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The effect of subcutaneous administration of graded doses of C19 (androstene or androstane) steroids on serum levels of LH and FSH and on weights of accessory reproductive organs in gonadectomized, adult male rats were investigated. The C19 steroids were administered during 7 days in doses of 100, 50, 25, 12.5 or 6.25 μg per 100 g body weight per day. With the amounts of steroids used, 5α-dihydrotestosterone and 5α-androstane-3α,17β-diol had a high potency in preventing the rise of serum gonadotrophin concentrations and in curbing the decrease of weights of ventral prostates and seminal vesicles following orchidectomy. 5α-Androstane-3β,17β-diol showed no such effects. Positive feedback effects on serum gonadotrophins in castrates were observed following injection of certain doses of some steroids. Effects of steroids on accessory reproductive organs did not always correlate with those on gonadotrophic function of the hypothalamic-pituitary unit.
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Most (90%) cases of CAH are due to mutations in the 21-hydroxylase gene (CYP21A2). CAH due to 21-hydroxylase deficiency is diagnosed by confirming elevations of OHPG and androstenedione with decreased cortisol. By contrast, in 2 less common forms of CAH, due to 17-hydroxylase or 11-hydroxylase deficiency, OHPG and androstenedione levels are not significantly elevated and measurement of progesterone (PGSN / Progesterone, Serum) and deoxycorticosterone (DCRN / 11-Deoxycorticosterone, Serum), respectively, are necessary for diagnosis.
Diagnosis and differential diagnosis of congenital adrenal hyperplasia (CAH) always requires the measurement of several steroids. Patients with CAH due to 21-hydroxylase gene (CYP21A2) mutations usually have very high levels of androstenedione, often 5- to 10-fold elevations. 17-Hydroxyprogesterone (OHPG) levels are usually even higher, while cortisol levels are low or undetectable. All 3 analytes should be tested.
In the much less common CYP11A mutation, androstenedione levels are elevated to a similar extent as in CYP21A2 mutation, and cortisol is also low, but OHPG is only mildly, if at all, elevated.
Also less common is 3 beta-hydroxysteroid dehydrogenase type 2 (3 beta HSD-2) deficiency, characterized by low cortisol and substantial elevations in dehydroepiandrosterone sulfate (DHEA-S) and 17-alpha-hydroxypregnenolone, while androstenedione is either low, normal, or rarely, very mildly elevated (as a consequence of peripheral tissue androstenedione production by 3 beta HSD-1).
In the also very rare 17-alpha-hydroxylase deficiency, androstenedione, all other androgen-precursors (17-alpha-hydroxypregnenolone, OHPG, DHEA-S), androgens (testosterone, estrone, estradiol), and cortisol are low, while production of mineral corticoid and its precursors, in particular progesterone, 11-deoxycorticosterone, corticosterone, and 18-hydroxycorticosterone, are increased.
The goal of CAH treatment is normalization of cortisol levels and, ideally, also of sex-steroid levels. OHPG is measured to guide treatment, but this test correlates only modestly with androgen levels. Therefore, androstenedione and testosterone should also be measured and used to guide treatment modifications. Normal prepubertal levels may be difficult to achieve, but if testosterone levels are within the reference range, androstenedione levels up to 100 ng/dL are usually regarded as acceptable.
5-androstene-3β,7β,17β-triol (β-AET), an active metabolite of dehydroepiandrosterone (DHEA), reversed glucocorticoid (GC)-induced suppression of IL-6, IL-8 and osteoprotegerin production by human osteoblast-like MG-63 cells and promoted osteoblast differentiation of human mesenchymal stem cells (MSCs). In a murine thermal injury model that includes glucocorticoid-induced osteopenia, β-AET significantly (p
In females, the outer part of the adrenal glands (known as the cortex) and the ovaries release androstenedione into the bloodstream where it is converted to provide around half of all testosterone and almost all of the body's oestrone, a form of oestrogen. Although the testes produce large amounts of androstenedione in males, they secrete little of this into the blood and, instead, rapidly convert it into testosterone within the testes. The adrenal glands also produce androstenedione in men, but this contribution is swamped by the testes' overwhelming production of the other androgenic hormone, testosterone.
In men, too much androstenedione may lead to an imbalance in oestrogen and testosterone production, leading to changes such as breast development. Depending on the cause of the excess androstenedione, other changes, such as the testes becoming smaller, might also occur.
Although androstenedione is often abused by bodybuilders in an effort to build muscle bulk, a small number of studies have suggested that its long-term use may actually decrease muscle strength. The precise consequences of having too much androstenendione are, therefore, still unclear.
Boys with too little androstenedione may fail to develop the sexual characteristics associated with puberty, including pubic and body hair, growth of the sexual organs and deepening of the voice. Similarly, girls may fail to start their periods and may not undergo many of the changes usually seen in puberty. In addition, if a male foetus has too little androstenedione, he may be born with abnormal genitalia. Too little androstenedione in later life would cause the same changes for both men and women as too little testosterone and oestrogen.
FSH, follicle-stimulating hormone; LH, luteinizing hormone.Because of the changes in estrogen production, the ratio of estradiol to estrone changes after the menopause, with the estrone level exceeding that of estradiol.9 The absolute levels of estrogen are influenced by weight, sex, and age. Obese women have a higher concentration of free estradiol because of decreased sex hormone-binding globulin and an increased rate of aromatization.6,16 Stress raises the estrogen level by increasing adrenal secretion, whereas liver disease and congestive heart disease raise serum estrogen by decreasing the metabolic clearance of androstenedione.
Androgens continue to be produced by the ovarian stromal and hilus cells in response to the increased levels of circulating LH. There is a 25% increase in testosterone secretion by the postmenopausal ovary; however, circulating levels of testosterone decrease to slightly less, approximately 250 pg/ml, than those of premenopausal women.11,13,20,21 This reduction has been attributed to a significant fall in the conversion of androstenedione to testosterone after the menopause. In premenopausal women, 50% of androstenedione is secreted by the adrenal gland and 50% by the ovary; 14% of androstenedione is converted to testosterone to account for 50% of circulating testosterone. After menopause, only 20% of androstenedione is secreted by the ovary, and the percentage of androstenedione converted to estrone rises from approximately 1.3% to 2.8%. Circulating concentrations of androstenedione are reduced after menopause from 1500 pg/ml to approximately 800 to 900 pg/ml.11,13,20,21 The levels of androstenedione in postmenopausal women are similar to those of young surgically castrated women, but the level of testosterone in intact postmenopausal women is twice that of oophorectomized younger women.20
Endocrine studies have shown that hot flushes occur in menopausal women together with pulses of LH (Fig. 2). Although not every LH pulse is accompanied by a hot flush, virtually every hot flush occurs simultaneously with the onset of a pulse of LH.37 Circulating estrone and estradiol levels do not vary before or after the flush; however, the adrenal steroids cortisol, dehydroepiandrosterone, and androstenedione increase significantly at the time of the flush. Corticotropin (ACTH) and cortisone also increase in a pulsatile fashion with the temperature changes.38
Androstenedione production during life mimics the pattern of other androgen precursors. Fetal serum concentrations increase throughout embryonal development and peak near birth at approximately young adult levels. Levels then fall rapidly during the first year of life to low prepubertal values. With the onset of adrenarche, androstenedione rises gradually, a process that accelerates with the onset of puberty, reaching adult levels around age 18. Adrenarche is a poorly understood phenomenon peculiar to higher primates that is characterized by a gradual rise in adrenal androgen production. It precedes puberty, but is not causally linked to it. Early adrenarche is not associated with early puberty, or with any reduction in final height, or overt androgenization, and is generally regarded as a benign condition not requiring intervention. However, girls with early adrenarche may be at increased risk of polycystic ovarian syndrome as adults, and some boys may develop early penile enlargement.
Elevated androstenedione levels can cause symptoms or signs of hyperandrogenism in women. Men are usually asymptomatic, but through peripheral conversion of androgens to estrogens can occasionally experience mild symptoms of estrogen excess, such as gynecomastia.
In children, adrenal and gonadal tumors are uncommon, but many forms of congenital adrenal hyperplasia can increase serum androstenedione concentrations. Diagnosis always requires measurement of other androgen precursors (eg, OHPG, 17-alpha-hydroxypregnenolone, and DHEA-S) and cortisol, in addition to androstenedione.
Elevated androstenedione levels indicate increased adrenal or gonadal androgen production. Mild elevations in adults are usually idiopathic, or related to conditions such as polycystic ovarian syndrome (PCOS) in women, or use of androstenedione supplements in men and women. However, levels greater than or equal to 500 ng/dL can suggest the presence of an androgen-secreting adrenal, or less commonly, a gonadal, tumor. Androstenedione levels are elevated in more than 90% of patients with benign androgen-producing adrenal tumors, usually well above 500 ng/dL. Most androgen-secreting adrenal carcinomas also exhibit elevated androstenedione levels, but more typically show relatively larger elevations in 17-alpha-hydroxyprogesterone (OHPG) and dehydroepiandrosterone sulfate (DHEA-S) than in androstenedione, as they have often lost the ability to produce downstream androgens. 041b061a72