Relevant bibliographies by topics / Syndrome de Stein-Leventhal

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Academic literature on the topic 'Syndrome de Stein-Leventhal'

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Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Syndrome de Stein-Leventhal"

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Sanfilippo, Joseph S. "Polycystic Ovarian Syndrome Since Stein and Leventhal." Journal of Pediatric and Adolescent Gynecology 28, no. 6 (December 2015): 411. http://dx.doi.org/10.1016/j.jpag.2015.10.001.

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Matevosyan, Naira R. "Schizophrenia and Stein–Leventhal syndrome: comorbidity features." Archives of Gynecology and Obstetrics 284, no. 4 (July 30, 2011): 1035–41. http://dx.doi.org/10.1007/s00404-011-1963-1.

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Kurzrock, Razelle, and Philip R. Cohen. "Polycystic ovary syndrome in men: Stein–Leventhal syndrome revisited." Medical Hypotheses 68, no. 3 (January 2007): 480–83. http://dx.doi.org/10.1016/j.mehy.2006.03.057.

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Edward, H., T. Cobb, and E. William. "Cognitive and affective symptoms in Stein-Leventhal syndrome." Archives of Clinical Neuropsychology 6, no. 3 (January 1, 1991): 192–93. http://dx.doi.org/10.1093/arclin/6.3.192a.

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Raboch, Jan, Jitka Kobilkov�, Ji?� Raboch, and Luboslav St�rka. "Sexual life of women with the Stein-Leventhal Syndrome." Archives of Sexual Behavior 14, no. 3 (June 1985): 263–70. http://dx.doi.org/10.1007/bf01542108.

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Singh, Richa, Poonam Yadav, and Roohi Parveen. "Adolescent Polycystic Ovary Syndrome: A Management Dilemma." Journal of South Asian Federation of Obstetrics and Gynaecology 4, no. 3 (2012): 123–25. http://dx.doi.org/10.5005/jp-journals-10006-1192.

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ABSTRACT Since the description by Stein and Leventhal the enigma of polycystic ovarian syndrome keeps on unfolding day by day. Recently due to changes in lifestyle the incidence of adolescent PCOS is on rise and form the basis of metabolic and endocrinological diseases in later life. Hence, it is of utmost importance to recognize the pathology at earliest and treat it before the features become resistant. How to cite this article Singh R, Yadav P, Parveen R. Adolescent Polycystic Ovary Syndrome: A Management Dilemma. J South Asian Feder Obst Gynae 2012;4(3):123-125.
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Kiryushkina, D. A. "From the history of polycystic ovary syndrome." Obstetrics, Gynecology and Reproduction 13, no. 3 (September 21, 2019): 261–64. http://dx.doi.org/10.17749/2313-7347.2019.13.3.261-264.

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Polycystic ovary syndrome (PCOS) is a gynecological disease manifested in polycystic ovarian morphology, oligo/ anovulation, hyperandrogenism, hirsutism, alopecia, and acne. PCOS affects 5–10 % of women of reproductive age. The first histological description of polycystic ovaries was made by Antonio Vallisneri. Then, Kronid Fedorovich Slavyanskiy, for the first time, described the clinical picture of PCOS, and Sergey Kuzmich Lesnoy proposed ovary wedge resection for surgical treatment. Irving Stein and Michael Leventhal studied the PCOS symptom complex and provided the recommendations on its diagnosis and treatment to restore normal menstrual cycle and fertility in such patients.
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Khankoev, IM, BI Kazakov, OA Magerlamov, and VN Pigarev. "Comparative evaluation of the effect of the combined treatment of stein-leventhal syndrome with high-level prolactin." Journal of the American Association of Gynecologic Laparoscopists 1, no. 4 (August 1994): S17. http://dx.doi.org/10.1016/s1074-3804(05)80923-5.

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Dey, Prabha. "Quality of life of women with polycystic ovarian syndrome." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 7, no. 7 (June 27, 2018): 2586. http://dx.doi.org/10.18203/2320-1770.ijrcog20182447.

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Background: Polycystic ovary syndrome (PCOS), also known as hyper androgenic anovolation (HA or Stein-Leventhal syndrome) is a well-recognised and common condition that causes considerable morbidity. The objective of the present study was to find out the quality of life of women with polycystic ovarian syndrome.Methods: Patients with PCOD diagnosed clinically at out patients department were selected for the study. SF 36 was applied to find out the Quality of life of women with polycystic ovarian syndrome.Results: A total of 84 patients were participated and 75% of the sample were student, 56.7% were graduate and 86.7% were non-vegetarian. The mean height of the sample was 155±4.81 centimeters. The mean weight of sample was 59.35±6.63 kgs and BMI mean was 24.70±3.47. Among 35% the duration of diagnosis was less than one year and for 65% it was more than one year. Means of the all sub set scores, across shorter and longer duration of being diagnosed as PCOD were significantly same on t test.Conclusions: Measured by SF 36, women with poly cystic ovarian disease/symptoms are suffering from significantly lowered quality of life, but independent of their duration of illness.
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Donesky, Barry W. "The role of laparoscopic ovarian electrocautery in the new millennium." Reproductive Medicine Review 7, no. 2 (July 1999): 111–29. http://dx.doi.org/10.1017/s0962279999000241.

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With the introduction of bilateral ovarian wedge resection (BOWR) in 1935, Stein and Leventhal were the first to describe an effective treatment for the chronic anovulation and associated infertility resulting from what was later to become known as polycystic ovary syndrome (PCOS). Since that time, many less invasive methods of ovulation induction and enhancement have been developed. While the success of medical ovulation induction led to the almost complete replacement of BOWR by the late 1970's, the presence of a group of women who are not optimally treated by medical methods has maintained the interest in surgical approaches. Surgical and nonsurgical methods of treatment for anovulatory women have continued to be refined. This manuscript reviews this literature and attempts to provide a framework for the role that modern surgical methods of ovulation induction might play in the current scheme of treatment for anovulatory infertility in women with PCOS.
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Dissertations / Theses on the topic "Syndrome de Stein-Leventhal"

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Angles, Michel. "Le syndrome de stein-leventhal de l'adolescente." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20311.

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Schattman, Linda. "The role of testosterone in aspects of cognition, aggression, and sexual functioning in women with polycystic ovary syndrome and in healthy young women /." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=85094.

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Sex differences have been established in a number of behaviours, including aspects of cognition, aggression, and sexuality. Although there has been a considerable amount of research concerning the influence of estrogen on sexually dimorphic behaviours, there has been a dearth of investigations on the role of testosterone (T) in these behaviours in women. The studies presented here were undertaken to elucidate the role of T in sexually-dimorphic aspects of psychological functioning in women. In Study 1, users and non-users of oral contraceptives were tested with a battery of neuropsychological tests and questionnaires at two different phases of the menstrual cycle. Results showed that women with chronic low levels of free T induced by oral contraceptives demonstrated better verbal fluency and visuospatial memory performance and reported lower levels of verbal aggression than naturally-cycling women whose free T levels were within the normal female range. Furthermore, although self-ratings of hostility fluctuated across test sessions concomitant with changes in free T levels, performance on cognitive tests did not appear to be influenced by the fluctuations in T levels across the menstrual cycle. In Study 2, women with elevated free T levels due to polycystic ovary syndrome (PCOS) demonstrated worse verbal fluency, verbal memory, manual dexterity, and visuospatial working memory performance, but reported higher levels of anger than healthy, matched control women. Women with PCOS also reported lower levels of sexual cognition and arousal than healthy controls. In Study 3, women with PCOS were randomly assigned to receive 3 months of treatment with an anti-androgen or placebo. Anti-androgen treatment resulted in significant reductions in free T levels and in improvements in verbal fluency performance. Taken together, the results of these three studies suggest that T has a detrimental effect on aspects of cognitive functioning in women, particu
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Boutes, Chantal. "Syndrome des ovaires polykystiques et fécondation in vitro." Montpellier 1, 1988. http://www.theses.fr/1988MON11027.

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Attaoua, Redha. "Déterminisme génétique de la résistance à l'insuline dans les maladies complexes : application des stratégies de criblage dense du génome basées sur les profils de déséquilibre de liaison dans la génétique du syndrome des ovaires polykystiques." Montpellier 1, 2009. http://www.theses.fr/2009MON1T011.

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La résistance à l'insuline est un désordre métabolique caractérisé par la diminution de l'action de l'insuline sur ses tissus cibles. Elle caractérise un ensemble de maladies mendéliennes comme le syndrome de type A, ou complexes comme le diabète de type 2 ou le syndrome des ovaires polykystiques (SOPK). Dans ma thèse, nous avons étudié l'association de trois gènes au SOPK dans une population de femmes d' Europe Centrale. Il s'agit du VNTR du gène de l'insuline, du gène du récepteur de l'insuline (INSR) et du FTO (fat mass ans obesity associated gene). Les marqueurs génétiques utilisés dans ces études sont les SNP, des polymorphismes mononucléotidiques et bialléliques que nous avons génotypés par séquençage en fluorescence ou par SSO-PCR (sequence specific oligonucleotide-PCR). Dans l'exploration de INSR, le microsatellite D19S884 situé à 1 mb du gène a été criblé par PCR fluorescente. Le déséquilibre de liaison (DL) entre les SNP a été mesuré par HAPLOVIEW 3. 31 et la combinaison de ces polymorphismes en haplotypes dans la population a été déterminée par le logiciel PHASE 2. 1. Le logiciel StatView and SAS a été utilisé pour calculer les associations génétiques par régression logistique ou pour mesurer les corrélations génotype-phénotype par ANOVA. L'étude du VNTR (en criblant 7 SNP) a été réalisée chez 160 femmes avec SOPK et 95 contrôles. L'exploration du gène INSR (par génotypage de 5 SNP et de 1 microsatellite) a été établie chez 115 femmes avec SOPK et 111 contrôles tandis que l'investigation du FTO (en criblant le SNP rs1421085) a été effectuée chez 207 cas et 100 contrôles. Le gène FTO a été également exploré dans l'obésité de la population générale des femmes, dans une cohorte du Sud de la France (71 avec obésité simple, 48 avec obésité morbide et 128 contrôles). Nous avons constaté l'association du VNTR, par SNP et par son haplotype H5, à un effet protecteur contre le SOPK (OR=0,54, P<0,03), tandis que le gène INSR nous est apparu plutôt pathogène en s'associant par son haplotype H9 au SOPK et à l'infertilité (OR=3,0; P<3,1. 10 ˉ³) et en corrélant avec l'hyperandrogénisme et avec les degrés de sévérité du syndrome. Le FTO quant à lui ne s'associe pas au phénotype SOPK comme l'est INSR, mais s'associe plutôt à l'obésité, au syndrome métabolique (SMet) et à la résistance à l'insuline dans la maladie (OR = 3,2; P < 0,0001). Cette donnée a été confirmée dans l'obésité de la population générale des femmes, où FTO a été associé au phénotype obèse comme c'est d'ailleurs le cas du gène IRS-2, un gène également génotypé dans cette étude. Cependant, et contrairement au FTO, l'association de IRS-2 se limite à l'obésité (OR = 4,4; P < 0,01) mais pas au SMet et à ses composantes comme l'intolérance au glucose (IGT) et l'insulinorésistance. En conclusion, cette thèse m'a permis d'une part de montrer l'intérêt de l'utilisation des haplotypes comme marqueurs dans l'étude génétique des maladies complexes, et d'autre part de constater la nécessité de l'exploration génétique des désordres métaboliques dans SOPK pour rechercher des inividus à risque cardiovasculaire ou de diabète de type 2
Insulin resistance is a metabolic disorder characterized by a decrease of insulin activity on its target issues. It characterizes a panel of Mendelian diseases as type A syndrome or complex affections as type 2 diabetes or polycystic ovary syndrome (PCOS). In my thesis, we focused on the study of 3 genes in PCOS, in a women population from Central Europe. Genes explored were VNTR of insulin gene, insulin receptor gene (INSR) and FTO (fat mass and obesity associated gene). Genetic markers used in these studies were SNPs, a mononucleotidic and biallelic polymorphisms which we genotyped using fluorescent sequencing or SSO-PCR (sequence specific oligonucleotide-PCR). For INSR, the microsatellite D19S884 located at 1 Mb from the gene genotyped by fluorescent PCR. Linkage disequilibrium between SNPs was measured using HAPLOVIEW 3. 31 and the combination of these polymorphisms into haplotypes in the population was determined by the software PHASE 2. 1. The software StatView ans SAS was used to calculate genetic association by logistic regression or to assess genotype-phenotype correlations by ANOVA. Exploration of VNTR (by genotyping 7 SNPs) was achieved in a population of 160 women with PCOS and 95 controls. INSR was explored (by genotyping 5 SNPs and one microsatellite) in a population of 115 women with PCOS and 11 controls, while FTO gene was investigated (by genotyping one SNP : rs1421085) in 207 cases and 100 controls. FTO was also studied in the obesity of the general women population, in a cohort from Southern France (71 women with simple obesity, 48 others with morbid obesity and 128 controls). We observed that VNTR associates to a prospective effect against PCOS by its SNPs and haplotype H5 (OR = 0. 54; P< 0. 03) while insulin receptor gene appeared as pathogenic by its haplotype H9 which associates to PCOS and infertility (OR = 3. 0, P < 3. 1. 10ˉ³) and correlates with hyperandrogenism and the severity of the disease. FTO did not associate to the phenotype PCOS like INSR but to metabolic syndrome (MetS) and insulin resistance in PCOS (OR = 3. 2; p <0. 0001). This findind was confirmed in obesity of the general women population where FTO was associated as IRS-2, also genotyped in this cohort, to obesity. However, the association of IRS-2 was limited to obesisty (P < 0. 01, OR = 4. 4) and did not extend to MetS and its components as impaired glucose tolerance (IGT) and insulin resistance. In conclusion, my thesis demonstrates the importance of using haplotypes as markers in genetic studies of complex diseases but also allows to note the necessity of investigating the genetic background of metabolic disorders in PCOS aiming individuals of a high cardiovascular and type 2 diabetes risk
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Chhuon, Danielle. "Le syndrome des ovaires polykystiques : réactualisation des données de la littérature et application à l'étude de quelques dossiers cliniques." Paris 5, 1998. http://www.theses.fr/1998PA05P032.

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Macari, Françoise. "Déterminisme génétique de la résistance à l'insuline : identification de défauts moléculaires dans les syndromes de type A, d'Alström et des ovaires polykystiques." Montpellier 1, 1999. http://www.theses.fr/1999MON13505.

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Rehme, Marta Francis Benevides. "O hiperandrogenismo influencia no desenvolvimento de síndrome metabólica em pacientes com síndrome dos ovários policísticos?" Botucatu : [s.n.], 2009. http://hdl.handle.net/11449/106373.

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Orientador: Anaglória Pontes
Banca: Tamara Goldberg
Banca: Marcos Felipe Silva de Sá
Banca: José Alcione Macedo Almeida
Banca: Cleusa Cascaes Dias
Resumo: A síndrome dos ovários policísticos (SOP) afeta 5 a 8% das mulheres no menacme e é caracterizada pela anovulação crônica e hiperandrogenismo. A obesidade central e a resistência insulínica (RI) são freqüentes na SOP e desempenham um papel fundamental na etiopatogenia da síndrome metabólica (SM). O hiperandrogenismo tem sido questionado como um fator importante no desenvolvimento da SM em mulheres com SOP. Verificar se o hiperandrogenismo influencia no desenvolvimento de síndrome metabólica em pacientes com SOP. Foram avaliados retrospectivamente os dados clínicos, bioquímicos e ultrassonográficos de 180 mulheres com SOP diagnosticadas pelos critérios de Rotterdam e de 70 mulheres com obesidade simples. As pacientes com SOP foram classificadas de acordo com o índice de massa corporal (IMC) em SOP não obesas e SOP obesas. As pacientes obesas simples não apresentaram hiperandrogenismo clínico nem bioquímico. O índice de sensibilidade à insulínica (ISI) foi avaliado pelo HOMA-IR e ISI de Matsuda e DeFronzo. A SM foi diagnosticada pelos critérios do NCEP-ATP III com modificações sugeridas pelo consenso de Rotterdam. A média de idade das pacientes foi de 27,3 + 4,7 no grupo das pacientes SOP não obesas; 28,8 + 5,0 nas SOP obesas e 27,4 + 5,2 nas obesas simples (p=0, 0773), e o IMC foi de 25,1+3,0 kg/m2; 37,0+ 5,5 kg/m2 e 36,0+ 4,2 kg/m2 respectivamente (p<0, 001). A prevalência de RI e SM não diferiu entre as pacientes obesas com e sem SOP e foi significativamente maior do que nas SOP não obesas (p<0, 001). Entretanto a prevalência de SM foi maior nas SOP obesas com hiperandrogenismo... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Polycystic ovary syndrome (PCOS) affects 5-8% of women at menacme and is characterized by chronic anovulation and hyperandrogenism. Central obesity and insulin resistance (IR) are frequent in PCOS and play a leading role in the etiopathogeny of metabolic syndrome (MS). Hyperandrogenism has been suggested as an important factor in the development of MS in women with PCOS. To determine whether hyperandrogenism influences the development of metabolic syndrome in patients with PCOS. Clinical, biochemical and ultrasonographic data on 180 women with PCOS, as diagnosed by the Rotterdam criteria, and 70 women with simple obesity were retrospectively analyzed. According to body mass index, PCOS patients were classified as nonobese with PCOS and obese with PCOS. No clinical or biochemical hyperandrogenism was observed in patients with simple obesity. Insulin sensitivity indices (ISI) were assessed as proposed by HOMA-IR and ISI (Matsuda and De Fronzo). MS was diagnosed based on NCEP-ATP III criteria with modifications suggested by the Rotterdam consensus. Mean age was 27.3 + 4.7 among non-obese patients with PCOS, 28.8 + 5.0 in obese patients with POS, and 27.4 + 5.2 in those with simple obesity (p=0.0773), while BMI was 25.1+3.0 kg/m2, 37.0+ 5.5 kg/m2 and 36.0+ 4.2 kg/m2, respectively (p<0.001). The prevalence of IR and MS did not differ between obese patients with and without PCOS, and was significantly higher in these patients than in non-obese women with PCOS (p<0.001). The prevalence of MS, however, was higher... (Complete abstract click electronic access below)
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Barbotin, Anne-Laure. "Plasticité neuro-structurale de l’hypothalamus dans le syndrome des ovaires polykystiques." Thesis, Lille, 2019. http://www.theses.fr/2019LILUS043.

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L’hormone anti-Müllerienne (AMH) dont les taux dans le sérum sont élevés dans le Syndrome des Ovaires Polykystiques (SOPK) est connue pour augmenter la sécrétion de LH/GnRH. Comme mis en évidence récemment, cette augmentation de la sécrétion de GnRH pourrait être liée à une hyperactivité des neurones à GnRH en réponse à une action directe de l’AMH mais pourrait également s’exercer indirectement via une augmentation des afférences excitatrices sur les neurones à GnRH. Par ailleurs, les tanycytes, qui enchâssent les terminaisons des neurones à GnRH, expriment le récepteur à l’AMH et sont connus pour moduler la plasticité neuro-structurale de l’hypothalamus. Ainsi, notre objectif est de tester les deux hypothèses suivantes dans un modèle animal et chez la femme. Est-ce que la physiopathologie du SOPK : 1- Est liée à une rétraction des tanycytes provoquée par l’AMH, entraînant l’augmentation des sécrétions de GnRH / LH ? Et/ou 2- Est liée à une augmentation de l’activité des neurones à GnRH AMH-dépendante ?Nous avons étudié la modification de la plasticité morphologique de l’hypothalamus en microscopie électronique en comparant la distance entre les terminaisons des neurones à GnRH et l’espace péri-capillaire entre des éminences médianes de rates en phase de dioestrus de leur cycle oestral (au moment où ces terminaisons sont normalement enfouies par les tanycytes) traitées par de l’AMH et des contrôles. Puis, nous avons comparé cette même distance entre des éminences médianes issues d’un modèle de souris SOPK en comparaison à des contrôles. Enfin, nous avons étudié la plasticité neuro-structurale de l’hypothalamus chez des femmes SOPK et des témoins par une approche en imagerie en comparant les métabolites cérébraux.Nous avons observé une augmentation significative du nombre de terminaisons de neurones à GnRH situées à proximité de l’espace péri-capillaire dans le groupe traité par l’AMH par rapport aux contrôles et nous avons fait les mêmes observations chez les souris SOPK comparées aux contrôles. Par ailleurs, nous avons mis en évidence une augmentation de l’activité neuronale dans le noyau arqué de l’hypothalamus chez des souris SOPK. Or, cette région est particulièrement impliquée dans la régulation de la sécrétion de GnRH. Chez les femmes atteintes de SOPK, nous avons pour la première fois mis en évidence des concentrations plus élevées de GnRH mesurées par spectroscopie de masse par rapport à des femmes normo-ovulantes. Notre étude par IRM, chez les femmes SOPK et contrôles, vient conforter ce résultat en montrant une augmentation de la viabilité/activité neuronale. Cette étude translationnelle suggère que l’augmentation des sécrétions de GnRH/LH rencontrées dans le SOPK serait dépendante d’une part d’un rapprochement de terminaisons à GnRH à l’espace péri-capillaire et d’autre part d’une augmentation de l’activité neuronale hypothalamique
Polycystic ovary syndrome (PCOS) is the most common reproductive disorder (10% of women worldwide). Anti-Müllerian hormone (AMH) levels are found to be 2-3-fold higher in PCOS women than in those with normal ovaries. AMH induces LH secretion by stimulating the activation of GnRH secretion. As recently demonstrated, this increase in GnRH secretion could be related to hyperactivity of GnRH neurons in response to a direct action of AMH but could also be exerted indirectly via an increase in excitatory inputs on GnRH neurons.Our team has previously demonstrated that tanycytes, which unsheathe the terminals of GnRH neurons, regulate GnRH secretion and express AMH receptor. Thus, we aim to determine (1) whether elevated AMH could be responsible for the retraction of the tanycyte coverage leading to increased GnRH/LH secretion in PCOS and (2) whether neuronal hyperactivity in hypothalamus could contribute to higher GnRH activity in PCOS women.Firstly, we have performed ultrastructural studies in rodents’ median eminence (ME) explants challenged with AMH. Then, we compared tanycytic retraction using electron microscopy. We have performed the same experiments in a PCOS mouse model. In humans, we have used metabolic magnetic resonance imaging approaches (i.e. proton magnetic resonance spectra). In order to assess neuronal activity, we have compared N-acetyl-aspartate/creatine ratios in the hypothalamus between PCOS women versus controls.Using electron microscopy, we have shown that tanycytes displayed a significant retraction of their end-feet after AMH treatment ex vivo. This is followed by the sprouting of GnRH terminals towards the pericapillary space. Such processes could significantly favor the sustained delivery of peak levels of GnRH, which could contribute to the rise in LH levels typical of PCOS condition. We have found the same results in PCOS-mouse model with higher GnRH terminals towards the pericapillary space in PCOS mice than in controls. In addition, we found an increase in neuronal activity in the arcuate nucleus of the hypothalamus in PCOS mice. Moreover, this region is particularly involved in the regulation of GnRH secretion. For the first time, we have demonstrated that PCOS women exhibit higher concentrations of GnRH measured by mass spectroscopy than GnRH levels in normo-ovulatory women. Our proton magnetic resonance spectroscopy analysis has revealed that PCOS women exhibit higher N-acetyl aspartate/creatine ratio than controls. These results are predicted to be correlated with increased hypothalamic activity.This translational study suggests that the increase in GnRH / LH secretions found in PCOS could be explained by neurostructural hypothalamic plasticity in link with tanycytes retraction and by an increase of neuronal activity in the hypothalamus
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Aït, El Mkadem Samira. "Déterminisme génétique de la résistance à l'insuline : identification de défauts moléculaires dans le syndrome des ovaires polykistiques, l'obésité et le diabète sucré." Saint-Etienne, 2000. http://www.theses.fr/2000STET004T.

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Gürber, Peter. "Das "Stein-Leventhal-Syndrom" /." [S.l : s.n.], 1987. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Books on the topic "Syndrome de Stein-Leventhal"

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PCOS: The silent epidemic. Indianapolis, Ind: Perspectives Press, 2000.

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Best-Boss, Angie. Living with PCOS: Polycystic ovary syndrome. 2nd ed. Omaha, Neb: Addicus Books, 2009.

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Best-Boss, Angie. Living with P.C.O.S.: Polycystic ovary syndrome. Omaha, Neb: Addicus Books, 2001.

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Y, Boutaleb, and Gzouli A, eds. The treatment of endometriosis--and other disorders and infections. Carnforth, Lancs, UK: Parthenon Pub. Group, 1991.

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Andrea, Dunaif, ed. Polycystic ovary syndrome. Boston: Blackwell Scientific Publications, 1992.

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What to Do When the Doctor Says It's PCOS: (Polycystic Ovarian Syndrome). Fair Winds Press, 2003.

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W, Shaw Robert, Imperial Chemical Industries, ltd. Pharmaceutical Division., and Workshop in Reproductive Endocrinology (3rd : 1990 : Kings College, Cambridge), eds. Polycystic ovaries: A disorder or a symptom? Carnforth, Lancs., England: Parthenon Pub. Group, 1991.

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T, Kovacs Gabor, ed. Polycystic ovary syndrome. Cambridge, U.K: Cambridge University Press, 2000.

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Polycystic Ovary Syndrome. Cambridge University Press, 2012.

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George, Tolis, Bringer Jacques, and Chrousos George P, eds. Intraovarian regulators and polycystic ovarian syndrome: Recent progress on clinical and therapeutic aspects. New York, N.Y: New York Academy of Sciences, 1993.

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Book chapters on the topic "Syndrome de Stein-Leventhal"

1

"Polycystic Ovarian Disease (Stein-Leventhal syndrome)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1528. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_13178.

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2

"Polycystic Ovarian Syndrome (PCOS, Stein-Leventhal Disease)." In The APRN and PA’s Complete Guide to Prescribing Drug Therapy. New York, NY: Springer Publishing Company, 2019. http://dx.doi.org/10.1891/9780826179357.0312.

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3

"Polycystic Ovarian Syndrome (PCOS, Stein-Leventhal Disease)." In The APRN and PA’s Complete Guide to Prescribing Drug Therapy. New York, NY: Springer Publishing Company, 2019. http://dx.doi.org/10.1891/9780826179340.0312.

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