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Page 1: Disclosures PCOS –enigma and challenges€¦ · PCOS compared with women without PCOS. Given the potential for throm-boticdiseaseamongwomenwithPCOS, the purpose of this study was

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S v e n O . S ko u b y, M D , D M S c

R e p ro d u c t iv e M e d ic in e U n it

D e p . O b / G y n . H e r le v / G e n to fte H o s p ita l, Fa c u lty o f M e d ic a l a n d

H e a lth S c ie n c e s U n iv e rs ity o f C o p e n h a g e n , D e n m a rk

PCOS – enigma and challenges

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Disclosures

T h e N O R D IC

M E N O P A U S E S o c ie ty

• Pharma Research funding

• Pharma Advisory Boards

• ESC Past President

• EMAS Past President

• IMS Board• NOMS Past

President• Conflicts of

interests: nil

21.10201524.102015

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• P r e v a le n c e o f P C O S : > 1 0 %

• T h e m o s t p r e v a le n t e n d o c r in e d y s fu n c t io n a m o n g f e r t i le

w o m e n

• E t io lo g y : u n k n o w n

L e a rn in g o b je c tiv e s

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• A p a r t f r o m o v a r ia n d y s fu n c t io n c l in ic a l p e n e t r a t io n o f

m e t a b o l ic d is t u r b a n c ie s a n d C V D r is k a r e l in k e d t o P C O S

p h e n o t y p e s

L e a rn in g o b je c tiv e s

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Natural history

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G u r E B e t a l, W J D , 2 0 1 5 , 9 3 6 -4 2

F e ta l p ro g ra m m in g o f P C O S H o rm o n a l in te ra c t io n s in P C O S

Natural history of PCOS. PCOS has a multifactorial aetiology that includes intra-uterine, genetic and environmental factors which might or might not be interrelated.

Anderson Sanches de Melo et al. Reproduction 2015;150:R11-R24

© 2015 Society for Reproduction and Fertility

Consequenses of IR Consequenses of IR

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• The Rotterdam criteria

1. Oligo-/amenorrhoea

2. Clinical and/or biochemical hyperandrogenism

3. Polycystic ovaries (PCO)

And exclusion of other related disorders

Fauser B.C.et el, Hum Repod 2004 Jan;19(1):41-7

D e fin it io n o f P C O STekst starter uden

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PCOS phenotypes according to the Rotterdam criteria

FeaturesPhenotype

1Phenotype

2Phenotype

3Phenotype

4

Oligo-/amenorrhoea + + +

Clinical and/or biochemical

hyperandrogenemia+ + +

Polycystic ovaries + + +

Herlev /Gentofte Hospital

8

Heterogeneity!

PCOS and BMI

• 40-60% BM I > 30

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•Insulin resistance (IR)

• Impaired glucose tolerance

• Dyslipidemia

• Type 2 diabetes

• Cardiovascular disease (CVD)

M etabolic associations/co-m orbidity

F e rtil S te r il 2 0 1 4 ; 1 0 2 :1 4 4 4 -5 1

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Obesity (BMI ≥30 kg/m2), overweight (BMI 25–29.9 kg/m2), hypertension (BP ≥140/90 mm Hg), enlargedwaist circumference (≥88 cm), hyperglycemia (fasting glucose >6.0 mmol/L), insulin resistance (1/HOMA-IR <0.47), dyslipidemia (TC ≥5.0 mmol/L, TG >1.7 mmol/L, LDL-C ≥3.0 mmol/L, HDL-C <1.2 mmol/L) and presenceof metabolic syndrome (MetS; ATP III criteria, presenceof three or more of any of the following clinical features: waist ≥88 cm, fasting glucose ≥5.6 mmol/L, BP ≥130/85 mm Hg, HDL <1.3 mmol/L, TG ≥1.7 mmol/L)

Assessment of Cardiometabolic Profilebetween the different PCOS phenotypes

F e rtil S te r il 2 0 1 4 ; 1 0 2 :1 4 4 4 -5 1

Women with hyperandrogenic PCOS have a worse cardiometabolic profile and higher prevalence of CV risk factors compared with women with nonhyperandrogenic PCOS.

C o n c lu s io n (s )

PCOS phenotypes translate to different endocrine and metabolic

consequences

- However, for m ost benefical intervention attem pts increase in insulin sensitivity seem s to be pivotal

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•A re p h e n o ty p e s o f w o m e n w it h P C O S

•b a s e d o n B M I a n d in s u l in r e s is ta n c e a re m o re c a u s a l ly

a s s o c ia t e d w it h d is t in c t C V D r is k p ro f i le s

PCOS: CVD in relation to phenotypes

B M I

IR

+ IR

+ O b e s ity

+ IR

� O b e s ity

� IR

� O b e s ity

� IR

+ O b e s ity

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A th ro m b o g ra m

35

Herlev Hospital

0

10

20

30

40

50

60

70

BMI≤25-IR BMI≤25+IR BM I> 25- IR BM I> 25+ IR

lo w CR P, Low ETPHi gh C RP, Hig h ET P

BMI/IR phenotypes

%

D is tr ib u tio n o f B M I/IR -p h e n o ty p e s a c c c o rd in g to th e le v e l o f E T P a n d C R P

GENERAL GYNECOLOGY

Is polycystic ovary syndrome another risk factor for venousthromboembolism? United States, 2003–2008Ekwutosi M. Okoroh, MD; W. Craig Hooper, PhD; Hani K. Atrash, MD; Hussain R. Yusuf, MD; Sheree L. Boulet, DrPH

OBJECTIVE: We sought to determine prevalence and likelihood of ve-nous thromboembolism (VTE) among women with and without polycys-tic ovary syndrome (PCOS).

STUDY DESIGN: We performed a cross-sectional analysis using ThomsonReuters MarketScan Commercial databases for the years 2003 through 2008.TheassociationbetweenVTEandPCOSamongwomenaged18-45yearswasassessed using age-stratified multivariable logistic regression models.

RESULTS: Prevalence of VTE per 100,000 was 374.2 for PCOS womenand 193.8 for women without PCOS. Compared with women withoutPCOS, those with PCOS were more likely to have VTE (adjusted odds

ratio [aOR] 18-24 years, 3.26; 95% confidence interval [CI], 2.61–4.08; aOR 25-34 years, 2.39; 95% CI, 2.12–2.70; aOR 35-45 years,2.05; 95% CI, 1.84–2.38). A protective association (odds ratio, 0.8;95% CI, 0.73–0.98) with oral contraceptive use was noted for PCOSwomen.

CONCLUSION: PCOS might be a predisposing condition for VTE, partic-ularly among women aged 18-24 years. Oral contraceptive use mightbe protective.

Key words: polycystic ovary syndrome, prevalence, venousthromboembolism

Cite this article as: Okoroh EM, Hooper WC, Atrash HK, et al. Is polycystic ovary syndrome another risk factor for venous thromboembolism? United States,2003–2008. Am J Obstet Gynecol 2012;207:377.e1-8.

Venous thromboembolism (VTE) isa chronic condition that includes

both deep vein thrombosis (DVT) andpulmonary embolism (PE). Initial pre-sentation might be leg pain, tenderness,shortness of breath, or pleuritic chestpain, or there might be no symptoms.1

VTE is the third most common cardio-vascular disease–after myocardial infarc-tion and stroke–among the general pop-ulation.2,3 The overall annual incidenceof VTE is estimated to be 1-2 per 1000adults per year.4-7 These incident esti-mates, however, might not represent theentire population because VTE inci-dence differs by age and race, and slightlyby sex. VTE is a multifactorial diseasewith both inherited and acquired riskfactors. In 26-47% of first-time VTEcases, the etiology is unknown4,5,8; a pos-sible predisposing condition not yet as-sessed is polycystic ovary syndrome(PCOS).

PCOS is the most common endocrinedisorder affecting women of reproduc-tive age. Estimates of its prevalence varyand range from 4 – 6%.9-12 Its exact eti-ology is unknown, but it is characterizedby a heterogeneous presentation of hy-perandrogenism, ovulatory dysfunction,and polycystic ovaries.13 PCOS is also as-sociated with insulin-induced elevationsof plasminogen activator inhibitor (PAI)-1,which is a potent inhibitor of fibrinolysis.14

While some studies have found PCOS tobe associated with coronary heart diseaserisk factors,15-20 other studies have shown

that women with PCOS were 3 timesmore likely to have a family history ofvenous thrombosis.21 Mak and Dokras22

hypothesized that women with PCOSlikely have an increased baseline risk fordeveloping thrombosis compared withother women in the general population.However, no study has evaluated theprevalence of VTE among women withPCOS compared with women withoutPCOS. Given the potential for throm-botic disease among women with PCOS,the purpose of this study was to: (1) de-termine the prevalence of VTE amongwomen with and those without PCOS;and (2) assess the association betweenPCOS and VTE.

MATERIALS AND METHODSData sourceData for the study were derived fromthe 2003 through 2008 Thomson Reu-ters MarketScan Commercial data-bases.23 These databases compriselongitudinal, deidentified health in-surance claims data from large em-ployers and health plans across theUnited States and contain informationon inpatient admissions, outpatientvisits, and pharmaceutical claims. Thedata are derived from multiple USstates that are geographically diverse.23

From the Division of Blood Disorders, NationalCenter on Birth Defects and DevelopmentalDisabilities, Centers for Disease Control andPrevention, Atlanta, GA.

Received May 24, 2012; revised July 17, 2012;accepted August 1, 2012.

The findings and conclusions in this report arethose of the authors and do not necessarilyrepresent the official position of the Centers forDisease Control and Prevention.

The authors report no conflict of interest.

Presented orally at the 60th Annual EpidemicIntelligence Service Conference, Atlanta, GA,April 11-15, 2011.

Reprints: Ekwutosi M. Okoroh, MD, Division ofBlood Disorders, National Center on BirthDefects and Developmental Disabilities,Centers for Disease Control and Prevention,1600 Clifton Rd., Mailstop E64, Atlanta, GA30333. [email protected]/free© 2012 Mosby, Inc. All rights reserved.http://dx.doi.org/10.1016/j.ajog.2012.08.007

For Editors’ Commentary, seeContents

Research www.AJOG.org

NOVEMBER 2012 American Journal of Obstetrics & Gynecology 377.e1

GENERAL GYNECOLOGY

Is polycystic ovary syndrome another risk factor for venousthromboembolism? United States, 2003–2008Ekwutosi M. Okoroh, MD; W. Craig Hooper, PhD; Hani K. Atrash, MD; Hussain R. Yusuf, MD; Sheree L. Boulet, DrPH

OBJECTIVE: We sought to determine prevalence and likelihood of ve-nous thromboembolism (VTE) among women with and without polycys-tic ovary syndrome (PCOS).

STUDY DESIGN: We performed a cross-sectional analysis using ThomsonReuters MarketScan Commercial databases for the years 2003 through 2008.TheassociationbetweenVTEandPCOSamongwomenaged18-45yearswasassessed using age-stratified multivariable logistic regression models.

RESULTS: Prevalence of VTE per 100,000 was 374.2 for PCOS womenand 193.8 for women without PCOS. Compared with women withoutPCOS, those with PCOS were more likely to have VTE (adjusted odds

ratio [aOR] 18-24 years, 3.26; 95% confidence interval [CI], 2.61–4.08; aOR 25-34 years, 2.39; 95% CI, 2.12–2.70; aOR 35-45 years,2.05; 95% CI, 1.84 –2.38). A protective association (odds ratio, 0.8;95% CI, 0.73– 0.98) with oral contraceptive use was noted for PCOSwomen.

CONCLUSION: PCOS might be a predisposing condition for VTE, partic-ularly among women aged 18-24 years. Oral contraceptive use mightbe protective.

Key words: polycystic ovary syndrome, prevalence, venousthromboembolism

Cite this article as: Okoroh EM, Hooper WC, Atrash HK, et al. Is polycystic ovary syndrome another risk factor for venous thromboembolism? United States,2003–2008. Am J Obstet Gynecol 2012;207:377.e1-8.

Venous thromboembolism (VTE) isa chronic condition that includes

both deep vein thrombosis (DVT) andpulmonary embolism (PE). Initial pre-sentation might be leg pain, tenderness,shortness of breath, or pleuritic chestpain, or there might be no symptoms.1

VTE is the third most common cardio-vascular disease–after myocardial infarc-tion and stroke–among the general pop-ulation.2,3 The overall annual incidenceof VTE is estimated to be 1-2 per 1000adults per year.4-7 These incident esti-mates, however, might not represent theentire population because VTE inci-dence differs by age and race, and slightlyby sex. VTE is a multifactorial diseasewith both inherited and acquired riskfactors. In 26-47% of first-time VTEcases, the etiology is unknown4,5,8; a pos-sible predisposing condition not yet as-sessed is polycystic ovary syndrome(PCOS).

PCOS is the most common endocrinedisorder affecting women of reproduc-tive age. Estimates of its prevalence varyand range from 4 – 6%.9-12 Its exact eti-ology is unknown, but it is characterizedby a heterogeneous presentation of hy-perandrogenism, ovulatory dysfunction,and polycystic ovaries.13 PCOS is also as-sociated with insulin-induced elevationsof plasminogen activator inhibitor (PAI)-1,which is a potent inhibitor of fibrinolysis.14

While some studies have found PCOS tobe associated with coronary heart diseaserisk factors,15-20 other studies have shown

that women with PCOS were 3 timesmore likely to have a family history ofvenous thrombosis.21 Mak and Dokras22

hypothesized that women with PCOSlikely have an increased baseline risk fordeveloping thrombosis compared withother women in the general population.However, no study has evaluated theprevalence of VTE among women withPCOS compared with women withoutPCOS. Given the potential for throm-botic disease among women with PCOS,the purpose of this study was to: (1) de-termine the prevalence of VTE amongwomen with and those without PCOS;and (2) assess the association betweenPCOS and VTE.

MATERIALS AND METHODSData sourceData for the study were derived fromthe 2003 through 2008 Thomson Reu-ters MarketScan Commercial data-bases.23 These databases compriselongitudinal, deidentified health in-surance claims data from large em-ployers and health plans across theUnited States and contain informationon inpatient admissions, outpatientvisits, and pharmaceutical claims. Thedata are derived from multiple USstates that are geographically diverse.23

From the Division of Blood Disorders, NationalCenter on Birth Defects and DevelopmentalDisabilities, Centers for Disease Control andPrevention, Atlanta, GA.

Received May 24, 2012; revised July 17, 2012;accepted August 1, 2012.

The findings and conclusions in this report arethose of the authors and do not necessarilyrepresent the official position of the Centers forDisease Control and Prevention.

The authors report no conflict of interest.

Presented orally at the 60th Annual EpidemicIntelligence Service Conference, Atlanta, GA,April 11-15, 2011.

Reprints: Ekwutosi M. Okoroh, MD, Division ofBlood Disorders, National Center on BirthDefects and Developmental Disabilities,Centers for Disease Control and Prevention,1600 Clifton Rd., Mailstop E64, Atlanta, GA30333. [email protected]/free© 2012 Mosby, Inc. All rights reserved.http://dx.doi.org/10.1016/j.ajog.2012.08.007

For Editors’ Commentary, seeContents

Research www.AJOG.org

NOVEMBER 2012 American Journal of Obstetrics & Gynecology 377.e1

GENERAL GYNECOLOGY

Is polycystic ovary syndrome another risk factor for venousthromboembolism? United States, 2003–2008Ekwutosi M. Okoroh, MD; W. Craig Hooper, PhD; Hani K. Atrash, MD; Hussain R. Yusuf, MD; Sheree L. Boulet, DrPH

OBJECTIVE: We sought to determine prevalence and likelihood of ve-nous thromboembolism (VTE) among women with and without polycys-tic ovary syndrome (PCOS).

STUDY DESIGN: We performed a cross-sectional analysis using ThomsonReuters MarketScan Commercial databases for the years 2003 through 2008.TheassociationbetweenVTEandPCOSamongwomenaged18-45yearswasassessed using age-stratified multivariable logistic regression models.

RESULTS: Prevalence of VTE per 100,000 was 374.2 for PCOS womenand 193.8 for women without PCOS. Compared with women withoutPCOS, those with PCOS were more likely to have VTE (adjusted odds

ratio [aOR] 18-24 years, 3.26; 95% confidence interval [CI], 2.61–4.08; aOR 25-34 years, 2.39; 95% CI, 2.12–2.70; aOR 35-45 years,2.05; 95% CI, 1.84–2.38). A protective association (odds ratio, 0.8;95% CI, 0.73–0.98) with oral contraceptive use was noted for PCOSwomen.

CONCLUSION: PCOS might be a predisposing condition for VTE, partic-ularly among women aged 18-24 years. Oral contraceptive use mightbe protective.

Key words: polycystic ovary syndrome, prevalence, venousthromboembolism

Cite this article as: Okoroh EM, Hooper WC, Atrash HK, et al. Is polycystic ovary syndrome another risk factor for venous thromboembolism? United States,2003–2008. Am J Obstet Gynecol 2012;207:377.e1-8.

Venous thromboembolism (VTE) isa chronic condition that includes

both deep vein thrombosis (DVT) andpulmonary embolism (PE). Initial pre-sentation might be leg pain, tenderness,shortness of breath, or pleuritic chestpain, or there might be no symptoms.1

VTE is the third most common cardio-vascular disease–after myocardial infarc-tion and stroke–among the general pop-ulation.2,3 The overall annual incidenceof VTE is estimated to be 1-2 per 1000adults per year.4-7 These incident esti-mates, however, might not represent theentire population because VTE inci-dence differs by age and race, and slightlyby sex. VTE is a multifactorial diseasewith both inherited and acquired riskfactors. In 26-47% of first-time VTEcases, the etiology is unknown4,5,8; a pos-sible predisposing condition not yet as-sessed is polycystic ovary syndrome(PCOS).

PCOS is the most common endocrinedisorder affecting women of reproduc-tive age. Estimates of its prevalence varyand range from 4 – 6%.9-12 Its exact eti-ology is unknown, but it is characterizedby a heterogeneous presentation of hy-perandrogenism, ovulatory dysfunction,and polycystic ovaries.13 PCOS is also as-sociated with insulin-induced elevationsof plasminogen activator inhibitor (PAI)-1,which is a potent inhibitor of fibrinolysis.14

While some studies have found PCOS tobe associated with coronary heart diseaserisk factors,15-20 other studies have shown

that women with PCOS were 3 timesmore likely to have a family history ofvenous thrombosis.21 Mak and Dokras22

hypothesized that women with PCOSlikely have an increased baseline risk fordeveloping thrombosis compared withother women in the general population.However, no study has evaluated theprevalence of VTE among women withPCOS compared with women withoutPCOS. Given the potential for throm-botic disease among women with PCOS,the purpose of this study was to: (1) de-termine the prevalence of VTE amongwomen with and those without PCOS;and (2) assess the association betweenPCOS and VTE.

MATERIALS AND METHODSData sourceData for the study were derived fromthe 2003 through 2008 Thomson Reu-ters MarketScan Commercial data-bases.23 These databases compriselongitudinal, deidentified health in-surance claims data from large em-ployers and health plans across theUnited States and contain informationon inpatient admissions, outpatientvisits, and pharmaceutical claims. Thedata are derived from multiple USstates that are geographically diverse.23

From the Division of Blood Disorders, NationalCenter on Birth Defects and DevelopmentalDisabilities, Centers for Disease Control andPrevention, Atlanta, GA.

Received May 24, 2012; revised July 17, 2012;accepted August 1, 2012.

The findings and conclusions in this report arethose of the authors and do not necessarilyrepresent the official position of the Centers forDisease Control and Prevention.

The authors report no conflict of interest.

Presented orally at the 60th Annual EpidemicIntelligence Service Conference, Atlanta, GA,April 11-15, 2011.

Reprints: Ekwutosi M. Okoroh, MD, Division ofBlood Disorders, National Center on BirthDefects and Developmental Disabilities,Centers for Disease Control and Prevention,1600 Clifton Rd., Mailstop E64, Atlanta, GA30333. [email protected]/free© 2012 Mosby, Inc. All rights reserved.http://dx.doi.org/10.1016/j.ajog.2012.08.007

For Editors’ Commentary, seeContents

Research www.AJOG.org

NOVEMBER 2012 American Journal of Obstetrics & Gynecology 377.e1

In 2008, !35 million individuals wereenrolled, including employees andtheir dependents who were aged "65years and geographically distributedthroughout the United States.23

This commercial database has met orexceeded requirements of the US HealthInsurance Portability and Accountabil-ity Act of 1996 and, accordingly, does notrequire specific patient consent to partic-ipate in the study.24

PopulationWe restricted the analysis to women18-45 years of age. The upper limit of agewas set at 45 years to keep within the agelimit used by other prevalence studies.1-4

Women with PCOS were defined by thepresence of hyperandrogenism, the pres-ence of ovulatory dysfunction, and/orthe presence of polycystic ovaries. Inter-national Classification of Diseases, NinthRevision, Clinical Modification (ICD-9-

CM) codes were used to identify theseconditions in the database. Each condi-tion was defined as follows.

“Clinical hyperandrogenism” wasdefined as the presence of ICD-9-CMcodes for acne (706.0 or 706.1), alope-cia (704.0x), or hirsutism (704.1). Ele-vated testosterone, another character-istic of clinical hyperandrogenism, wasnot included because no ICD-9-CMcodes were available for this laboratoryvalue in the database.

“Ovulatory dysfunction” was definedby the presence of any 1 of the ICD-9-CM codes for the 626 series, which arecodes dealing with disorders of menstru-ation and other abnormal bleeding fromthe female genital tract: 626.0, 626.1,626.2, 626.3, 626.4, 626.5, 626.6, 626.7,626.8, or 626.9.

“Polycystic ovaries” were defined byICD-9-CM code 256.4.

Exclusion of other conditionsWe excluded women who met the crite-ria for any of the PCOS phenotypes andhad !1 of the following conditions: ad-renal hyperplasia (255.0 or 255.9), hy-perprolactinemia (253.1), or thyroid dis-order (244.0, 244.1, 244.2, 244.3, 244.8,244.9, 242.90, or 242.91).

Combinations of these conditionswere used to create 4 mutually exclusivePCOS phenotypes based on the 3 avail-able criterion recommendations (Na-tional Institutes of Health, Rotterdam,and Androgen Society). Women withphenotype A, or classic PCOS, were de-fined by the presence of hyperandro-genism (704.1, 706.0 or 706.1, or 704.0x)and ovulatory dysfunction (626.0, 626.1,626.2, 626.3, 626.4, 626.5, 626.6, 626.7,626.8, or 626.9); but polycystic ovaries(256.4), adrenal hyperplasia (255.0 or255.9), hyperprolactinemia (253.1), andthyroid disorder (244.0, 244.1, 244.2,244.3, 244.8, 244.9, 242.90, or 242.91)were absent. Definitions of the remain-ing PCOS phenotypes are found in theAppendix.

Due to the heterogenic nature ofPCOS and its complex presentation anddefinition, we also assessed the preva-lence of associated conditions seenamong women with PCOS (eg, obesity[278.0, 278.00-278.02, 783.1, or V77.8];infertility [628.0 or 628.9]; syndrome Xor metabolic syndrome [277.7]; and di-abetes [250.00, 250.02, 250.90, or250.92]) to provide additional informa-tion on the frequency of these conditionswithin the different PCOS phenotypes.For all conditions related to PCOS, diag-noses reported on inpatient claims wereconsidered valid; diagnoses based solelyon outpatient claims required that thediagnoses were reported on !2 claimsthat occurred !30 days apart.

Women with possible VTE during thestudy period also were identified usingICD-9-CM codes for DVT (671.3x,671.4x, 671.5x, 671.9x, 451.11, 451.19,451.2, 451.81, 451.9, 453.1, 453.2,453.40-453.42, 453.8, or 453.9), PE(673.2x, 673.8x, 415.11, or 415.19), orboth on any inpatient or outpatientclaim. To reduce inaccurate reporting ofDVT and PE diagnoses, we restricted

FIGURE 1Prevalence of VTE during study period, 2003 through 2008

A, Women with clinical hyperandrogenism; and menstrual or ovulatory dysfunction, or both. B,Women with hyperandrogenism and polycystic ovaries. C, Women with menstrual or ovulatory dys-function, or both; and polycystic ovaries. D, Women with clinical hyperandrogenism; menstrual orovulatory dysfunction, or both; and polycystic ovaries. Any PCOS # Women with any polycystic ovarysyndrome (PCOS) phenotype (A-D). No PCOS # Women without any PCOS phenotype (A-D).VTE, venous thromboembolism.

Okoroh. Polycystic ovary syndrome and venous thromboembolism. Am J Obstet Gynecol 2012.

Research General Gynecology www.AJOG.org

377.e2 American Journal of Obstetrics & Gynecology NOVEMBER 2012

A , W o m e n w ith c lin ic a l h y p e ra n d ro g e n is m ; a n d m e n s tru a l o r o v u la to ry

d y s fu n c tio n , o r b o th . B , W o m e n w ith h y p e ra n d ro g e n is m a n d p o ly c y s tic o v a r ie s . C , W o m e n w ith m e n s tru a l o r o v u la to ry d y s fu n c tio n , o r b o th ; a n d p o ly c y s tic

o v a r ie s . D , W o m e n w ith c lin ic a l h y p e ra n d ro g e n is m ; m e n s tru a l o r o v u la to ry d y s fu n c tio n , o r b o th ; a n d p o ly c y s tic o v a r ie s .

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6

Uncertainty Rem ains in W om en w ith PCOS

Regarding the Increased Incidence of Cardiovascular D isease Later in Life,

Despite the Indisputable Presence of

Multiple Cardiovascular R isk Factors at a Young Age

B a r t C . J . M . F a u s e r , a n d P h i l ip p e B o u c h a r d

CVD in PCOS

A b s tra c t S e n d to

J C lin E n d o c r in o l M e ta b . 2 0 11 D e c ;9 6 (1 2 ):3 6 7 5 -7 . d o i: 1 0 .1 2 1 0 /jc .2 0 11 -2 9 3 5 .

Tekst starter uden

Enhedens Sted og

Enhedens

Classical PCOS follow up studies

A u th o r P a t ie n ts In te rm e d ia te

o u tc o m e s

C V D

O u tc o m e sD a h lg re n � 9 2 N = 3 5

2 2 -3 1 y rs fo llo w u p

M o re d ia b e te s

M o re h y p e rte n s io n

P ie rp o in t � 9 8 N = 9 8 6 , d ia g n o s e d

b e tw e e n 1 9 3 0 -1 9 7 9

S M R 0 .9

(9 5 % C I 0 .7 -1 .2 )

W ild � 0 0 N = 2 4 0 d ia g n o s e d

b e fo re 1 9 7 97 2 0 c o n tro ls

M o re c e re b ra l

d is e a s eM o re

D ia b e te s

S im ila r C H D

m o rb id ity a n d m o rta lity

E lt in g � 0 1 N = 3 4 6

2 -3 2 y rs fo llo w u p

M o re d ia b e te s

M o re h y p e rte n s io n

Tekst starter uden

Enhedens Sted og

Enhedens

Tekst starter uden

Enhedens Sted og

Enhedens

Tekst starter uden

Enhedens Sted og

Enhedens

S te in L e v e n th a l, w e d g e re s e c tio n 1 9 5 6 -1 9 6 5

S c re e n in g 2 1 y rs la te r (n = 3 5 ; D a h lg re n 1 9 9 2 )

S c re e n in g 2 0 y rs la te r (6 1 -7 9 y rs n = 3 3 v s 1 2 0 C )

Tekst starter uden

Enhedens Sted og

Enhedens

C VD N S

Page 7: Disclosures PCOS –enigma and challenges€¦ · PCOS compared with women without PCOS. Given the potential for throm-boticdiseaseamongwomenwithPCOS, the purpose of this study was

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Tekst starter uden

Enhedens Sted og

Enhedens

M a y 2 2 , 2 0 1 6

T h e s e le c tio n o f s tu d ie s

in c lu d e d (n = 1 0 4 3 9 2 )

M e ta -a n a ly s is o f th e a s s o c ia tio n b e tw e e n

P C O S a n d C V D

C H D ; O R :1 .4 4 P = 0 ,0 4

M I; O R :1 .0 1 P = 0 .9 5

1. Polycystic ovary syndrome (PCOS) is a complex and heterogeneous disease that involves reproductive and metabolic elements

2. The Rotterdam PCOS critria are not valid for CVD prediction

3. There should be two names for the PCOS phenotypes: those with primarily reproductive consequences , and those with important metabolic consequences

Take home message:

1. PCOS increases DVT risk dependent on phenotype and linked metabolic disturbancies

2. Life-long PCOS metabolic disturbanciesexaggerates CVD risk according to all validated risk markers

3. Uncertainties to whether PCOS per se increases clinical CVD should probably be explained by differences in metabolic impact modulated by phenotypes and medical intervention.

Take home message: