Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertil
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Common pathophysiological mechanisms involved in luteal phase deficiency and polycystic ovary syndrome. Impact on fertility Georgios Boutzios • Maria Karalaki Evangelia Zapanti
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Received: 8 July 2012 / Accepted: 17 August 2012 / Published online: 29 August 2012 Ó Springer Science+Business Media, LLC 2012
Abstract Luteal phase deficiency (LPD) is a consequence of the corpus luteum (CL) inability to produce and preserve adequate levels of progesterone. This is clinically manifested by short menstrual cycles and infertility. Abnormal follicular development, defects in neo-angiogenesis or inadequate steroidogenesis in the lutein cells of the CL have been implicated in CL dysfunction and LPD. LPD and polycystic ovary syndrome (PCOS) are independent disorders sharing common pathophysiological profiles. Factors such as hyperinsulinemia, AMH excess, and defects in angiogenesis of CL are at the origin of both LPD and PCOS. In PCOS ovulatory cycles, infertility could result from dysfunctional CL. The aim of this review was to investigate common mechanisms of infertility in CL dysfunction and PCOS. Keywords Corpus luteum Luteal phase defect Polycystic ovary syndrome Infertility
Introduction Luteal phase defect (LPD), an ovulatory dysfunction, is defined as a defect of the corpus luteum (CL) to produce and secrete adequate amounts of progesterone during the luteal phase of the menstrual cycle [1]; it includes the defect of the CL to preserve high levels of progesterone during the second half of the menstrual cycle, as well as the defect of the endometrium to respond to the circulating G. Boutzios (&) M. Karalaki E. Zapanti Division of Endocrinology, First Department of Internal Medicine, Laiko General Hospital, Medical School, University of Athens, Aghiou Thoma 17 Street Goudi, Athens, Greece e-mail: [email protected]
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progesterone levels [2]. Polycystic ovary syndrome (PCOS) is a heterogeneous disorder of unknown etiology, which affects 6–10 % of women of reproductive age [3]. The diagnostic criteria for PCOS include two of the three following: chronic anovulation or oligomenorrhea, clinical or biochemical hyperandrogenism, and polycystic ovarian morphology [4]. The pathogenesis of PCOS is not clarified as yet [5]. LPD and PCOS are independent disorders, but they share common pathophysiological profiles. Although the literature on this matter is limited, it would be interesting to investigate in what extent LPD is involved in subfertility observed in women with PCOS. Etiology and pathogenesis of corpus luteum deficiency Clinically, LPD may present with short menstrual cycles or without any significant change in menstrual cycle length, despite prolonged follicular phases and shortened progesterone-deficient luteal phases [6]. LPD is a clinical expression of CL deficiency caused by various pathophysiological mechanisms, including (a) abnormal follicular development and (b) secretory dysfunction of CL. Both mechanisms lead to the inadequate transformation of the endometrium to secretory, resulting
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