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Larry R. Boots

Researcher at University of Alabama at Birmingham

Publications -  67
Citations -  5498

Larry R. Boots is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Dehydroepiandrosterone sulfate & hirsutism. The author has an hindex of 27, co-authored 67 publications receiving 5267 citations.

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Prevalence of the polycystic ovary syndrome in unselected Black and White women of the Southeastern United States : A prospective study

TL;DR: In a consecutive population of unselected women the prevalence of hirsutism varied from 2-8% depending on the chosen cut-off F-G score, with no significant difference between White and Black women.
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Androgen Excess in Women: Experience with Over 1000 Consecutive Patients

TL;DR: Specific identifiable disorders (NCAH, CAH, HAIRAN syndrome, and androgen-secreting neoplasms) were observed in approximately 7% of subjects, whereas functional androgen excess, principally PCOS, was observed in the remainder.
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Prevalence of polycystic ovary syndrome (PCOS) in first-degree relatives of patients with PCOS.

TL;DR: The rates of PCOS in mothers and sisters of patients with PCOS were 24% and 32%, respectively, although the risk was higher when considering untreated premenopausal women only, and suggest the involvement of a major genetic component in the disorder.
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Screening for 21-hydroxylase-deficient nonclassic adrenal hyperplasia among hyperandrogenic women: a prospective study.

TL;DR: A basal 17-HP level is a useful screening tool for NCAH, with little loss in sensitivity if testing is performed in the morning and during the follicular phase, and a lower cutoff level (e.g., 2 or 3 ng/mL) is preferable ifTesting is performed at odd hours of the day, as is common in many practices, and maximum sensitivity is desired.
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Adrenal androgen excess in the polycystic ovary syndrome : Sensitivity and responsivity of the hypothalamic-pituitary-adrenal axis

TL;DR: It is postulated that excess AAs in PCOS arises from dysfunction of the hypothalamic-pituitary-adrenal axis, due to exaggerated pituitary secretion of ACTH in response to hypothalamic CRH, and excess sensitivity/responsivity of AAs to ACTH stimulation.