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Etiology and Prevalence of Obesity
Published in Claude Bouchard, The Genetics of Obesity, 2020
The syndrome of polycystic ovaries was originally described in 1844 as sclerocsystic ovaries. It is characterized clinically by oligomenorrhea or amenorrhea, hirsutism, hyperandrogenism, an elevated luteinizing hormone follicle-stimulating hormone (LH)/(FSH) ratio, and polycystic ovaries.8 Obesity is present in 16 to 49% of the cases in various series. When a group of very obese women with polycystic ovaries was compared to a group of women with a similar degree of obesity but without polycystic ovaries, the SHBG (Sex Hormone Binding Globulin) concentration was found to be reduced in both groups compared to control women. However, testosterone and albumin-bound testosterone levels were higher than normal, as were Δ4-androstenedione levels in the women with polycystic ovaries. The level of dehydroepiandrosterone-sulfate (DHEA-S) was not increased. Estradiol and estrone were significantly higher in the women with polycystic ovaries than in the control women. An increased and pulsatile pattern of LH secretion was seen in both groups, but the value was higher in the less obese women.
Androgen production over the female life span
Published in Barry G. Wren, Progress in the Management of the Menopause, 2020
H. M. Buckler, W. R. Robertson
Androstenedione, T and DHEA are produced by the ovary and the adrenals, with secretion from the latter being partially controlled by adrenocorticotropin hormone (ACTH); dehydroepiandrosterone sulfate (DHEAS) synthesis is entirely adrenal in origin. Androgen secretion from the ovary is under luteinizing hormone (LH) control and as it arises from the theca cells of the follicle, the corpus luteum and the stromal cells, it varies somewhat during the normal menstrual cycle. Examination of the androgen content of ovarian venous blood has shown that both T and Adione are secreted by the ovary with the dominant follicle9 but the other ovary also contributes. Testosterone varies less than its major precursor Adione as at least 50% of circulating T is derived from the peripheral conversion of Adione and DHEA.
Menstrual-Cycle-Related Disorders
Published in Jane M. Ussher, Joan C. Chrisler, Janette Perz, Routledge International Handbook of Women’s Sexual and Reproductive Health, 2019
Nancy Fugate Woods, Nancy J. Kenney
Although research on menopause in women with PCOS is limited, one study revealed that age at menopause was 1–2 years later than average for women with PCOS (Minooee, Tehrani, Rahmati, Mansournia, & Azizi, 2018). Hyperandrogenism of ovarian and adrenal origin and insulin resistance persist after menopause in women with PCOS. Although androgen levels tend to decrease in women over 70 years of age, lower levels of sex hormone binding globulin (SHBG) and FSH persist. Markopoulos and colleagues (2011) found that postmenopausal women with PCOS demonstrated higher than average levels of total testosterone and adrenal androgens (androstenedione, dehydroepiandrosterone sulfate [DHEAS]), 17-hydroxyprogesterone, and free androgen index. SHBG levels were significantly lower among women with PCOS. In a prospective study of women diagnosed with PCOS based on ovarian histology from ovarian wedge resection for PCOS and subsequently re-studied in their 70s, the PCOS group had higher free androgen index (FAI) and lower FSH and SHBG levels than those without PCOS. In addition, DHEAS, total testosterone, and androstenedione levels were higher in premenopausal women with PCOS than those without, but similar after menopause, which suggests that differences became less marked among women in their 80s (Schmidt, Brannstrom, Landin-Wilhelmsen, & Dahlgren, 2011). Endometrial cancer risk is elevated among women with PCOS (attributed to hyperestrogenic anovulation), which results in exposure to estrogen in the absence of progesterone and menses in which endometrial cells are shed (Azziz et al., 2016).
An evaluation of the available pharmacotherapy for the treatment of hirsutism
Published in Expert Opinion on Pharmacotherapy, 2023
Leila Asfour, Ahmed Kazmi, Rodney Sinclair
Hirsutism can result from increased levels of tissue androgens or a low activation threshold for the androgen receptors [16]. Testosterone is the key circulating androgen, which is secreted in equal amounts from the ovaries (promoted by luteinizing hormone (LH) and insulin) and adrenal glands promoted by adrenocorticotropic hormone (ACTH) [17]. However, circulating testosterone comes mostly from peripheral conversion of other androgens, especially androstenedione and dehydroepiandrosterone sulfate (DHAS), in the liver and skin. Direct secretion by ovaries and adrenals contributes weakly. Free testosterone is the main bioactive portion of plasma testosterone, but most of the circulating testosterone is bound by sex hormone‐binding globulin (SHBG) and can modulate the bioavailability of free testosterone [18]. The lower the concentration of serum SHBG, the higher the concentration of free testosterone there will be in the circulation. The more potent dihydrotestosterone is then generated from testosterone by 5‐alpha‐reductase (5α‐reductase) in the hair follicle and stimulates the dermal papilla to produce terminal hairs instead of vellus hairs [18]. Androstenedione and dehydroepiandrosterone (DHEA) are weaker androgens and may also be metabolized in the skin into testosterone and dihydrotestosterone [19].
Assessment of insulin resistance and metabolic syndrome in young reproductive aged women with polycystic ovarian syndrome: analogy of surrogate indices
Published in Archives of Physiology and Biochemistry, 2022
Nadia Rashid, Aruna Nigam, Sana Kauser, Prem Prakash, S. K. Jain, Saima Wajid
Study subjects included women of age group 16–35 years attending the outpatient department (OPD) of Gynaecology and Obstetrics, HAH Centenary Hospital, Jamia Hamdard, New Delhi from August 2014 to September 2016 with menstrual and infertility complaints. Subjects fulfilling the Rotterdam criteria (2004) were recruited into the PCOS group (n = 95). Clinical hyperandrogenism was defined by the presence of hirsutism (modified Ferriman–Gallwey score of ≥8) whereas biochemical hyperandrogenism was defined by increased levels of total/free testosterone levels. In 20–35 years old females, cut-off points for hyperandrogenaemia (the 95th percentiles): serum level of total testosterone (T) – 1.68 nmol/L, dehydroepiandrosterone sulphate (DHEAS – 10.42 mmol/L, free androgen index (FAI)) – 2.94. Amenorrhoea was defined as per FIGO guidelines as the absence of menstrual bleeding for a period of 90 days. Oligo-ovulation was defined by the presence of menstrual cycles of >35 days in length or less than 6–9 menstrual cycles in a year whereas anovulation was defined by complete absence of at least six menstrual cycles. Polycystic ovarian morphology was defined by the presence of ≥12 antral follicles measuring 9–12 mm in diameter in one/both ovaries and/or ovarian volume of ≥10 cm3 with increased stromal echogenicity.
Continuum of Symptoms in Polycystic Ovary Syndrome (PCOS): Links with Sexual Behavior and Unrestricted Sociosexuality
Published in The Journal of Sex Research, 2021
Rebecca Tzalazidis, Kirsten A. Oinonen
PCOS is “above all a disorder of androgen excess in women” (Azziz et al., 2006, p. 23). Approximately 60% to 80% of women with PCOS have elevated circulating androgen levels (Azziz et al., 2006), and more than 80% of women with symptoms of androgen excess have PCOS (Azziz et al., 2004). Hirsutism has been associated with higher testosterone levels (Conway, Honour, & Jacobs, 1989) and androgens are credited with changing light vellus hairs into larger terminal pigmented hairs (Randall, 2008). Elevated dehydroepiandrosterone sulfate (DHEAS) levels, an adrenal androgen metabolite often used as a measure of hyperandrogenism in women, are seen in 40% to 65% of women with PCOS (Kumar, Woods, Bartolucci, & Azziz, 2005; Mostafa et al., 2017). Huang, Brennan, and Azziz (2010) reported the following in women with PCOS: a 75.3% prevalence of hyperandrogenemia, 57.6% had supranormal levels of free testosterone, 33% had supranormal levels of serum total testosterone, and 32.7% had elevated levels of DHEAS. Thus, there is heterogeneity between women with PCOS in terms of their hyperandrogenic profile.