evaluation of insulin resistance and metabolic syndrome in patients with polycystic ovary syndrome

REVIEW PAPER

Evaluation of insulin resistance and metabolic syndrome in patientswith polycystic ovary syndrome

MAHNAZ LANKARANI1 NEDA VALIZADEH1 RAMIN HESHMAT1

MARYAM PEIMANI1 amp FARNAZ SOHRABVAND2

1Endocrinology and metabolism Research Center Tehran University of Medical Sciences Tehran Iran and 2Obstetrics and

Gynecology Department Vallie-Asr Hospital Imam Khomeini Medical Center Tehran Iran

(Received 14 December 2008 revised 31 March 2009 accepted 6 April 2009)

AbstractAim Polycystic ovary syndrome (PCOS) is associated with the clustering of states including insulin resistance (IR) obesityelevated blood pressure and dyslipidemia that are termed as metabolic syndrome (MBS) This study was designed to assessthe differences between homeostatic model assessment (HOMA) values in PCOS and healthy womenMethods In a casendashcontrol study 55 women with PCOS and 59 women with normal cycles (control group) aged 15ndash40years old were evaluated In all the subjects (after obtaining written informed consent) blood pressure body weight heightbody mass index (BMI) waist hip ratio(WHR) and fasting blood glucose (FBG) triglycerides (TG) HDL C-peptideinsulin HOMA Index and FGIR (fasting glucose to insulin ratio) were measuredResults In this study the prevalence of MBS was significantly higher in PCOS group compared with the control group(pfrac14 0028) There were no significant differences in age waisthip ratio fasting glucose insulin and C-peptide levelsbetween patients with PCOS and control group Furthermore the prevalence of impaired fasting glucose (IFG) and themean of HOMA and FGIR did not differ significantly between PCOS and control groupConclusion Criteria of MBS are frequently present in young women with PCOS and may be more useful as a prognosticfactor than IR indexes in this age group We suggest evaluation of IR in older age women with PCOS

Keywords Polycystic ovary syndrome insulin resistance HOMA index metabolic syndrome

Introduction

Polycystic ovary syndrome (PCOS) is a common

medical condition that is manifested by oligoanovou-

lation and hyperandrogenemia The exact pathogen-

esis of this heterogenous disorder has not yet been

clarified The condition is usually associated with

insulin resistance (IR) reflected by hyperinsulinemia

Subjects with PCOS have androgen excess secondary

to the insulin influences in diminishing sex hormone

binding globulin (SHBG) synthesis and also enhance-

ment of androgen production by ovarian tissue [1] IR

is a main factor in the pathogenesis of metabolic

syndrome (MBS) [2] PCOS is associated with the

clustering of states [including IR obesity elevated

blood pressure (BP) and unfavorable lipid profile]

that is termed MBS [3] Hyperinsulinemia as a

consequence of severe IR aggravates the reproductive

disorders in PCOS [4] It has been described that

IR promotes PCOS elevated BP and dyslipidemia

[5] Currently homeostatic model assessment

(HOMA) score that applies fasting glucose and

insulin levels has been used by investigators to

determine IR [6] Detection of IR in women with

PCOS may be beneficial for management by insulin

sensitizer agents such as metformin to decrease

insulin levels [4] This study was designed to

determine the differences between HOMA values

in women with PCOS and healthy women without

PCOS We also investigated the differences between

FGIRs in these two groups

Subjects and methods

In a casendashcontrol study 55 women with PCOS from

the endocrine and gynecology clinics of Shariati

Correspondence Neda Valizadeh Endocrinology and Metabolism Research Center 5th floor Shariati Hospital North Kargar Avenue Tehran Iran

Tel thorn9821-88026902 Fax thorn9821-88029399 E-mail neda_valizadeh2003yahoocom

Gynecological Endocrinology August 2009 25(8) 504ndash507

ISSN 0951-3590 printISSN 1473-0766 online ordf 2009 Informa UK Ltd

DOI 10108009513590902972083

Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly

Hospital and 59 women with normal cycles (control

group) aged 15ndash40 year old were evaluated Diag-

nosis of PCOS was based on the criteria adopted at

the 1990 National Institute of Child Health and

Human Development conference on PCOS [7]

PCOS was defined as having oligoanovoulation with

hyperandrogenism Other causes of hyperandrogen-

ism such as adult onset congenital adrenal hyperpla-

sia hyperprolactinemia and androgen secreting

tumors were ruled out Control healthy women were

selected among the patientsrsquo visitors medical stu-

dents and hospital workers Subjects that were

taking any agents that influence on hormonal profile

or glucose metabolism (oral contraceptive agents

glucocorticoids thiazides and metformin) in the last

3 months before beginning of the study were

excluded Written informed consent was obtained

from all participants before beginning the study

protocol Control women were matched for age to

the women with PCOS We measured body

weight height body mass index (BMI) waisthip

ratio (WHR) and blood pressure in all subjects

Samples of venous blood were obtained in the

morning after 12 h of fasting for measuring fasting

blood glucose (FBG) triglycerides (TG) HDL

C-peptide and insulin The concentrations of

FBG TG and HDL were analyzed by enzymatic

assay and radioimmunoassay (RIA) was used for

insulin and C-peptide

MBS was defined (based on the guidelines from

the 2005 National Cholesterol Education program

[Adult Treatment Panel ATP III]) as the presence of

at least three of the following criteria

Abdominal obesity (a waist circumference greater

than 88 cm in women)

Serum TG 150 mgdl or taking any medication

for hypertriglyceridemia

Serum HDL5 50 mgdl or taking any medica-

tion for reduced HDL level

BP 130 85 mmHg or taking any medication

for hypertension

Fasting blood glucose100 mgdl or taking any

medication for hyperglycemia [8]

We use HOMA and FGIR for comparing of IR

between PCOS and control women [9]

The FGIR was calculated with fasting glucose (in

milligrams per deciliter) divided by fasting insulin (in

micro units per milliliter)

HOMA was assessed using the following formula

[9]

HOMA frac14 frac12Fasting insulin ethmU=mlTHORN Fasting glucoseethmmol=literTHORN=225

Impaired fasting glucose was defined as FBS100 mgdl but125 mgdl and the diagnosis of

diabetes mellitus (DM) was made as FBS126 mg

dl [10]

Data were analyzed by MannndashWhitney U-test T-

test Fisherrsquos exact test and w2 test using the

statistical package SPSS version 115 The level of

statistical significance was considered as p5 005

Results

The demographic characteristics and biochemical

parameters of the PCOS and control women are

demonstrated in Table I

Intentionally there was no significant difference in

age between two groups WHRs and BMIs were

significantly higher in the women with PCOS than in

the control women (Table I)

There were no statistically significant differences in

fasting glucose insulin and C-peptide levels be-

tween patients with PCOS and healthy women

(Table I) The prevalence of IFG was 55 and

68 in PCOS and healthy women respectively

(pfrac14 100) The prevalence of the IFG did not differ

significantly between the two groups None of the

subjects had the diabetes mellitus

The mean HOMA Index did not differ signifi-

cantly between PCOS and control women

294+ 125 vs 298+ 110 respectively (Values

are mean+SD pfrac14 0569)

The mean of FGIR did not differ significantly

between the PCOS and the control women



Prevalence of the NCEP ATP III-defined MBS

was 127 in women with PCOS (7 of 55 patients)

in comparison with 17 (1 of 59) in control women

(Table II) The prevalence of MBS was significantly

higher in the PCOS group compared to the control

group (pfrac14 0028)

Discussion

PCOS is the most frequent endocrinopathy in

childbearing females Many of these patients tend

to have high insulin levels due to IR Affected

Table I Demographic characteristics and biochemical parameters

of subjects

Parameter PCOS (nfrac1455) Controls (nfrac1459) p-value

Age(years) 2375+ 526 2449+540 0457

BMI (kgm2) 2493+ 532 2156+256 0001

Waisthip ratio 079+ 007 076+004 0007

Fasting glucose

(mgdl)

8166+ 1153 7971+915 0318

Fasting insulin

(ngdl)

058+ 022 060+021 0577

C-peptide (ngdl) 281+ 161 294+163 0611

Values are means+SD

Insulin resistance in PCOS 505

Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly

patients also have higher prevalence of glucose

intolerance type II DM and MBS contributing to

greater risk for cardiovascular complications in these

patients [23]

On the basis of our findings although fasting

insulin in PCOS was higher than in control group

there were no statistically significant differences in

fasting glucose and fasting insulin In the study by

Legro et al fasting glucose levels did not differ

between PCOS and control women but women with

PCOS had significantly higher fasting insulin levels

than control group [4]

Robinson et al reported that fasting glucose values

did not differ between PCOS and weight-matched

controls but the plasma glucose area that was

assessed by applying oral glucose (75 g) was greater

in the lean and obese women with PCOS than in the

controls [11]

In the study by Vrbıkova et al both lean and obese

European women with PCOS had significantly

greater levels of basal glucose and fasting insulin in

comparison with the control group [12]

In our study the prevalence of MBS was 127 in

women with PCOS and low HDL cholesterol were

the most frequent criteria of MBS (818 )

Apridonize et al [2] reported that in 106 women

with PCOS the prevalence of MBS was 43 and

low HDL cholesterol had higher frequency than

other criteria of MBS (68) [13] Park et al referred

in their article to a German study by Hahn et al that

have shown 31 of patients with PCOS had MBS

and the most common component of MBS was high

waist circumference [13] Apridonize et al in their

study demonstrated that in PCOS subjects MBS

rate was approximately two times greater than in age-

matched controls They also demonstrated that

higher rate of the MBS in women with PCOS is

independent of age and BMI [2] In our patients the

prevalence of MBS is less common but significantly

higher than in the healthy women

Some investigators have pointed out that the

greater rates of the MBS in PCOS may be linked to

the greater rates of obesity in them [14] Some

studies have obtained the same results but others

have reported that higher rates of MBS in women

with PCOS are independent of age and obesity [2]

Based on the present study HOMA did not differ

between PCOS and control women In the study by

Kurioka et al (2007) there were not significant

differences in HOMA values between Japanese

PCOS and controls Moreover HOMA values

differed significantly between obese and normal

body-weighted patients but in the normal body-

weighted subjects HOMA tests did not differ in

PCOS women and controls [15] However

DeUgarte et al study showed that the mean adjusted

HOMA (with the race age and BMI) was higher in

women with PCOS compared with control women

In their study 644 of patients with PCOS had a

HOMA value above the normal ranges [16] Despite

the fact that in our study the patients with PCOS had

higher BMIs than controls the mean of HOMA or

FGIR were similar in these two groups

In the study by Kauffman et al the means of BMI

fasting insulin and HOMA were significantly higher

in Mexican American women with PCOS in com-

parison with white women but the former group had

significantly lower mean FGIRs than the later group

Kauffman et al considered HOMA value greater

than 38 and 45 in white women and Mexican

American women respectively for detecting IR in

their patients They pointed that cut off values for

detecting of IR in the PCOS is influenced by the race

and ethnicity [17]

In the study by DeUgarte et al in patients with

PCOS HOMA has a positive correlation with BMI

but did not significantly depend on race or age

Within controls HOMA depended significantly on

age BMI and race (black patients had more IR than

whites) [16] Fulghesu et al showed the failure of the

HOMA score for exhibiting metabolic abnormalities

in young adolescent patients with PCOS They

described that a normal HOMA score is not

sufficient to exclude early metabolic abnormalities

such as hyperinsulinemia in young normal-weight

patients with PCOS On the other hand HOMA

values cannot detect the prevalence of hyperinsuli-

nemia in young normal-weight patients with PCOS

In their study 18 of patients had IR by applying

HOMA test but 44 of patients were hyperinsuli-

nemic based on the assessment by euglycemic

glucose clamp test [6] Like in the study of Fulghesu

and coworkers in our study women with PCOS

were young and the failure of present study in

detection of difference in HOMA values between

PCOS and controls may be due to the young age of

patients However Bahrami reported that the pre-

valences of IGT and type 2 DM were significantly

higher in both obese and non-obese young women

with PCOS (mean age 24+ 6 years) He recom-

mended screening of all patients with PCOS for IGT

and DM [18] In a study by Sheikholeslami et al in

Table II The prevalence for each component of metabolic

syndrome

Parameter

in PCOS

(nfrac1455)

in

Controls

(nfrac1459) p-value

Waist4 88( cm) 255 (14) 51 (3) 0002

TG150 (mgdl) 309 (17) 68 (4) 0001

HDL5 50 (mgdl) 818 (45) 797 (47) 0771

BP 13085 (mmHg) 73 (4) 0 0051

Sys BP130 (mmHg) 36 (2) 0 0231

Dia BP 85 (mmHg) 36 (2) 0 0231

Fasting Glu 100 (mgdl) 55 (3) 68(4) 100

Metabolic syn 127 (7) 17 (1) 0028

506 M Lankarani et al

Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly

Iran women with PCOS (mean age 312+ 37

years) had higher basal insulin HOMA scores and

FBS in comparison with women with idiopathic

hirsutism [19]

Several studies have failed in documentation of the

link between IR and PCOS particularly in lean

subjects Cibula has explained that it may be arising

from different ethnicity andor lifestyle modifications

in women with PCOS [20]

Previous studies have exhibited that patients with

PCOS have a detrimental lipid profile including high

LDL and TG and low HDL levels [3] Insulin excess

inhibits lipolysis and leads to elevation of non-

esterified fatty acids levels that in turn contributes

to hypertriglyceridemia and decreased HDL levels

[3] In our study the prevalence of TG4 150 mgdl

was significantly higher in PCOS than in the control

group but there was no significant difference in the

occurrence of HDL5 50 between two groups

Small sample size is one of the limitations of this

study Another limitation is focusing the study on

young patients with PCOS Future studies with

larger sample size and older age group of PCOS

women seem reasonable

Conclusions

In our study HOMA and FGIR were not signifi-

cantly different in young PCOS and healthy women

but MBS was significantly more common in women

with PCOS The conflicts between different studies

in regard to IR in PCOS may be related to different

age groups ethnicity and lifestyle modifications in

various geographic regions Criteria of MBS are

frequently seen in Iranian young women with PCOS

MBS might be more useful as a prognostic factor

than IR indexes in this young age group Further

surveillance of MBS in women with PCOS will be

required We also suggest evaluation of IR by using

HOMA and FGIR tests in older age group of patients

with PCOS

Acknowledgements

This study was supported by Endocrinology and

Metabolism Research Center of Tehran University of

Medical Science in Iran

References

1 Legro RS Azziz R Ehrmann D Fereshetian AG Orsquokeefe M

Ghazzi MN Minimal response of circulating lipids in women

with polycystic ovary syndrome to improvement in insulin

sensitivity with troglitazone J Clin Endocr Metab 2003

885137ndash5144

2 Apridonidze T Essah PA Iuorno MJ Nestler JE Prevalence

and characteristics of the metabolic syndrome in women with

polycystic ovary syndrome J Clin Endocr Metab 200590

1929ndash1935

3 Leo VD Marca AL Petraglia F Insulin ndash lowering Agents in

the management of polycystic overy syndrome Endocr Rev

200324633ndash667

4 Legro RS Finegood D Dunaif A A fasting glucose to insulin

ratio is a useful measure of insulin sensitivity in women with


2694ndash2698

5 Flier JS Insulin resistance the metabolic syndrome X New

Engl J Med 19993411402

6 Fulghesu AM Angioni S Portoghese E Milano F Batetta B

Paoletti AM Melis GB Failures of the homeostatic model

assessment calculation score for detecting metabolic deteriora-

tion in young patients with polycystic ovary syndrome Fertil

Steril 200686398ndash404

7 Zawadzki JK Dunaif A Diagnostic criteria for polycystic

ovary syndrome towards a rational approach In Dunaif A

Givens JR Haseltine F Merriam GM editors Polycystic

ovary syndrome Boston Black well scientific 1992 pp 377ndash

384

8 Grundy SM Cleeman JI Daniels SR Donato KA Eckel RH

Franklin BA Gordon DJ Krauss RM Savage PJ Smith SC Jr

et al Diagnosis and management of the metabolic syndrome

an American Heart AssociationNational Heart Lung and

Blood Institute Scientific Statement Circulation 2005112

2735

9 Lergo RS Castracane VD Kauffman RP Detecting insulin

resistance in polycystic ovary syndrome purposes and pitfalls

Obstet Gynecol Surv 200459141ndash154

10 Genuth S Alberti KG Bennett P Follow-up report on the

diagnosis of diabetes mellitus Diabetes care 2003263160

11 Robinson S Henderson AD Gelding SV Kiddy D

Niththyananthan R Bush A Richmond W Johnston DG

Franks S Dyslipidemia is associated with insulin resistance in

women polycystic ovaries Clin Endocrinol 199644277ndash284

12 Vrbikova J Cibula D Dvorakova K Stanicka S Sindelka G

Hill M Fanta M Vondra K Skrha J Insulin Sensitivity in

women with polycystic ovary syndrome J Clin Endocr Metab

2004892942ndash2945

13 Park HR Choi Y Lee HJ Oh JY Hong YS Sung YA The

metabolic syndrome in young Korean women with polycystic

ovary syndrome Diabetes Res Clin PR 200777SS243ndashS246

Available online at wwwsciencedirectcom

14 Cussons AJ Stuckey BGA watts GF Metabolic and

cardiovascular risk in the polycystic ovary syndrome Pract

Diabetes Int 200522261ndash265

15 Kurioka H Takahashi K Miyazaki K Glucose intolerance in

japanese patients with polycystic ovary syndrome Arch

Gynecol Obstet 2007275169ndash173

16 DeUgarte CM Bartolucci AA Azziz R Prevalence of

insulin resistance in the polycystic ovary syndrome using the

homeostasis model assessment Fertil Steril 2005831454ndash

1460

17 Kauffman RP Baker VM DiMarino P Gimpel T castracane

VD Polycystic ovarian syndrome and insulin resistance in

white and Mexican American women a comparison of two

distinct populations Am J Obstet Gynecol 20021871362ndash

1369

18 Bahrami A Evaluation of impaired glucose tolerance and type

2 diabetes mellitus prevalence in PCOS and necessity for

screening in patients with PCOS Iran J Diabetes Lipid

Disord Spring Summer 20043141ndash148

19 Sheikholeslami H Mirdamadi M Ziaee A Kani C Insulin

resistance in patients with polycystic ovary syndrome In

European congress of endocrinology 2008 May 3ndash7 Berlin

Germany Bioscientifica publishers Endocrine Abstracts

(2008) 16 P648

20 Cibula D Is insulin resistance an essential component of

PCOS The influence of confounding factors Hum Reprod

200419757ndash759


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly

Hospital and 59 women with normal cycles (control

group) aged 15ndash40 year old were evaluated Diag-

nosis of PCOS was based on the criteria adopted at

the 1990 National Institute of Child Health and

Human Development conference on PCOS [7]

PCOS was defined as having oligoanovoulation with

hyperandrogenism Other causes of hyperandrogen-

ism such as adult onset congenital adrenal hyperpla-

sia hyperprolactinemia and androgen secreting

tumors were ruled out Control healthy women were

selected among the patientsrsquo visitors medical stu-

dents and hospital workers Subjects that were

taking any agents that influence on hormonal profile

or glucose metabolism (oral contraceptive agents

glucocorticoids thiazides and metformin) in the last

3 months before beginning of the study were

excluded Written informed consent was obtained

from all participants before beginning the study

protocol Control women were matched for age to

the women with PCOS We measured body

weight height body mass index (BMI) waisthip

ratio (WHR) and blood pressure in all subjects

Samples of venous blood were obtained in the

morning after 12 h of fasting for measuring fasting

blood glucose (FBG) triglycerides (TG) HDL

C-peptide and insulin The concentrations of

FBG TG and HDL were analyzed by enzymatic

assay and radioimmunoassay (RIA) was used for

insulin and C-peptide

MBS was defined (based on the guidelines from

the 2005 National Cholesterol Education program

[Adult Treatment Panel ATP III]) as the presence of

at least three of the following criteria

Abdominal obesity (a waist circumference greater

than 88 cm in women)

Serum TG 150 mgdl or taking any medication

for hypertriglyceridemia

Serum HDL5 50 mgdl or taking any medica-

tion for reduced HDL level

BP 130 85 mmHg or taking any medication

for hypertension

Fasting blood glucose100 mgdl or taking any

medication for hyperglycemia [8]

We use HOMA and FGIR for comparing of IR

between PCOS and control women [9]

The FGIR was calculated with fasting glucose (in

milligrams per deciliter) divided by fasting insulin (in

micro units per milliliter)

HOMA was assessed using the following formula

[9]

HOMA frac14 frac12Fasting insulin ethmU=mlTHORN Fasting glucoseethmmol=literTHORN=225

Impaired fasting glucose was defined as FBS100 mgdl but125 mgdl and the diagnosis of

diabetes mellitus (DM) was made as FBS126 mg

dl [10]

Data were analyzed by MannndashWhitney U-test T-

test Fisherrsquos exact test and w2 test using the

statistical package SPSS version 115 The level of

statistical significance was considered as p5 005

Results

The demographic characteristics and biochemical

parameters of the PCOS and control women are

demonstrated in Table I

Intentionally there was no significant difference in

age between two groups WHRs and BMIs were

significantly higher in the women with PCOS than in

the control women (Table I)

There were no statistically significant differences in

fasting glucose insulin and C-peptide levels be-

tween patients with PCOS and healthy women

(Table I) The prevalence of IFG was 55 and

68 in PCOS and healthy women respectively

(pfrac14 100) The prevalence of the IFG did not differ

significantly between the two groups None of the

subjects had the diabetes mellitus

The mean HOMA Index did not differ signifi-

cantly between PCOS and control women



The mean of FGIR did not differ significantly

between the PCOS and the control women



Prevalence of the NCEP ATP III-defined MBS

was 127 in women with PCOS (7 of 55 patients)

in comparison with 17 (1 of 59) in control women

(Table II) The prevalence of MBS was significantly

higher in the PCOS group compared to the control

group (pfrac14 0028)

Discussion

PCOS is the most frequent endocrinopathy in

childbearing females Many of these patients tend

to have high insulin levels due to IR Affected

Table I Demographic characteristics and biochemical parameters

of subjects

Parameter PCOS (nfrac1455) Controls (nfrac1459) p-value

Age(years) 2375+ 526 2449+540 0457

BMI (kgm2) 2493+ 532 2156+256 0001

Waisthip ratio 079+ 007 076+004 0007

Fasting glucose

(mgdl)

8166+ 1153 7971+915 0318

Fasting insulin

(ngdl)

058+ 022 060+021 0577

C-peptide (ngdl) 281+ 161 294+163 0611

Values are means+SD


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly




patients [23]














controls [11]
























































and ethnicity [17]






























syndrome

Parameter

in PCOS

(nfrac1455)

in

Controls

(nfrac1459) p-value

Waist4 88( cm) 255 (14) 51 (3) 0002

TG150 (mgdl) 309 (17) 68 (4) 0001

HDL5 50 (mgdl) 818 (45) 797 (47) 0771

BP 13085 (mmHg) 73 (4) 0 0051

Sys BP130 (mmHg) 36 (2) 0 0231

Dia BP 85 (mmHg) 36 (2) 0 0231

Fasting Glu 100 (mgdl) 55 (3) 68(4) 100

Metabolic syn 127 (7) 17 (1) 0028


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly




hirsutism [19]





















Conclusions














with PCOS

Acknowledgements




References





885137ndash5144




1929ndash1935



200324633ndash667




2694ndash2698


Engl J Med 19993411402










384






2735













2004892942ndash2945














1460





1369









(2008) 16 P648



200419757ndash759


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly




patients [23]














controls [11]
























































and ethnicity [17]






























syndrome

Parameter

in PCOS

(nfrac1455)

in

Controls

(nfrac1459) p-value

Waist4 88( cm) 255 (14) 51 (3) 0002

TG150 (mgdl) 309 (17) 68 (4) 0001

HDL5 50 (mgdl) 818 (45) 797 (47) 0771

BP 13085 (mmHg) 73 (4) 0 0051

Sys BP130 (mmHg) 36 (2) 0 0231

Dia BP 85 (mmHg) 36 (2) 0 0231

Fasting Glu 100 (mgdl) 55 (3) 68(4) 100

Metabolic syn 127 (7) 17 (1) 0028


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly




hirsutism [19]





















Conclusions














with PCOS

Acknowledgements




References





885137ndash5144




1929ndash1935



200324633ndash667




2694ndash2698


Engl J Med 19993411402










384






2735













2004892942ndash2945














1460





1369









(2008) 16 P648



200419757ndash759


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly




hirsutism [19]





















Conclusions














with PCOS

Acknowledgements




References





885137ndash5144




1929ndash1935



200324633ndash667




2694ndash2698


Engl J Med 19993411402










384






2735













2004892942ndash2945














1460





1369









(2008) 16 P648



200419757ndash759


Gyn

ecol

End

ocri

nol D

ownl

oade

d fr

om in

form

ahea

lthca

rec

om b

y Fr

eie

Uni

vers

itaet

Ber

lin o

n 11

05

14Fo

r pe

rson

al u

se o

nly

evaluation of insulin resistance and metabolic syndrome in patients with polycystic ovary syndrome

Documents