Diagnosis of Polycystic Ovary Syndrome

Chang, R. Jeffrey; Katz, Seth E.

doi:10.1016/s0889-8529(05)70076-1

Cited by 57 publications

(46 citation statements)

References 74 publications

(77 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Patients with Cushing's syndrome have elevated levels of circulating androgen, as well as abnormal secretion of cortisol, manifested by increased basal levels of cortisol and failure of suppression after stimulation with dexamethasone. [16][17][18] In patients who have HAIR-AN syndrome without underlying ovarian tumors or adrenal abnormalities, testosterone levels can become significantly elevated while DHEAS and 17␣-hydroxyprogesterone concentrations are normal. The levels of gonadotropins are also normal.…”

Section: Laboratory Studiesmentioning

confidence: 99%

Clinical Presentation and Differential Diagnosis

Scott

2013

Myelodysplastic Syndromes

View full text Add to dashboard Cite

Section: Laboratory Studiesmentioning

confidence: 99%

Clinical Presentation and Differential Diagnosis

Scott

2013

Myelodysplastic Syndromes

View full text Add to dashboard Cite

“…Follicular monitoring was performed in all patients to detect a preovulatory follicle, the day of ovulation and the development of the corpus luteum (8,9). The presence of a dominant follicle (>16-18 mm in diameter) and of an echogenic mass projecting into the follicle were the potential signs of impending ovulation.…”

Section: Ultrasonographic Analysismentioning

confidence: 99%

Effects of metformin treatment on luteal phase progesterone concentration in polycystic ovary syndrome

Meenakumari

Agarwal

Krishna

et al. 2004

Braz J Med Biol Res

View full text Add to dashboard Cite

The causes of luteal phase progesterone deficiency in polycystic ovary syndrome (PCOS) are not known. To determine the possible involvement of hyperinsulinemia in luteal phase progesterone deficiency in women with PCOS, we examined the relationship between progesterone, luteinizing hormone (LH) and insulin during the luteal phase and studied the effect of metformin on luteal progesterone levels in PCOS. Patients with PCOS (19 women aged 18-35 years) were treated with metformin (500 mg three times daily) for 4 weeks prior to the test cycle and throughout the study period, and submitted to ovulation induction with clomiphene citrate. Blood samples were collected from control (N = 5, same age range as PCOS women) and PCOS women during the late follicular (one sample) and luteal (3 samples) phases and LH, insulin and progesterone concentrations were determined. Results were analyzed by one-way analysis of variance (ANOVA), Duncan's test and Karl Pearson's coefficient of correlation (r). The endocrine study showed low progesterone level (4.9 ng/ml) during luteal phase in the PCOS women as compared with control (21.6 ng/ml). A significant negative correlation was observed between insulin and progesterone (r = -0.60; P < 0.01) and between progesterone and LH (r = -0.56; P < 0.05) concentrations, and a positive correlation (r = 0.83; P < 0.001) was observed between LH and insulin. The study further demonstrated a significant enhancement in luteal progesterone concentration (16.97 ng/ml) in PCOS women treated with metformin. The results suggest that hyperinsulinemia/insulin resistance may be responsible for low progesterone levels during the luteal phase in PCOS. The luteal progesterone level may be enhanced in PCOS by decreasing insulin secretion with metformin.

show abstract

“…The cardinal features of this syndrome include hyperandrogenism, chronic anovulation, and polycystic ovaries; however, of most concern is the observation that these young women demonstrate a greater propensity towards the development of metabolic disease as well as infertility and recurrent miscarriage (Chang & Katz 1999). Nearly, 40% of women with PCOS exhibit insulin resistance, a condition that is only aggravated by the increased prevalence of obesity in women with this syndrome (Legro et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Transgenic overexpression of plasminogen activator inhibitor-1 promotes the development of polycystic ovarian changes in female mice

Devin¹,

Johnson²,

Eren³

et al. 2007

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Reproductive age women (5-10%) are affected by the polycystic ovarian syndrome (PCOS), a diagnosis which confers lifelong cardiovascular and reproductive health implications. Plasminogen activator inhibitor-1 (PAI-1), the main physiological inhibitor of plasminogen activation, is consistently elevated in women with PCOS, regardless of metabolic status. Interestingly, the plasminogen system has long been implicated in proteolytic processes within the dynamic ovary. A non-physiologic elevation in PAI-1 may thus contribute systemically to endothelial dysfunction and locally to abnormal ovarian phenotype and function. We herein characterize the phenotypic alterations in ovaries from transgenic mice, which constitutively express a stable form of human PAI-1 and determine the plasma testosterone level in these mice as opposed to their unaffected counterparts. Over half of the ovaries from transgenic mice were found to contain large cystic structures, in contrast to wild-type controls of the same genetic background (53% (NZ17) vs 5% (NZ22); PZ0 . 001). Plasma testosterone was nearly twofold elevated in transgenic female mice versus wild-type females (0 . 312 ng/mlG 0 . 154 (NZ10) vs 0 . 181 ng/mlG0 . 083 (NZ8); PZ0 . 014). An elevation in PAI-1 therefore appears to predispose mice to the development of this abnormal architecture, which in turn is associated with an increase in plasma testosterone. Therefore, we propose that an inappropriate elevation in PAI-1 contributes to the development of polycystic structures; these findings may thus reorient the efforts aimed at the development of therapeutic agents for the treatment of this increasingly common syndrome.

show abstract

Diagnosis of Polycystic Ovary Syndrome

Cited by 57 publications

References 74 publications

Clinical Presentation and Differential Diagnosis

Clinical Presentation and Differential Diagnosis

Effects of metformin treatment on luteal phase progesterone concentration in polycystic ovary syndrome

Transgenic overexpression of plasminogen activator inhibitor-1 promotes the development of polycystic ovarian changes in female mice

Contact Info

Product

Resources

About