scholarly journals Nephrolithiasis and Polycystic Ovary Syndrome: A Case-Control Study Evaluating Testosterone and Urinary Stone Metabolic Panels

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Donald Fedrigon ◽  
Kareem Alazem ◽  
Sri Sivalingam ◽  
Manoj Monga ◽  
Juan Calle
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Sodium Excretion ◽  
Polycystic Ovary ◽  
Stone Formation ◽  
Free Testosterone ◽  
Case Control ◽  
Composition Analysis ◽  
Ovary Syndrome ◽  
Stone Composition ◽  
Stone Formers

Introduction. Both elevated testosterone and polycystic ovary syndrome (PCOS) have been speculated as possible risk factors for kidney stone formation; however, the details of this potential relationship with regards to 24-hour urine metabolic panels and stone composition have not previously been characterized. Methods. A total of 74 PCOS patients were retrospectively identified and matched with a cohort of female stone formers at a 3 : 1 ratio (by age and BMI). All patients had 24-hour urinary metabolic panels and stone compositions. These groups were compared using Pearson chi-square and Student t-tests. Additionally, the PCOS group was differentiated based on free testosterone using multivariate analysis. Results. The case-control cohort showed that PCOS patients had significantly lower sodium excretion p=0.015 and hypernatriuria rates (28.9% vs 50.9%, p=0.009). The PCOS-testosterone cohort demonstrated that high testosterone patients had significantly higher citrate values p=0.041 and significantly lower odds of hypocitraturia (36.7% vs 54.2%, OR = 0.2, p=0.042). The high testosterone group also had higher sodium excretion p=0.058 with significantly higher odds of having hypernatriuria (40.0% vs 13.6%, OR = 13.3, p=0.021). No significant patterns were revealed based on stone composition analysis. Conclusions. Compared to healthy stone formers, PCOS patients did not demonstrate significant differences in 24-hour urine and stone composition values. Elevated free testosterone in PCOS patients has a significant association with higher urinary citrate and sodium values: findings that in and of themselves do not confirm the hypothesized increased risk of stone formation. This patient cohort may provide deeper insight into the interplay between androgens and stone formation; however, further study is needed to fully characterize the possible relationship between PCOS and stone formation.

Free testosterone is related to aspects of cognitive function in women with and without polycystic ovary syndrome

2021 ◽  
Author(s):  
Mayouri Sukhapure ◽  
Kate Eggleston ◽  
Katie Douglas ◽  
Anna Fenton ◽  
Christopher Frampton ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Free Testosterone ◽  
Ovary Syndrome

Carotid atherosclerosis in women with polycystic ovary syndrome: Initial results from a case-control study

1996 ◽  
Vol 174 (4) ◽  
pp. 1224-1232 ◽  
Author(s):  
David S. Guzick ◽  
Evelyn O. Talbott ◽  
Kim Sutton-Tyrrell ◽  
Holly C. Herzog ◽  
Lewis H. Kuller ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Carotid Atherosclerosis ◽  
Case Control Study ◽  
Polycystic Ovary ◽  
Case Control ◽  
Ovary Syndrome ◽  
Initial Results ◽  
Control Study

scholarly journals Association of CYP3A7*1C and Serum Dehydroepiandrosterone Sulfate Levels in Women with Polycystic Ovary Syndrome

2008 ◽  
Vol 93 (7) ◽  
pp. 2909-2912 ◽  
Author(s):  
Mark O. Goodarzi ◽  
Ning Xu ◽  
Ricardo Azziz
Keyword(s):  
Los Angeles ◽  
Polycystic Ovary Syndrome ◽  
White Women ◽  
Polycystic Ovary ◽  
Medical Center ◽  
Free Testosterone ◽  
Total Testosterone ◽  
Adrenal Androgen ◽  
Androgen Excess ◽  
Ovary Syndrome

Abstract Context: Adrenal androgen excess is common in polycystic ovary syndrome (PCOS) and appears to be heritable. CYP3A7 metabolizes dehydroepiandrosterone and its sulfate (DHEAS). A promoter variant, CYP3A7*1C, which results in persistent expression in adults, was associated with reduced DHEAS levels in a previous study, which led us to consider CYP3A7*1C as a modulator of adrenal androgen excess in patients with PCOS. Objective: The objective was to replicate the association between CYP3A7*1C and reduced DHEAS levels in PCOS patients and assess its possible role in modulating testosterone levels. Design: Women with and without PCOS were genotyped for CYP3A7*1C, and this variant was tested for association with DHEAS and total and free testosterone. Setting: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. Genotyping took place at Cedars-Sinai Medical Center (Los Angeles, CA). Participants: A total of 287 white women with PCOS and 187 controls were studied. Main Measurements: CYP3A7*1C genotype, PCOS risk, and androgen levels were measured. Results: PCOS subjects who carried the CYP3A7*1C variant had lower levels of serum DHEAS and total testosterone (P = 0.0006 and 0.046, respectively). The variant was not associated with PCOS risk. Conclusion: This study replicated prior work of the association of CYP3A7*1C and decreased DHEAS in a different population of young PCOS women, providing further genetic evidence that CYP3A7 plays a potential role in modulation of DHEAS levels. Adult expression of CYP3A7 may modify the PCOS phenotype by ameliorating adrenal androgen excess.

The frequency of late-onset 21-hydroxylase and 11 beta-hydroxylase deficiency in women with polycystic ovary syndrome

1997 ◽  
pp. 670-674 ◽  
Author(s):  
Y Sahin ◽  
F Kelestimur
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Late Onset ◽  
Polycystic Ovary ◽  
Serum Testosterone ◽  
Free Testosterone ◽  
Sex Hormone Binding Globulin ◽  
Acth Stimulation ◽  
Hydroxylase Deficiency ◽  
Ovary Syndrome ◽  
Biochemical Features

OBJECTIVE: To determine the frequency of late-onset adrenal hyperplasia (LOCAH) due to 21-hydroxylase (21-OH) and 11 beta-hydroxylase (11 beta-OH) deficiency in women with clinical and biochemical features of polycystic ovary syndrome (PCOS). DESIGN: Eighty-three consecutively selected women with PCOS and eighteen normal women were included in the study. METHODS: Ultrasound, clinical and hormonal parameters were used to define PCOS. Basal FSH, LH, testosterone, free testosterone, androstenedione, dehydroepiandrosterone sulfate (DHEA-S), sex hormone-binding globulin (SHBG) and cortisol levels were measured. Serum 17-hydroxyprogesterone (17-OHP) and 11-deoxycortisol (11-DOC) levels were also measured before, 30 and 60 min after a single bolus injection of 0.25 mg ACTH (1-24) at 0900 h during the mid-follicular phase of the cycle. ACTH-stimulated 17-OHP levels > 30 nmol/l were considered as the criteria of 21-OH deficiency. The diagnosis 11 beta-OH deficiency was made if the adrenal 11-DOC response to ACTH stimulation exceeded threefold the 95th percentile of controls. RESULTS: Basal serum testosterone, free testosterone, androstenedione, DHEA-S, cortisol and 11-DOC levels were significantly higher in PCOS than in control subjects. ACTH-stimulated 17-OHP (P < 0.05) and 11-DOC (P < 0.0005) levels were found to be significantly higher in patients with PCOS than in controls. Seven (8.4%) patients had an 11-DOC response to ACTH higher than threefold the 95th percentile of controls, while no patients showed evidence of 21-OH deficiency. CONCLUSIONS: We have found that 8.4% of the women with clinical and biochemical features of PCOS could be presumed to have 11 beta-OH deficiency. No patients among the women with PCOS showed evidence of 21-OH deficiency. 11 beta-OH deficiency is unexpectedly more common than 21-OH deficiency in women with PCOS.

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