Insights into hypothalamic-pituitary dysfunction in polycystic ovary syndrome

Hall, Janet E.; Taylor, Ann E.; Hayes, Frances J.; Crowley, William F.

doi:10.1007/bf03350785

Cited by 60 publications

(31 citation statements)

References 65 publications

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“…The ovary has been implicated as the prime suspect, 2 as has the hypothalamicpituitary axis, 25,27 and currently some defect in insulin ac- The peripheral small follicles lined up are often referred to as the "black pearl necklace sign." The ovary is also larger (dimensions 4.44 cm ϫ 2.57 cm) in cross section than a normal ovary.…”

Section: Pathophysiology Of Pcosmentioning

confidence: 99%

A 27-Year-Old Woman With a Diagnosis of Polycystic Ovary Syndrome

Legro

2007

JAMA

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Background: Polycystic ovary syndrome and oligomenorrhea which is one of its complications are considered as the most common causes of menstrual disorders which increases the risk of depression and psychological effects complications. The prevalence of oligomenorrhea is predicted to be 12 to 15 percent. This syndrome occurs with symptoms such as obesity, impaired glucose metabolism, dysmenorrhea, oligomenorrhea and other symptoms. In addition, incidence of decreased libido, painful sexual intercourse and decreased libido are also observed in the patients concurrently which must be considered during the treatment. Case Presentation: The case is a 27 year old woman married 2 years ago without children, unprotected, housewife who has been referred to the clinic of traditional medicine in June 2016 with palpitation complaints, dizziness, extreme tiredness, poor sleep, fatigue, darkening of skin along with syncopal attacks. She was the candidate for standard treatment for depression with diagnosis of depression by a psychiatrist. Based on the history of the patient, she has experienced delayed period for up to three months, severe pain prior to and during menstruation, dyspareunia and fear of sexual intercourse, decreased libido and progressive lack of sexual satisfaction over the past two years. She suffered from epileptic attack every 7-10 days without falling resulting in organ and head damage. After taking history, medical tonic treatment of ovarian and treatment using sitz-bath and training for sexual intercourse were conducted simultaneously from the perceptive of modern and Iranian medicine and menstruation was regulated in the first three months and sexual intercourse gradually became possible in the next three months and patient experienced regular menstruation and complete sexual intercourse with sexual pleasure at the end of six months. Conclusion: Treatment of this patient by modification of her uterus and ovaries function, creation of menstrual regularity and possibility of sexual intercourse along with sexual pleasure based on sexual pleasure highlights the necessity of more attention to the connection between the different organs in the human body. A woman's uterus and femininity functions make her sick in the case of disorder, one of such is termed strangulation of uterus (Ekhtenagh in Persian) in Iranian medicine.

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Section: Pathophysiology Of Pcosmentioning

confidence: 99%

A 27-Year-Old Woman With a Diagnosis of Polycystic Ovary Syndrome

Legro

2007

JAMA

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“…It is due to a combination of genetic and environmental factors. A dysfunction of the hypothalamicpituitary-ovarian or adrenal axis was proposed to be the cause of hyperandrogenemia in women with PCOS (Hall et al 1998, Baptiste et al 2010. Risk factors for the…”

Section: Introductionmentioning

confidence: 99%

Hormonal alterations in PCOS and its influence on bone metabolism

Krishnan¹,

Muthusami²

2017

Journal of Endocrinology

129

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According to the World Health Organization (WHO) polycystic ovary syndrome (PCOS) occurs in 4-8% of women worldwide. The prevalence of PCOS in Indian adolescents is 12.2% according to the Indian Council of Medical Research (ICMR). The National Institute of Health has documented that it affects approximately 5 million women of reproductive age in the United States. Hormonal imbalance is the characteristic of many women with polycystic ovarian syndrome (PCOS). The influence of various endocrine changes in PCOS women and their relevance to bone remains to be documented. Hormones, which include gonadotrophin-releasing hormone (GnRH), insulin, the leutinizing/follicle-stimulating hormone (LH/FSH) ratio, androgens, estrogens, growth hormones (GH), cortisol, parathyroid hormone (PTH) and calcitonin are disturbed in PCOS women. These hormones influence bone metabolism in human subjects directly as well as indirectly. The imbalance in these hormones results in increased prevalence of osteoporosis in PCOS women. Limited evidence suggests that the drugs taken during the treatment of PCOS increase the risk of bone fracture in PCOS patients through endocrine disruption. This review is aimed at the identification of the relationship between bone mineral density and hormonal changes in PCOS subjects and identifies potential areas to study bone-related disorders in PCOS women.

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“…To what extent reduced sensitivity to E 2 negative feedback contributes to the hypergonadotropism and what are the consequences of this feedback disruption in terms of fertility remain to be determined. The prenatal T females exhibit several characteristic features that are typical of the majority of women with polycystic ovary syndrome (PCOS), namely hypergonadotropism, and an increase in LH to FSH ratio and multifollicular ovaries (53)(54)(55). The hypergonadotropism in women with PCOS is a contributing factor in development of hyperandrogenism, multifollicular ovaries, and infertility because treatment with GnRH-A helps correct hyperandrogenism of ovarian origin in women with PCOS (56)(57)(58)(59).…”

Section: Implications Of Reduced E 2 Negative Feedbackmentioning

confidence: 99%

Fetal Programming: Excess Prenatal Testosterone Reduces Postnatal Luteinizing Hormone, But Not Follicle-Stimulating Hormone Responsiveness, to Estradiol Negative Feedback in the Female

Sarma¹,

Manikkam²,

Herkimer³

et al. 2005

Endocrinology

100

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Exposure of female sheep fetuses to excess testosterone (T) during early to midgestation produces postnatal hypergonadotropism manifest as a selective increase in LH. This hypergonadotropism may result from reduced sensitivity to estradiol (E 2 ) negative feedback and/or increased pituitary sensitivity to GnRH. We tested the hypothesis that excess T before birth reduces responsiveness of LH and FSH to E 2 negative feedback after birth. Pregnant ewes were treated with T propionate (100 mg/kg in cotton seed oil) or vehicle twice weekly from d 30 -90 gestation. Responsiveness to E 2 negative feedback was assessed at 12 and 24 wk of age in the ovaryintact female offspring. Our experimental strategy was first to arrest follicular growth and reduce endogenous E 2 by administering the GnRH antagonist (GnRH-A), Nal-Glu (50 g/kg sc every 12 h for 72 h), and then provide a fixed amount of exogenous E 2 via an implant. Blood samples were obtained every 20 min at 12 wk and every 10 min at 24 wk before treatment, during and after GnRH-A treatment both before and after E 2 implant. GnRH-A ablated LH pulsatility, reduced FSH by approximately 25%, and E 2 production diminished to near detection limit of assay at both ages in both groups. Prenatal T treatment produced a precocious and selective reduction in responsiveness of LH but not FSH to E 2 negative feedback, which was manifest mainly at the level of LH/GnRH pulse frequency. Collectively, these findings support the hypothesis that prenatal exposure to excess T decreases postnatal responsiveness to E 2 inhibitory feedback of LH/GnRH secretion to contribute to the development of hypergonadotropism. (Endocrinology 146: 4281-4291, 2005)

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Insights into hypothalamic-pituitary dysfunction in polycystic ovary syndrome

Cited by 60 publications

References 65 publications

A 27-Year-Old Woman With a Diagnosis of Polycystic Ovary Syndrome

A 27-Year-Old Woman With a Diagnosis of Polycystic Ovary Syndrome

Hormonal alterations in PCOS and its influence on bone metabolism

Fetal Programming: Excess Prenatal Testosterone Reduces Postnatal Luteinizing Hormone, But Not Follicle-Stimulating Hormone Responsiveness, to Estradiol Negative Feedback in the Female

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