AUCGLU were positive correlated with PCOM ( P =0.03, OR=1.24; P =0.02,

OR=1.13), HOMA-IR was negative correlated with PCOM ( P =0.02, OR=0.37), it indicates

that the more serious IR is, the lower incidence of PCOM is (Table 9).

Table 9 Correlation of glucose and lipid metabolism level and PCOM in PCOS

Indicator r P OR   95%CI (minimum-maximum)

FI

I60

I12 0

FG

G60

HOMA-IR 

HOMA-β

I60-FI/G60-FG

ISI

AUCGLU

DI

TC

TG

HDL

LDL

0.22

0.03

-0.06

0.57

0.04

-1.00

0.00

-0.02

-0.29

0.13

0.03

0.07

-0.12

0.24

-0.24

0.03

0.20

0.55

0.23

0.92

0.02

0.94

0.49

0.54

0.02

0.76

0.91

0.24

0.21

0.50

1.24

1.03

0.94

1.77

1.04

0.37

1.00

0.98

0.75

1.13

0.87

1.08

0.89

1.27

0.79

1.03-1.50

0.99-1.08

0.76-1.16

0.70-4.45

0.52-2.07

0.16-0.85

1.00-1.01

0.93-1.03

0.31-1.86

1.02-1.26

0.74-0.98

0.30-3.89

0.72-1.08

0.88-1.84

0.40-1.56

Discussion

The characteristics of PCOS include: abnormal ovarian function, increased follicle

number and ovarian hyperfunction which is the inherent feature, IR which is the common

 pathophysiological mechanisms of abnormal ovarian function and glucose metabolic

abnormalities; insulin sensitizers could improve IR and ovarian function abnormalities[6].

The follicle development abnormality can lead to PCOM. There are influences for HA,

hyperinsulinemia and IR on the follicle development respectively. But PCOM is not

necessary for the diagnosis of PCOS. In the 2003 Rotterdam Criteria[3], PCOM is one of the

diagnostic criteria. But many scholars consider that HA is the basic pathogen of PCOS,

PCOM is also found in other diseases, particularly in functional hypothalamic anovulation

(FHA). In 2006, Androgen Excess Society (AES) made HA as one of necessary diagnostic

criteria, however, it is not widely recognized. Many studies[7,8] showed that simple PCOM may

 be the early manifestation of PCOS, there is a tendency of varity on the hormone level in

these patients, which showed that ovarian morphology may affect on endocrine metabolism.

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There are only several studies on ovarian morphology.

Our study showed that BMI of B-PCOM and U-PCOM increased significantly, the

incidence of stage I obesity in the three PCOS subgroups increased significantly compared

with control group, which is in according with the conclusion of previous studies. But there

was no difference in obesity incidence among PCOS patients with different ovarian morphology.

More than 50% PCOS patients are obese. IR and hyperinsulinemia are more severe in

PCOS with obesity than those without. Studies showed that losing weight could improve

ovulation and HA. Losing 5%-10% of weight and reducing abdominal fat could improve

menstrual situation, ovulation, infertility and serum hormone level[9]. In this study, the duration

of menstrual cycle was significantly longer in the three PCOS subgroups than in the control,

 but there was no significant difference in the three PCOS subgroups, which showed that

PCOM was not an important factor affecting the menstrual cycle.

Endometrial thickness was thicker in B-PCOM subgroup than in control group, and

thinner in N-PCOM group than in B-PCOM group, the difference was significant. Endome-

trial thickness was mainly affected by estrogen level, the traditional opinion was that follicles

of PCOS were atrophic follicles, but the research on the follicular fluid test and estradiol

synthesis in follicle granular cell showed that the function of synthesis for steroid hormones

in PCOS patients was higher than in normal female[10]. Compared with normal female, there

were higher serum level of estrodiol, more follicles and higher rate of ovarian hyperstimulation

syndrome (OHSS) in PCOS patients when ovulation induction was done using the same

amount of gonadotropin. That means the ovaries of PCOS patients are in high functional

status which estrogen synthetic is hyperfunctional and there are more follicles in basic state,

which is similarly to OHSS in ovulation induction. We could take PCOS as a basic OHSS.

Endometrial thickness was significantly thicker in B-PCOM group than in N-PCOM group

( P 

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selective growth, and induce follicle apoptosis and atresia, ultimately lead to ovulation dys-

function[11]. Rice et al.[12] confirmed that there was androgen receptor expression in the thecal

cell of ovary when the follicle began to grow, and the expression abundance increased with

follicular development. Study of Laven showed that serum level of anti-Müllerian hormone

(AMH) in PCOS correlated positively with follicle numbers whose diameter is 2-5 mm[13]. In

this study, serum level of androgen was statistically higher in PCOS subgroups than in the

control, and the level of androgen in N-PCOM group was higher than that in B-PCOM and

U-PCOM groups. The reason was perhaps that high androgen level inhibit follicular selective

growth, caused follicular apoptosis and atresia, eventually made disorders during the time of 

follicle growth and ovulation, made the number of follicles less in N-PCOM patients than in

other PCOS patients who reached the standard of PCOM. However, how the high level of 

androgen suppresses the follicular selective growth, the specific mechanism is not very clear.

Small follicles collected by androgen excess inhibit follicle to grow continuely, through the

follicle interaction to promote granular cell secreting AMH[12].

 There are important effects for hyperinsulinemia and IR on the follicle development,

which is recognized widely as one of factors playing a criticial role in PCOS pathogenesis.

When insulin combine insulin receptors which located in theca cells, follicular raising level

can increase, and steroid hormone synthesis can promote in theca cells and granular cell[14].

Through 17-α hydroxylase activation, insulin stimulates theca cells to produce androgen,

enhances androgen generation by LH and insulin like growth factor-1 (IGF-1) action, mean-

while reduces liver sex hormone binding globulin (SHGB) level, increases serum free

testosterone level, suppresses IGF-1 binding protein and improves the biological activity of 

IGF-1. Insulin can also improve LH receptor regulation level which FSH induced in granulosa

cells, and promote progesterone reactivity on LH. The regulation disorder of signaling

 pathway of the insulin receptor appeared in PCOS patients, leading to insulin sensitivity

damaged, and mediating glucose absorption rate decreased, but did not affect the steroid

hormone synthesis. So PCOS patients with IR, whether obese or not, all exhibit damaged

glucose-insulin internal environment and increased synthesis of ovarian steroid hormone. We

could deduce that the hyperinsulinemia status in PCOS patients with IR can stimulate

androgen producing, and induce granulosa cells prematurely luteinizing, lead to stagnation of 

follicle proliferation and growth[15]. Some studies have found that the amount of insulin existing

in human follicle was decided by BMI and fasting serum insulin level[16]. Our study showed

that HOMA-IR was significantly higher in N-PCOM group, HOMA-β, ∆I60/∆G60 and DI

were significantly lower in N-PCOM group than in the B-PCOM and U-PCOM groups. It

showed that the patients with N-PCOM had more serious insulin resistance. HOMA-β,

∆I60/∆G60 and DI were evaluation index of insulin β-cell function, insulin β-cell secretion

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function deficiency may be one of the important reasons of IR in PCOS patients, particularly

in PCOS patients without PCOM. The study shows that compared to control group, TC is

significantly elevated, HDL-C was decreased significantly in the three PCOS subgroups,

and more obviously in N-PCOM group. TG in N-PCOM group was increased compared

with in the control. Among the three PCOS subgroups, abnormal lipid metabolism in N-

PCOM group was more obviously, particularly HDL-C. IR is also an important reason of 

abnormal lipid metabolism in PCOS patients, because of IR, TG in the adipose tissue

decomposites strongly, makes overload of free fatty acid, strengthens the synthesis of 

glycogen, TG biosynthesis and very low density lipoprotein cholesterol (VLDL-C) secretion

in the liver. Conversely, following VLDL-C arising in cycle, HDL-C reduces and LDL-C

 particles increases, increasing the load of free fatty acid could also lead to IR of surrounding

tissue[17].

 It is generally believed that there are intrinsically connection between IR and HA, but

which is exactly the first effect on PCOS is still not clear [18]. The possible mechanisms

through which hyperinsulinemia strengthens androgen synthesis are as follows: 1) the

insulin directly stimulates the pituitary to secret LH and affects the ovarian function, makes

ovarian theca cells prolifera tion, increases 17 alpha-hydroxylase/17,20-lyase (CYP-17)

enzyme activity and androgen synthesis excessiveness; 2) hyperinsulinemia indirectly

 promotes ovarian androgen production, through its influence on the hypothalamus gonadotropin

effect; 3) high level insulin in the serum can promote IGF-1 synthesis of ovarian stromal cell

in patients with PCOS, make androgen synthesis increase; 4) high level insulin makes the

reduction of synthesis and secretion of SHBG in the liver, drops of the serum SHBG level,

increases the serum level of free testosterone (FT), makes the androgen exploitation degree

increasing[18].

In this study, PCOS patients without PCOM had higher androgen level and more severe

IR, to a certain extent, that embodies the relationship between HA and IR. Hyperinsulinemia

and IR increase serum FT level, the high level androgen suppresses the follicular selective

growth which is mentioned previously, HA, hyperinsulinemia and IR may interact with ovarian

morphology in PCOS through affecting follicular development. So in clinical practise, we

should pay more attention to PCOS patients without PCOM, who may be have serious

hyperinsulinemia or HA. We should know the HA and hyperinsulinemia are a glory and

honor, which both can lead to serious clinical consequences.

 In the related factors Logistic regression analysis of PCOM, we find that there are

significant correlations between oligomenorrhea, endometrial thickness and PCOM, positive

relationships between LH/FSH and PCOM, FINS, AUCGLU and PCOM, negative relation-

ship between HOMA-IR and PCOM. All these indicate that the more serious IR is, the lower 

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incidence of PCOM is. Results in our study show that IR and HA may result in the follicle

 proliferation and growth stagnation, and affect follicular development. So in clinical practice,

HA and hyperinsulinemia should be fully treated before ovulation induction, to avoid OHSS

and ovulation induction failure, especially in the COH process.

Conclusion

In patients with PCOS, obesity, type 2 diabetes, metabolic syndrome, IR, and hyperlipidemia

incidence are significantly higher than those in the normal population. There are higher 

androgen levels and IR in PCOS patients without PCOM. Therefore, HA and hyperinsulinemia

in these patients should been fully treated before ovulation induction in order to avoid OHSS.

HA, hyperinsulinemia and insulin resistance may interact with ovarian morphology in PCOS

through affecting follicular development.

In short, pathogen of PCOS is the interaction of multiple factors. PCOM under the

ultrasound may be the early status of PCOS. HA and IR are more severe in PCOS without

PCOM than with PCOM, accompanied by more obvious abnormalities in lipid metabolism,

which indicates more long-term complications such as DM, endometrial cancer, hypertension,

coronary heart disease, etc., need to be paid more clinical attentions and aggressive treatments.

References

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Conference Information

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Contact: Royal College of Obstetricians and Gynaecologists

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E-mail: events@rcog.org.uk 

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