Salivary microbiome differences in prepubertal children with and without adrenal androgen excess

2021 ◽  
Author(s):  
Brittany K. Wise-Oringer ◽  
Anne Claire Burghard ◽  
Heekuk Park ◽  
Richard J. Auchus ◽  
Sharon E. Oberfield ◽  
...  
Keyword(s):  
Adrenal Androgen ◽  
Androgen Excess ◽  
Prepubertal Children

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.

Adrenal androgen excess in hyperandrogenism: relation to age and body mass

1999 ◽  
Vol 71 (4) ◽  
pp. 671-674 ◽  
Author(s):  
Carlos Morán ◽  
Eric Knochenhauer ◽  
Larry R Boots ◽  
Ricardo Azziz
Keyword(s):  
Body Mass ◽  
Adrenal Androgen ◽  
Androgen Excess

Adrenal androgen excess and body mass index in polycystic ovary syndrome

2015 ◽  
pp. jc.0000-9999 ◽  
Author(s):  
Carlos Moran ◽  
Monica Arriaga ◽  
Fabian Arechavaleta-Velasco ◽  
Segundo Moran
Keyword(s):  
Body Mass Index ◽  
Polycystic Ovary Syndrome ◽  
Body Mass ◽  
Polycystic Ovary ◽  
Adrenal Androgen ◽  
Androgen Excess ◽  
Ovary Syndrome

scholarly journals Current Insights Into Adrenal Insufficiency in the Newborn and Young Infant

2020 ◽  
Vol 8 ◽  
Author(s):  
Federica Buonocore ◽  
Sinead M. McGlacken-Byrne ◽  
Ignacio del Valle ◽  
John C. Achermann
Keyword(s):  
Adrenal Insufficiency ◽  
Young Infant ◽  
Adrenal Androgen ◽  
Androgen Excess ◽  
The Family ◽  
Threatening Condition ◽  
Life Threatening ◽  
Glucocorticoid Deficiency ◽  
Poor Weight Gain ◽  
Prolonged Jaundice

Adrenal insufficiency (AI) is a potentially life-threatening condition that can be difficult to diagnose, especially if it is not considered as a potential cause of a child's clinical presentation or unexpected deterioration. Children who present with AI in early life can have signs of glucocorticoid deficiency (hyperpigmentation, hypoglycemia, prolonged jaundice, poor weight gain), mineralocorticoid deficiency (hypotension, salt loss, collapse), adrenal androgen excess (atypical genitalia), or associated features linked to a specific underlying condition. Here, we provide an overview of causes of childhood AI, with a focus on genetic conditions that present in the first few months of life. Reaching a specific diagnosis can have lifelong implications for focusing management in an individual, and for counseling the family about inheritance and the risk of recurrence.

scholarly journals Premature adrenarche: novel lessons from early onset androgen excess

2011 ◽  
Vol 165 (2) ◽  
pp. 189-207 ◽  
Author(s):  
Jan Idkowiak ◽  
Gareth G Lavery ◽  
Vivek Dhir ◽  
Timothy G Barrett ◽  
Paul M Stewart ◽  
...  
Keyword(s):  
Early Onset ◽  
Polycystic Ovary ◽  
Breast Development ◽  
Future Research ◽  
Adrenal Androgen ◽  
Androgen Excess ◽  
Adult Type ◽  
The Metabolic Syndrome ◽  
Premature Adrenarche ◽  
Increased Risk

Adrenarche reflects the maturation of the adrenal zona reticularis resulting in increased secretion of the adrenal androgen precursor DHEA and its sulphate ester DHEAS. Premature adrenarche (PA) is defined by increased levels of DHEA and DHEAS before the age of 8 years in girls and 9 years in boys and the concurrent presence of signs of androgen action including adult-type body odour, oily skin and hair and pubic hair growth. PA is distinct from precocious puberty, which manifests with the development of secondary sexual characteristics including testicular growth and breast development. Idiopathic PA (IPA) has long been considered an extreme of normal variation, but emerging evidence links IPA to an increased risk of developing the metabolic syndrome (MS) and thus ultimately cardiovascular morbidity. Areas of controversy include the question whether IPA in girls is associated with a higher rate of progression to the polycystic ovary syndrome (PCOS) and whether low birth weight increases the risk of developing IPA. The recent discoveries of two novel monogenic causes of early onset androgen excess, apparent cortisone reductase deficiency and apparent DHEA sulphotransferase deficiency, support the notion that PA may represent a forerunner condition for PCOS. Future research including carefully designed longitudinal studies is required to address the apparent link between early onset androgen excess and the development of insulin resistance and the MS.

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