Literature DB >> 12447098

New approach to polycystic ovary syndrome and other forms of anovulatory infertility.

Joop S E Laven1, Babak Imani, Marinus J C Eijkemans, Bart C J M Fauser.   

Abstract

UNLABELLED: Anovulation can be classified in the clinic on the basis of serum hormone assays. Low gonadotropins along with low estrogen concentrations are suggestive of a central origin of the disease, whereas low estrogen levels along with elevated gonadotropins indicate a primary defect at the ovarian level. Most anovulatory patients (approximately 80%) present with serum FSH and estradiol levels within the normal range (World Health Organization class II). Polycystic ovary syndrome (PCOS) is a common but poorly defined heterogeneous clinical entity. Historically, characteristic ovarian abnormalities represented a hallmark of the syndrome. Because several etiological factors may lead to a similar end point (i.e., polycystic ovaries), the development of a clinically applicable classification of the syndrome has proven difficult. Clinical, morphological, biochemical, endocrine, and, more recently, molecular studies have identified an array of underlying abnormalities and added to the confusion concerning the pathophysiology of the disease. Despite the vast literature regarding the etiology and classification of PCOS, no consensus has been reached regarding the validity of criteria used to diagnose the syndrome. For instance, the significance of elevated serum luteinizing hormone (LH) concentrations, insulin resistance or polycystic-appearing ovaries assessed by ultrasound for PCOS diagnosis remains uncertain. In contrast, hyperandrogenism and chronic anovulation generally are believed to be mandatory diagnostic features. Patients with PCOS might visit a dermatologist for hirsutism, a generalist, or internist for complaints related to obesity or a gynecologist for irregular or absent bleeding. However, most patients seek the care of a gynecologist because of cycle abnormalities (oligomenorrhea) and infertility. In PCOS, serum FSH and estradiol (E2) levels are usually found to be within the (broad) normal ranges, whereas LH may either be normal or elevated. Because PCOS with normal or high LH does not seem to represent different clinical entities, it seems justifiable to consider this syndrome as a subgroup of WHO-II patients, although estrogen levels may be tonically elevated in these patients. This review will focus on characteristics of the heterogeneous group of WHO-II patients in an attempt to identify factors involved in the etiology and possible ovulation induction outcome of PCOS. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING
OBJECTIVES: After completion of this article, the reader will be able to outline the current classification of anovulatory infertility and to explain the characteristics and features used for classification.

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Year:  2002        PMID: 12447098     DOI: 10.1097/00006254-200211000-00022

Source DB:  PubMed          Journal:  Obstet Gynecol Surv        ISSN: 0029-7828            Impact factor:   2.347


  41 in total

1.  Luteal-phase inhibin A and follicular-phase inhibin B levels are not characteristic of patients with an elevated LH-to-FSH ratio.

Authors:  Erik E Hauzman; Péter Fancsovits; Akos Murber; Thomas Rabe; Thomas Strowitzki; Zoltán Papp; János Urbancsek
Journal:  J Assist Reprod Genet       Date:  2006-03       Impact factor: 3.412

Review 2.  Managing anovulatory infertility and polycystic ovary syndrome.

Authors:  Adam H Balen; Anthony J Rutherford
Journal:  BMJ       Date:  2007-09-29

3.  Leutinizing hormone/choriogonadotropin receptor and follicle stimulating hormone receptor gene variants in polycystic ovary syndrome.

Authors:  Wassim Y Almawi; Bayan Hubail; Dana Z Arekat; Suhaila M Al-Farsi; Shadha K Al-Kindi; Mona R Arekat; Naeema Mahmood; Samira Madan
Journal:  J Assist Reprod Genet       Date:  2015-02-04       Impact factor: 3.412

4.  Comparison of embryological and clinical outcome in GnRH antagonist vs. GnRH agonist protocols for in vitro fertilization in PCOS non-obese patients. A prospective randomized study.

Authors:  Rafal Kurzawa; Przemyslaw Ciepiela; Tomasz Baczkowski; Krzysztof Safranow; Pawel Brelik
Journal:  J Assist Reprod Genet       Date:  2008-09-19       Impact factor: 3.412

5.  Polycystic ovary syndrome and risk of uterine leiomyomata.

Authors:  Lauren A Wise; Julie R Palmer; Elizabeth A Stewart; Lynn Rosenberg
Journal:  Fertil Steril       Date:  2007-01-22       Impact factor: 7.329

Review 6.  Diagnostic criteria for polycystic ovarian syndrome.

Authors:  F J Broekmans; B C J M Fauser
Journal:  Endocrine       Date:  2006-08       Impact factor: 3.633

7.  Association of the genetic variants of luteinizing hormone, luteinizing hormone receptor and polycystic ovary syndrome.

Authors:  Nana Liu; Yanmin Ma; Shuyu Wang; Xiaowei Zhang; Qiufang Zhang; Xue Zhang; Li Fu; Jie Qiao
Journal:  Reprod Biol Endocrinol       Date:  2012-04-30       Impact factor: 5.211

8.  Delayed endometrial decidualisation in polycystic ovary syndrome; the role of AR-MAGEA11.

Authors:  Kinza Younas; Marcos Quintela; Samantha Thomas; Jetzabel Garcia-Parra; Lauren Blake; Helen Whiteland; Adnan Bunkheila; Lewis W Francis; Lavinia Margarit; Deyarina Gonzalez; R Steven Conlan
Journal:  J Mol Med (Berl)       Date:  2019-06-29       Impact factor: 4.599

9.  Gonadal soma controls ovarian follicle proliferation through Gsdf in zebrafish.

Authors:  Yi-Lin Yan; Thomas Desvignes; Ruth Bremiller; Catherine Wilson; Danielle Dillon; Samantha High; Bruce Draper; Charles Loren Buck; John Postlethwait
Journal:  Dev Dyn       Date:  2017-09-25       Impact factor: 3.780

10.  LH suppression following different low doses of the GnRH antagonist ganirelix in polycystic ovary syndrome.

Authors:  F P Hohmann; J S E Laven; A G M G J Mulders; J J L Oberyé; B M J L Mannaerts; F H de Jong; B C J M Fauser
Journal:  J Endocrinol Invest       Date:  2005-12       Impact factor: 4.256

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