Zusammenfassung
Hintergrund
Das polyzystische Ovarsyndrom (PCOS) stellt mit einer Prävalenz von 6–20 % eine der häufigsten Erkrankungen von Frauen im reproduktionsfähigen Alter dar. Das PCOS ist durch einen Hyperandrogenismus und eine chronische Anovulation charakterisiert und eng mit einer Insulinresistenz assoziiert. Frauen mit PCOS weisen Zyklusunregelmäßigkeiten, einen unerfüllten Kinderwunsch, äußerliche Veränderungen, wie Hirsutismus, Akne oder androgenetische Alopezie, sowie eine Adipositas auf. Die klinische Symptomatik führt zu einer deutlichen Einschränkung der Lebensqualität betroffener Frauen. Die Pathophysiologie des PCOS ist multifaktoriell. Über eine genetische Disposition hinaus scheinen auch verschiedene Umweltfaktoren Einfluss auf die Entwicklung zu haben.
Ziel der Arbeit
Dieser Beitrag beleuchtet den Einfluss ausgewählter äußerer Faktoren auf die Charakteristika des PCOS und soll die Frage beantworten, welche Rolle die uterine Umwelt, die Adipositas und endokrine Disruptoren wie Bisphenol A (BPA) in der Entstehung des PCOS spielen.
Ergebnisse und Diskussion
Tiermodelle mit pränataler Androgenisierung deuten darauf hin, dass die intrauterine Exposition mit Androgenen durch die Mutter zur Entstehung eines PCOS-typischen Phänotyps beitragen kann. Eine Adipositas ist wahrscheinlich nicht Ursache eines PCOS, jedoch eng mit ausgeprägteren Formen des PCOS assoziiert. Sie moduliert wesentlich das mit dem PCOS verbundene metabolische Risiko. Endokrine Disruptoren wie BPA verstärken möglicherweise den Hyperandrogenismus beim PCOS.
Abstract
Background
With a prevalence of 6–20 %, polycystic ovary syndrome (PCOS) is one of the most frequent endocrinopathies among fertile women. It is characterized by hyperandrogenism and chronic anovulation and is highly associated with insulin resistance. Women with PCOS suffer from menstrual irregularity resulting probably in subfertility and from hirsutism, acne, and androgenetic alopecia. Furthermore, obesity is common in PCOS. Women with PCOS report a significant decrease in quality of life. Multiple factors are involved in the pathophysiology of PCOS. Besides a genetic background, environmental factors seem to influence development.
Aim
This article outlines the role of selected environmental factors in the pathophysiology of PCOS and describes the influence of intrauterine exposure to androgens, obesity, and endocrine disruptors like bisphenol A (BPA) on the PCOS phenotype.
Results and discussion
Intrauterine exposure to androgen excess due to hyperandrogenism of the mother may lead to the development of the PCOS phenotype including metabolic derangements. Obesity does not seem to cause PCOS, but is highly associated with a more severe phenotype of PCOS and aggravates metabolic risks associated with PCOS. BPA may enhance androgen synthesis and activity.
Literatur
Azziz R et al (2009) The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 91(2):456–488
Boomsma CM et al (2006) A meta-analysis of pregnancy outcomes in women with polycystic ovary syndrome. Hum Reprod Update 12(6):673–683
de Zegher F, Lopez-Bermejo A, Ibanez L (2009) Adipose tissue expandability and the early origins of PCOS. Trends Endocrinol Metab 20(9):418–423
Dechaud H et al (1999) Xenoestrogen interaction with human sex hormone-binding globulin (hSHBG). Steroids 64(5):328–334
Dewailly D et al (2006) Oligoanovulation with polycystic ovaries but not overt hyperandrogenism. J Clin Endocrinol Metab 91(10):3922–3927
Dumesic DA, Abbott DH, Padmanabhan V (2007) Polycystic ovary syndrome and its developmental origins. Rev Endocr Metab Disord 8(2):127–141
ESHRE (2004) Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 81(1):19–25
Fernandez M et al (2010) Neonatal exposure to bisphenol a and reproductive and endocrine alterations resembling the polycystic ovarian syndrome in adult rats. Environ Health Perspect 118(9):1217–1222
Hanioka N et al (1998) Suppression of male-specific cytochrome P450 isoforms by bisphenol A in rat liver. Arch Toxicol 72(7):387–394
Ibanez L, de Zegher F, Potau N (1998) Premature pubarche, ovarian hyperandrogenism, hyperinsulinism and the polycystic ovary syndrome: from a complex constellation to a simple sequence of prenatal onset. J Endocrinol Invest 21(9):558–566
Joham AE et al (2014) Gestational diabetes and type 2 diabetes in reproductive-aged women with polycystic ovary syndrome. J Clin Endocrinol Metab 99(3):E447–452
Kandaraki E et al (2011) Endocrine disruptors and polycystic ovary syndrome (PCOS): elevated serum levels of bisphenol A in women with PCOS. J Clin Endocrinol Metab 96(3):E480–484
Legro RS, Strauss JF (2002) Molecular progress in infertility: polycystic ovary syndrome. Fertil Steril 78(3):569–576
Lim SS et al (2012) Overweight, obesity and central obesity in women with polycystic ovary syndrome: a systematic review and meta-analysis. Hum Reprod Update 18(6):618–637
Maliqueo M et al (2013) Placental steroidogenesis in pregnant women with polycystic ovary syndrome. Eur J Obstet Gynecol Reprod Biol 166(2):151–155
Meas T et al (2002) Endocrine consequences of premature pubarche in post-pubertal Caucasian girls. Clin Endocrinol (Oxf) 57(1):101–106
Moran LJ, Norman RJ, Teede HJ (2015) Metabolic risk in PCOS: phenotype and adiposity impact. Trends Endocrinol Metab 26(3):136–143
Morgan CL et al (2012) Evaluation of adverse outcome in young women with polycystic ovary syndrome versus matched, reference controls: a retrospective, observational study. J Clin Endocrinol Metab 97(9):3251–3260
Rausch ME et al (2009) Predictors of pregnancy in women with polycystic ovary syndrome. J Clin Endocrinol Metab 94(9):3458–3466
Rochester JR (2013) Bisphenol A and human health: a review of the literature. Reprod Toxicol 42:132–155
Stepto NK et al (2013) Women with polycystic ovary syndrome have intrinsic insulin resistance on euglycaemic-hyperinsulaemic clamp. Hum Reprod 28(3):777–784
Takeuchi T et al (2006) Elevated serum bisphenol A levels under hyperandrogenic conditions may be caused by decreased UDP-glucuronosyltransferase activity. Endocr J 53(4):485–491
Welt CK, Carmina E (2013) Lifecycle of Polycystic Ovary Syndrome (PCOS): from in utero to menopause. J Clin Endocrinol Metab 98(12):4629–4638
Welt CK, Duran JM (2014) Genetics of polycystic ovary syndrome. Semin Reprod Med 32(3):177–182
Welt CK et al (2006) Characterizing discrete subsets of polycystic ovary syndrome as defined by the Rotterdam criteria: the impact of weight on phenotype and metabolic features. J Clin Endocrinol Metab 91(12):4842–4848
Wild RA et al (2010) Assessment of cardiovascular risk and prevention of cardiovascular disease in women with the polycystic ovary syndrome: a consensus statement by the Androgen Excess and Polycystic Ovary Syndrome (AE-PCOS) Society. J Clin Endocrinol Metab 95(5):2038–2049
Yildiz BO et al (2012) Prevalence, phenotype and cardiometabolic risk of polycystic ovary syndrome under different diagnostic criteria. Hum Reprod 27(10):3067–3073
Yildiz BO, Knochenhauer ES, Azziz R (2008) Impact of obesity on the risk for polycystic ovary syndrome. J Clin Endocrinol Metab 93(1):162–168
Zawadski JK, Dunaif A (1992) Diagnostic criteria for polycystic ovary syndrome: towards a rational approach. In: Dunaif A, Givens JR, Haseltine FP, Merriam GR (Hrsg) Polycystic ovary syndrome. Blackwell Scientific Publications, Boston, S 377–384
Zhou W et al (2008) Effect of bisphenol A on steroid hormone production in rat ovarian theca-interstitial and granulosa cells. Mol Cell Endocrinol 283(1–2):12–18
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S. Reger-Tan und D. Führer-Sakel geben an, dass kein Interessenkonflikt besteht.
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Reger-Tan, S., Führer-Sakel, D. Umwelteinflüsse beim polyzystischen Ovarsyndrom. Gynäkologische Endokrinologie 13, 163–167 (2015). https://doi.org/10.1007/s10304-015-0014-6
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DOI: https://doi.org/10.1007/s10304-015-0014-6