Disclosures PCOS –enigma and challenges · PDF file PCOS compared with women without...

Click here to load reader

  • date post

    29-Sep-2020
  • Category

    Documents

  • view

    1
  • download

    0

Embed Size (px)

Transcript of Disclosures PCOS –enigma and challenges · PDF file PCOS compared with women without...

  • 1

    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

    Tekst starter uden

    Enhedens Sted og

    Enhedens

    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

    Tekst starter uden

    Enhedens Sted og

    Enhedens 3

    Herlev/Gentofte Hospital

    • 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

    Tekst starter uden

    Enhedens Sted og

    Enhedens 4

    Herlev/Gentofte Hospital

    • 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

    Tekst starter uden

    Enhedens Sted og

    Enhedens

    Natural history

  • 2

    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

  • 3

    Tekst starter uden

    Enhedens Sted og

    Enhedens 18

    Herlev/Gentofte Hospital

    • 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 S Tekst starter uden

    Enhedens Sted og

    Enhedens

    PCOS phenotypes according to the Rotterdam criteria

    Features Phenotype

    1 Phenotype

    2 Phenotype

    3 Phenotype

    4

    Oligo-/amenorrhoea + + +

    Clinical and/or biochemical

    hyperandrogenemia + + +

    Polycystic ovaries + + +

    Herlev /Gentofte Hospital

    8

    Heterogeneity!

    PCOS and BMI

    • 40-60% BM I > 30

    Tekst starter uden

    Enhedens Sted og

    Enhedens 22

    Herlev/Gentofte Hospital

    •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

  • 4

    Obesity (BMI ≥30 kg/m2), overweight (BMI 25–29.9 kg/m2), hypertension (BP ≥140/90 mm Hg), enlarged waist circumference (≥88 cm), hyperglycemia (fasting glucose >6.0 mmol/L), insulin resistance (1/HOMA-IR 1.7 mmol/L, LDL-C ≥3.0 mmol/L, HDL-C

  • 5

    Tekst starter uden

    Enhedens Sted og

    Enhedens 32

    Herlev/Gentofte Hospital

    •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

    Tekst starter uden

    Enhedens Sted og

    Enhedens 34

    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 ETP Hi 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 venous thromboembolism? United States, 2003–2008 Ekwutosi 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 Thomson Reuters MarketScan Commercial databases for the years 2003 through 2008. TheassociationbetweenVTEandPCOSamongwomenaged18-45yearswas assessed using age-stratified multivariable logistic regression models.

    RESULTS: Prevalence of VTE per 100,000 was 374.2 for PCOS women and 193.8 for women without PCOS. Compared with women without PCOS, 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 PCOS women.

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

    Key words: polycystic ovary syndrome, prevalence, venous thromboembolism

    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) and pulmonary embolism (PE). Initial pre- sentation might be leg pain, tenderness, shortness of breath, or pleuritic chest pain, 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 incidence of VTE is estimated to be 1-2 per 1000 adults per year.4-7 These incident esti- mates, however, might not represent the entire population because VTE inci- dence differs by age and race, and slightly by sex. VTE is a multifactorial disease with both inherited and acquired risk factors. In 26-47% of first-time VTE cases, 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 endocrine disorder affecting women of reproduc- tive age. Estimates of its prevalence vary and range from 4 – 6%.9-12 Its exact eti- ology is unknown, but it is characterized by a heterogeneous presentation of hy- perandrogenism, ovulatory dysfunction, and polycystic ovaries.13 PCOS is also as- sociated with insulin-induced elevations of plasminogen activator inhibitor (PAI)-1, which is a potent inhibitor of fibrinolysis.14

    While some studies have found PCOS to be associated with coronary heart disease risk factors,15-20 other studies have shown

    that women with PCOS were 3 times more likely to have a family history of venous thrombosis.21 Mak and Dokras22

    hypothesized that women with PCOS likely have an increased baseline risk for developing thrombosis compared with other women in the general population. However, no study has evaluated the prevalence of VTE among women with PCOS compared with women without PCOS. 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 among women with and those without PCOS; and (2) assess the association between PCOS and VTE.

    MATERIALS AND METHODS Data source Data for the study were derived from the 2003 through 2008 Thomson Reu- ters MarketScan Commercial data- bases.23 These databases comprise longitudinal, deidentified health in- surance claims data from large em- ployers and health plans across the United States and contain information on inpatient admissions, outpatient visits, and pharmaceutical claims. The data are derived from multiple US states that are geographically diverse.23

    From the Division of Blood Disorders, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, Atlanta, GA.

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

    The findings and conclusions in this report are those of the authors and do not necessarily represent the official position of the Centers for Disease Control and Prevention.

    The authors report no conflict of interest.

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

    Reprints: Ekwutosi M. Okoroh, MD, Division of Blood Disorders, National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention, 1600 Clifton Rd., Mailstop E64, Atlanta, GA 30333. Eokoroh@cdc.gov. 0002-9378/free © 2012 Mosby, Inc. All rights reserved. http://dx.doi.org/10.1