Gonadal Steroid Hormones
Sex Hormone-Binding Globulin
Follicle Stimulating Hormone
Polycystic Ovary Syndrome
Adrenal Hyperplasia, Congenital
Radioisotope Dilution Technique
Cytochrome P-450 Enzyme System
Cholesterol Side-Chain Cleavage Enzyme
Cholestenone 5 alpha-Reductase
Cytochrome P-450 CYP2B1
Insulin-Like Growth Factor I
The treatment of insulin resistance does not improve adrenal cytochrome P450c17alpha enzyme dysregulation in polycystic ovary syndrome. (1/906)OBJECTIVE: To determine whether metformin. when given to non-diabetic women with polycystic ovary syndrome (PCOS), results in a reduction of insulin resistance and hyperinsulinemia while body weight is maintained. Also we aimed to see whether the reduction in insulin levels attenuates the activity of adrenal P450c17alpha enzyme in patients with PCOS. DESIGN: We investigated the 17-hydroxyprogesterone (17-OHP) and androstenedione responses to ACTH, insulin responses to an oral glucose tolerance test (OGTT) and glucose disposal rate in an insulin tolerance test before and after metformin therapy (500 mg, orally, twice daily, for 12 weeks). METHODS: The presence of hyperinsulinemia in 15 women with PCOS was demonstrated by an OGTT and results were compared with those of 10 healthy women. Insulin sensitivity was measured by the rate of endogenous glucose disposal after i.v. bolus injection of insulin. 17-OHP and androstenedione responses to ACTH were measured in all the women with PCOS and the normal women. RESULTS: Women with PCOS were hyperinsulinemic (102.0+/-13.0 (S.E.M.) VS 46.2+/-4.4 pmol/l) and hyperandrogenemic (free testosterone 15.3+/-1.7 vs 7.9+/-0.6 nmol/l; androstenedione 11.8+/-0.8 vs 8.2+/-0.6 nmol/l) and more hirsute (modified Ferriman-Gallwey score, 17.7+/-1.6 vs 3.0+/-0.3) than healthy women. In addition, women with PCOS had higher 17-OHP and androstenedione responses to ACTH when compared with healthy women. Metformin therapy resulted in some improvement in insulin sensitivity and reduced the basal and post-glucose load insulin levels. But 17-OHP and androstenedione responses to ACTH were unaltered in response to metformin. CONCLUSIONS: PCOS is characterized by hyperactivity of the adrenal P450c17alpha enzyme and insulin resistance. It seems that there is no direct relationship between insulin resistance and adrenal P450c17alpha enzyme dysregulation. (+info)
The aromatase inactivator 4-hydroxyandrostenedione (4-OH-A) inhibits tamoxifen metabolism by rat hepatic cytochrome P-450 3A: potential for drug-drug interaction of tamoxifen and 4-OH-A in combined anti-breast cancer therapy. (2/906)Tamoxifen (tam), an anti-breast cancer agent, is metabolized into tam-N-oxide by the hepatic flavin-containing monooxygenase and into N-desmethyl- and 4-hydroxy-tam by cytochrome P-450s (CYPs). Additionally, tam is metabolically activated by hepatic CYP3A, forming a reactive intermediate that binds covalently to proteins. Tam and 4-hydroxyandrostenedione (4-OH-A) are currently used to treat breast cancer, and it has been contemplated that 4-OH-A be given concurrently with tam to contravene potential tumor resistance to tam. Because alterations in tam metabolism may influence its therapeutic efficacy, the effect of 4-OH-A on tam metabolism was examined. Incubation of tam with liver microsomes from phenobarbital-treated rats, in the presence of 4-OH-A (10-100 microM), resulted in marked inhibition of tam-N-demethylation and tam covalent binding and in decreased tam-N-oxide accumulation; however, there was no inhibition of the formation of 4-hydroxy-tam and of 3,4-dihydroxytamoxifen. These findings indicate that 4-OH-A inhibits CYP3A, but not P-450(s) that catalyze tam 4-hydroxylation. The diminished tam-N-oxide accumulation could be due to decreased N-oxide formation and/or due to increased N-oxide reduction. Incubation of tam-N-oxide with liver microsomes containing heat-inactivated flavin-containing monooxygenase demonstrated that 4-OH-A increases the accumulation of tam, possibly by diminishing its P-450-mediated metabolism. Kinetic studies indicate that 4-OH-A is a competitive inhibitor of CYP3A, but not a time-dependent inactivator. Consequently, the concurrent treatment of tam and 4-OH-A may result in increased tam half-life and thus could potentiate the therapeutic efficacy of tam and diminish the potential side effects of tam by inhibiting its covalent binding to proteins and possibly to DNA. (+info)
Dihydrotestosterone, stanozolol, androstenedione and dehydroepiandrosterone sulphate inhibit leptin secretion in female but not in male samples of omental adipose tissue in vitro: lack of effect of testosterone. (3/906)Leptin, the product of the Ob gene, is a polypeptide hormone expressed in adipocytes which acts as a signalling factor from the adipose tissue to the central nervous system, regulating food intake and energy expenditure. It has been reported that circulating leptin levels are higher in women than in men, even after correction for body fat. This gender-based difference may be conditioned by differences in the levels of androgenic hormones. To explore this possibility, a systematic in vitro study with organ cultures from human omental adipose tissue, either stimulated or not with androgens (1 microM), was undertaken in samples obtained from surgery on 44 non-obese donors (21 women and 23 men). The assay was standardized in periods of 24 h, ending at 96 h, with no apparent tissue damage. Leptin results are expressed as the mean+/-s.e.m. of the integrated secretion into the medium, expressed as ng leptin/g tissue per 48 h. Spontaneous leptin secretion in samples from female donors (4149+/-301) was significantly higher (P<0.01) than that from male donors (2456+/-428). Testosterone did not exert any significant effect on in vitro leptin secretion in either gender (4856+/-366 in women, 3322+/-505 in men). Coincubation of adipose tissue with dihydrotestosterone (DHT) induced a significant (P<0.05) leptin decrease in samples taken from women (3119+/-322) but not in those taken from men (2042+/-430). Stanozolol, a non-aromatizable androgen, decreased (P<0.05) leptin secretion in female samples (2809+/-383) but not in male (1553+/-671). Dehydroepiandrosterone sulphate (DHEA-S) induced a significant (P<0.01) leptin decrease in female samples (2996+/-473), with no modifications in samples derived from males (1596+/-528). Exposure to androstenedione also resulted in a significant reduction (P<0.01) of leptin secretion in samples taken from women (2231+/-264), with no effect on male adipose tissue (1605+/-544). In conclusion, DHT, stanozolol, DHEA-S and androstenedione induced a significant inhibition of in vitro leptin secretion in samples from female donors, without affecting the secretion in samples from men. Testosterone was devoid of activity in either gender. (+info)
Ovarian hormone secretory response to gonadotropins and nitric oxide following chronic nitric oxide deficiency in the rat. (4/906)Ovarian hormone secretion is regulated by gonadotropins, and it has been demonstrated that this response is modulated by nitric oxide (NO). The focus of this study was to determine the effect of chronic NO deficiency on the secretion of ovarian steroids. Female rats were given N-nitro-L-arginine (L-NNA; 0.6 g/L) in their drinking water, and vaginal smears were obtained daily. By 4 wk of treatment, all the rats were in constant estrus or proestrus. At 6-8 wk the animals were killed; the ovaries were removed and incubated in the presence of eCG (1 IU/ml) and hCG (1 IU/ml) and/or S-nitroso-L-acetyl penicillamine (an NO donor, S-NAP; 0.1 mM) for 4 h. Medium was collected at 30-min intervals, and estradiol, progesterone, and androstenedione were measured. Ovaries from proestrous rats served as controls. Ovaries from L-NNA-treated animals had a greater basal and gonadotropin-stimulated release of estradiol but not of androstenedione or progesterone in comparison to ovaries from untreated controls. S-NAP decreased the gonadotropin-stimulated estradiol, progesterone, and androstenedione in ovaries from NO-deficient rats. Steroid secretion in controls was not responsive to S-NAP. We conclude that chronic NO inhibition produces constant estrus due to increased estradiol production and that NO acts to inhibit estradiol and androstenedione production. (+info)
YM116, 2-(1H-imidazol-4-ylmethyl)-9H-carbazole, decreases adrenal androgen synthesis by inhibiting C17-20 lyase activity in NCI-H295 human adrenocortical carcinoma cells. (5/906)The concentrations of androstenedione and dehydroepiandrosterone, products of C17-20 lyase, in the medium after a 6-hr incubation of NCI-H295 cells were decreased by YM116 (2-(1H-imidazol-4-ylmethyl)-9H-carbazole) (IC50: 3.6 and 2.1 nM) and ketoconazole (IC50: 54.9 and 54.2 nM). 17Alpha-hydroxyprogesterone, a product of 17alpha-hydroxylase, was increased by YM116 (1-30 nM) and by ketoconazole (10-300 nM) and then was decreased at higher concentrations of both agents (IC50: 180 nM for YM116, 906 nM for ketoconazole), indicating that YM116 and ketoconazole were 50- and 16.5-fold more specific inhibitors of C17-20 lyase, respectively, than 17alpha-hydroxylase. Compatible with these findings, progesterone, a substrate of 17alpha-hydroxylase, was increased by these agents. Cortisol production was inhibited by YM116 and ketoconazole (IC50: 50.4 and 80.9 nM, respectively). YM116 was a 14-fold more potent inhibitor of androstenedione production than cortisol production, whereas ketoconazole was a nonselective inhibitor of the production of both steroids. YM116 and ketoconazole inhibited the C17-20 lyase activity in human testicular microsomes (IC50: 4.2 and 17 nM, respectively). These results demonstrate that YM116 reduces the synthesis of adrenal androgens by preferentially inhibiting C17-20 lyase activity. (+info)
The effect of chronic treatment with GH on gonadal function in men with isolated GH deficiency. (6/906)Eleven adult males, previously submitted to neurosurgery because of a pituitary lesion (three with craniopharyngioma, three with clinically non-functioning adenoma and five with macroprolactinoma) were treated with recombinant GH for 12 months after the diagnosis of GH deficiency was made. Circulating FSH, LH, prolactin, testosterone, 17 beta-estradiol (E2), dehyroepiandrosterone (DHEA-S), androstenedione. 17-OH-progesterone (17OHP), IFG-I, and steroid hormone-binding protein (SHBG) levels were assayed before and after CG test at study entry and 6 and 12 months after GH treatment. A significant increase in plasma IGF-I levels was obtained after 6 and 12 months of GH treatment. In addition, CG-stimulated, but not baseline, testosterone levels showed a significant increase after 6 and 12 months of GH treatment when compared with study entry (9.6 +/- 0.5 and 9.9 +/- 0.5 vs 7.9 +/- 0.5 ng/ml; P < 0.05). Baseline, but not CG-stimulated, serum 17OHP levels were significantly increased only after 12 months of GH treatment (1.7 +/- 0.1 vs 1.4 +/- 0.1 ng/ml; P < 0.05). No significant difference was found as far as both basal and CG-stimulated E2, androstenedione, DHEA-S and SHBG were concerned. With regards to the semen analysis, only seminal plasma volume was significantly increased after 12 months of GH treatment (2.9 +/- 0.3 vs 1.7 +/- 0.3 ml; P < 0.05). No significant change in sperm count, motility and abnormal forms was observed. These data show that GH treatment displays a clear-cut effect upon Leydig cell function and increases the production of seminal plasma volume in fertile adult males with isolated GH deficiency. (+info)
Dynamics of periovulatory steroidogenesis in the rhesus monkey follicle after ovarian stimulation. (7/906)The temporal relationships and regulation of events in the primate follicle during the periovulatory interval are poorly understood. This study was designed to elucidate the dynamics of steroid synthesis in the macaque follicle during ovarian stimulation cycles in which serum/follicular fluid aspirates were collected at precise intervals before (0 h) and after (up to 36 h) administration of the ovulatory human chorionic gonadotrophin (HCG) bolus. Serum concentrations of progesterone increased (P < 0.05) within 30 min, and follicular fluid progesterone concentrations were elevated 180-fold within 12 h, of HCG injection, and remained elevated until the time of ovulation. In contrast, 17beta-oestradiol concentrations increased initially, but then declined (P < 0.05) by 36 h post-HCG. Acute incubation of granulosa cells with and without steroidogenic substrates demonstrated that: (i) 3beta-hydroxysteroid dehydrogenase and aromatase activities were present in equivalent amounts before and after HCG; whereas (ii) P450 side-chain cleavage activity increased (P < 0.05) within 12 h of HCG; and (iii) exogenous low-density lipoprotein and cholesterol were not utilized for steroidogenesis. This model should be useful for further studies on ovulation and luteinization in primates, and enable elucidation of the local actions of progesterone and other steroids at specific time points during the periovulatory interval. (+info)
Concentration of steroids in bovine peripheral plasma during the oestrous cycle and the effect of betamethasone treatment. (8/906)Testosterone, oestradiol and progesterone were measured in peripheral plasma during the oestrous cycle of 6 heifers. Oestradiol and progesterone results confirmed earlier reports. Concentration of testosterone on the day of oestrus was 40+/-3 pg/ml (mean+/-S.E.M.), and two peaks were detected during the cycle, one 7 days before oestrus (1809+/-603 pg/ml) and the other (78+/- 7 pg/ml) on the day before the onset of oestrus. The concentration of progesterone declined in most cases 1 day after the maximum concentration of testosterone. Betamethasone treatment in 5 heifers extended luteal function by an average of 10 days: plasma androstenedione and oestradiol concentrations were unaltered; cortisol values were depressed for at least 16 days after treatment; testosterone concentrations were lowered by 13+/-2-4% during treatment, and except in one heifer the peak on Day -7 was abolished. (+info)
1. Irregular menstrual cycles, or amenorrhea (the absence of periods).
2. Cysts on the ovaries, which are fluid-filled sacs that can be detected by ultrasound.
3. Elevated levels of androgens (male hormones) in the body, which can cause a range of symptoms including acne, excessive hair growth, and male pattern baldness.
4. Insulin resistance, which is a condition in which the body's cells do not respond properly to insulin, leading to high blood sugar levels.
PCOS is a complex disorder, and there is no single cause. However, genetics, hormonal imbalances, and insulin resistance are thought to play a role in its development. It is estimated that 5-10% of women of childbearing age have PCOS, making it one of the most common endocrine disorders affecting women.
There are several symptoms of PCOS, including:
1. Irregular menstrual cycles or amenorrhea
2. Weight gain or obesity
4. Excessive hair growth on the face, chest, and back
5. Male pattern baldness
6. Infertility or difficulty getting pregnant
7. Mood changes, such as depression and anxiety
8. Sleep apnea
PCOS can be diagnosed through a combination of physical examination, medical history, and laboratory tests, including:
1. Pelvic exam: A doctor will examine the ovaries and uterus to look for cysts or other abnormalities.
2. Ultrasound: An ultrasound can be used to detect cysts on the ovaries and to evaluate the thickness of the uterine lining.
3. Hormone testing: Blood tests can be used to measure levels of androgens, estrogen, and progesterone.
4. Glucose tolerance test: This test is used to check for insulin resistance, which is a common finding in women with PCOS.
5. Laparoscopy: A small camera inserted through a small incision in the abdomen can be used to visualize the ovaries and uterus and to diagnose PCOS.
There is no cure for PCOS, but it can be managed with lifestyle changes and medication. Treatment options include:
1. Weight loss: Losing weight can improve insulin sensitivity and reduce androgen levels.
2. Hormonal birth control: Birth control pills or other hormonal contraceptives can help regulate menstrual cycles and reduce androgen levels.
3. Fertility medications: Clomiphene citrate and letrozole are commonly used to stimulate ovulation in women with PCOS.
4. Injectable fertility medications: Gonadotropins, such as follicle-stimulating hormone (FSH) and luteinizing hormone (LH), can be used to stimulate ovulation.
5. Surgery: Laparoscopic ovarian drilling or laser surgery can improve ovulation and fertility in women with PCOS.
6. Assisted reproductive technology (ART): In vitro fertilization (IVF) and intracytoplasmic sperm injection (ICSI) can be used to help women with PCOS conceive.
7. Alternative therapies: Some complementary and alternative therapies, such as acupuncture and herbal supplements, may be helpful in managing symptoms of PCOS.
It is important for women with PCOS to work closely with their healthcare provider to develop a treatment plan that meets their individual needs and goals. With appropriate treatment, many women with PCOS can improve their menstrual regularity, fertility, and overall health.
Some of the symptoms of hirsutism include:
* Thick, dark hair on the face, chest, back, and buttocks
* Hair growth on the arms, legs, and other areas of the body
* Thinning or loss of hair on the head
* Acne and oily skin
Hirsutism can be caused by a variety of factors, including:
* Hormonal imbalances: Excessive levels of androgens, such as testosterone, can cause hirsutism.
* Genetics: Inheritance plays a role in the development of hirsutism.
* Medications: Certain medications, such as anabolic steroids and certain antidepressants, can cause hirsutism as a side effect.
* Other medical conditions: Polycystic ovary syndrome (PCOS), congenital adrenal hyperplasia (CAH), and other endocrine disorders can also cause hirsutism.
There are several treatment options for hirsutism, including:
* Medications such as anti-androgens and retinoids to reduce hair growth and improve skin texture
* Electrolysis and laser therapy to remove unwanted hair
* Hormonal therapies such as birth control pills and spironolactone to regulate hormone levels and reduce hair growth
* Plastic surgery to remove excess hair-bearing skin.
It is important for individuals with hirsutism to seek medical attention if they experience any of the following symptoms:
* Sudden or excessive hair growth
* Hair growth on the face, chest, back, or buttocks
* Thinning or loss of hair on the head
* Acne and oily skin.
Early diagnosis and treatment can help manage the symptoms of hirsutism and improve quality of life for individuals affected by this condition.
There are several possible causes of hyperandrogenism, including:
1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of cortisol and aldosterone hormones by the adrenal glands.
2. Polycystic ovary syndrome (PCOS): A hormonal disorder that affects women of reproductive age and is characterized by cysts on the ovaries, irregular menstrual cycles, and high levels of androgens.
3. Adrenal tumors: Tumors in the adrenal glands can cause excessive production of androgens.
4. Familial hyperandrogenism: A rare inherited condition that causes an overproduction of androgens.
5. Obesity: Excess body fat can lead to increased production of androgens.
The symptoms of hyperandrogenism can vary depending on the cause, but may include:
2. Hirsutism (excessive hair growth)
3. Virilization (male-like physical characteristics, such as deepening of the voice and clitoral enlargement in women)
4. Male pattern baldness
5. Increased muscle mass and strength
6. Irregular menstrual cycles or cessation of menstruation
8. Elevated blood pressure
9. Elevated cholesterol levels
Treatment options for hyperandrogenism depend on the underlying cause, but may include:
1. Medications to reduce androgen production or block their effects
2. Hormone replacement therapy (HRT) to restore normal hormone balance
3. Surgery to remove tumors or cysts
4. Weight loss programs to reduce excess body fat
5. Lifestyle changes, such as exercise and dietary modifications, to improve overall health.
It's important to note that hyperandrogenism can also be caused by other factors, such as congenital adrenal hyperplasia or ovarian tumors, so it's important to consult a healthcare professional for proper diagnosis and treatment.
There are three main forms of ACH:
1. Classic congenital adrenal hyperplasia (CAH): This is the most common form of ACH, accounting for about 90% of cases. It is caused by mutations in the CYP21 gene, which codes for an enzyme that converts cholesterol into cortisol and aldosterone.
2. Non-classic CAH (NCAH): This form of ACH is less common than classic CAH and is caused by mutations in other genes involved in cortisol and aldosterone production.
3. Mineralocorticoid excess (MOE) or glucocorticoid deficiency (GD): These are rare forms of ACH that are characterized by excessive production of mineralocorticoids (such as aldosterone) or a deficiency of glucocorticoids (such as cortisol).
The symptoms of ACH can vary depending on the specific form of the disorder and the age at which it is diagnosed. In classic CAH, symptoms typically appear in infancy and may include:
* Premature puberty (in girls) or delayed puberty (in boys)
* Abnormal growth patterns
* Distended abdomen
* Weight gain or obesity
* Easy bruising or bleeding
In NCAH and MOE/GD, symptoms may be less severe or may not appear until later in childhood or adulthood. They may include:
* High blood pressure
* Low blood sugar (hypoglycemia)
* Weight gain or obesity
* Mood changes
If left untreated, ACH can lead to serious complications, including:
* Adrenal gland insufficiency
* Heart problems
* Bone health problems
* Increased risk of infections
* Mental health issues (such as depression or anxiety)
Treatment for ACH typically involves hormone replacement therapy to restore the balance of hormones in the body. This may involve taking medications such as cortisol, aldosterone, or other hormones to replace those that are deficient or imbalanced. In some cases, surgery may be necessary to remove an adrenal tumor or to correct physical abnormalities.
With proper treatment, many individuals with ACH can lead healthy, active lives. However, it is important for individuals with ACH to work closely with their healthcare providers to manage their condition and prevent complications. This may involve regular check-ups, hormone level monitoring, and lifestyle changes such as a healthy diet and regular exercise.
Freemartinism is caused by the abnormal development of the reproductive system of the calves. During fetal development, the two female calves may fail to fully separate from each other, leading to a shared uterus and vagina. This can result in a range of physical and reproductive abnormalities, including:
* Unusual genitalia: The shared uterus and vagina can cause the genitalia to appear abnormal or incomplete.
* Reproductive difficulties: Freemartinism can make it difficult or impossible for the calves to breed or conceive.
* Health problems: Freemartinism can increase the risk of health problems, such as urinary tract infections and reproductive tract infections.
Freemartinism is typically diagnosed through ultrasound examination during pregnancy or after birth. Treatment options for freemartinism are limited, and may include surgery to correct physical abnormalities and hormone therapy to stimulate reproductive function. In some cases, euthanasia may be necessary due to the severity of the condition.
Prevention of freemartinism is not possible, as it is a congenital condition that occurs during fetal development. However, careful breeding practices and proper veterinary care can help reduce the risk of complications associated with this condition.
In the medical field, the term is often used to describe various conditions that affect gender development or sexual differentiation in individuals with variations in sex chromosomes, hormones, or genitalia. Feminization can occur in individuals assigned male at birth but who exhibit female physical characteristics, such as those with congenital adrenal hyperplasia (CAH) or other intersex traits.
The term is also used to describe the effects of estrogen on the male body, particularly during puberty. For example, boys taking estrogen medication for hormone therapy may experience feminization of their physical features, such as breast tissue growth and a softer voice.
It's important to note that the term feminization is sometimes used in medical contexts to describe a process or outcome that is perceived as negative or undesirable, particularly when it comes to gender identity or expression. However, it's essential to recognize that all individuals, regardless of their gender identity or expression, deserve respect and support in their healthcare needs.
In summary, feminization within the medical field refers to a process or condition whereby male characteristics are acquired by an individual or group, often as a result of hormonal or genetic factors. The term is used to describe various conditions affecting gender development or sexual differentiation and the effects of estrogen on the male body. However, it's important to recognize that the term can be perceived as negative, and healthcare providers should approach patients with respect and sensitivity regardless of their gender identity or expression.
The term "gynecomastia" comes from the Greek words "gyneco," meaning "womanlike," and "mastos," meaning "breast." The condition can occur at any age, but it is most common in infants, teenagers, and older men.
Gynecomastia can be caused by a variety of factors, including:
1. Hormonal imbalance: An imbalance of testosterone and estrogen hormones can lead to breast tissue growth.
2. Medications: Certain medications, such as antidepressants, anti-anxiety drugs, and heart medications, can cause gynecomastia as a side effect.
3. Medical conditions: Conditions such as hypogonadism (low testosterone levels), hyperthyroidism (high thyroid hormone levels), and liver or kidney disease can contribute to gynecomastia.
4. Genetic factors: Some men may inherit a tendency to develop gynecomastia due to genetic mutations.
5. Other factors: Gynecomastia can also be caused by other factors such as obesity, alcohol consumption, and certain types of foods or supplements.
Symptoms of gynecomastia may include:
* Enlarged breasts
* Breast tenderness
* Nipple sensitivity
* Pain in the breasts
* Swelling in the armpits
Gynecomastia is usually diagnosed through a physical examination and medical history. Imaging tests such as mammography or ultrasound may also be used to help rule out other conditions.
Treatment for gynecomastia depends on the underlying cause of the condition. In some cases, medications may be prescribed to address hormonal imbalances or other medical conditions that are contributing to the development of gynecomastia. Surgery may also be an option to remove excess breast tissue and improve the appearance of the chest.
In conclusion, gynecomastia is a relatively common condition in men that can have a significant impact on their self-esteem and quality of life. Understanding the causes and symptoms of gynecomastia is essential for proper diagnosis and effective treatment.
1. Polycystic ovary syndrome (PCOS): This is the most common cause of anovulation, affecting up to 75% of women with PCOS.
2. Hypothalamic dysfunction: The hypothalamus regulates hormonal signals that stimulate ovulation. Disruptions in these signals can lead to anovulation.
3. Thyroid disorders: Both hypothyroidism (underactive thyroid) and hyperthyroidism (overactive thyroid) can disrupt hormone levels and lead to anovulation.
4. Premature ovarian failure (POF): This condition is characterized by the premature loss of ovarian function before age 40.
5. Ovarian insufficiency: This occurs when the ovaries lose their ability to produce eggs, often due to aging or medical treatment.
6. Chronic diseases: Certain conditions like diabetes, hypertension, and obesity can increase the risk of anovulation.
7. Luteal phase defect: This occurs when the uterine lining does not properly thicken during the second half of the menstrual cycle, making it difficult for a fertilized egg to implant.
8. Ovulatory disorders: Disorders such as ovarian cysts, endometriosis, and pelvic inflammatory disease can interfere with ovulation.
9. Genetic factors: Some genetic mutations can affect ovulation, such as those associated with Turner syndrome or other rare genetic conditions.
10. Medications: Certain medications, such as hormonal contraceptives and antidepressants, can disrupt ovulation.
Anovulation is typically diagnosed through a combination of medical history, physical examination, and laboratory tests, including hormone levels and imaging studies. Treatment options for anovulation depend on the underlying cause and may include:
1. Hormonal medications to stimulate ovulation
2. Intrauterine insemination (IUI) or in vitro fertilization (IVF) to increase the chances of conception
3. Lifestyle modifications, such as weight loss and stress management
4. Surgery to correct anatomical abnormalities or remove any blockages in the reproductive tract
5. Assisted reproductive technologies (ART), such as IVF with egg donation or surrogacy.
It's important for women experiencing irregular periods or anovulation to seek medical attention, as timely diagnosis and treatment can improve their chances of conceiving and reduce the risk of complications during pregnancy.
The causes of virilism can be due to various factors including:
1. Congenital adrenal hyperplasia (CAH): A genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive levels of androgens such as testosterone.
2. Androgen insensitivity syndrome (AIS): A condition where the body is unable to respond to androgens, leading to virilization.
3. 5-alpha-reductase deficiency: A rare genetic disorder that affects the production of the enzyme 5-alpha-reductase, which is important for the development of male characteristics.
4. Genetic mutations: Some individuals may have genetic mutations that lead to the overproduction of androgens or the underproduction of anti-androgens.
5. Hormonal imbalances: Imbalances in hormone levels, such as high testosterone and low estrogen, can also cause virilism.
Virilism can be diagnosed through a combination of physical examination, medical history, and laboratory tests such as hormone level measurements. Treatment options for virilism depend on the underlying cause and may include hormone replacement therapy, surgery, or psychological counseling.
In summary, virilism is a condition characterized by the excessive development of male characteristics in individuals who are not biologically male, and it can be caused by various genetic or hormonal factors. It is important to seek medical attention if symptoms persist or worsen over time, as early diagnosis and treatment can improve outcomes.
The exact cause of follicular cysts is not known, but they may be related to hormonal changes, genetic factors, or blockages within the hair follicle. Treatment options include observation, antibiotics, and surgical removal if the cyst becomes inflamed or infected.
A Follicular Cyst is a benign cystic lesion that forms in the scalp or face and typically arises from the hair follicle. They are usually small, soft to the touch, and painless unless they become inflamed or infected.
Follicular cysts are more common in women than men, and often appear during childhood or adolescence. Although their exact cause is unknown, they may be related to hormonal changes, genetic factors, or blockages within the hair follicle.
Small, soft, painless cysts that form on the scalp or face are usually Follicular Cysts, which are benign and do not produce any symptoms unless they become inflamed or infected. They appear more frequently in women than men and often develop during childhood or adolescence. Their exact cause is unknown but may be related to hormonal fluctuations, genetic factors, or blockages within the hair follicle.
Treatment for oligomenorrhea depends on the underlying cause, but may include hormone replacement therapy, birth control pills, or other medications to regulate menstrual cycles. In some cases, surgery may be necessary to correct anatomical abnormalities or remove cysts that are interfering with normal menstruation.
Oligomenorrhea can have significant impacts on women's lives, including difficulty becoming pregnant due to irregular ovulation and increased risk of developing endometrial cancer. Therefore, early diagnosis and treatment are important to manage the condition and prevent potential complications.
Some common types of adrenal gland diseases include:
1. Cushing's syndrome: A hormonal disorder caused by excessive production of cortisol, a hormone produced by the adrenal glands. This can be caused by a tumor on one of the adrenal glands or by taking too much corticosteroid medication.
2. Addison's disease: A rare disorder caused by the destruction of the adrenal glands, typically due to an autoimmune response. This results in a deficiency of cortisol and aldosterone hormones, leading to symptoms such as fatigue, weight loss, and skin changes.
3. Adrenocortical carcinoma: A rare type of cancer that affects the adrenal glands. This can cause symptoms such as weight gain, skin changes, and abdominal pain.
4. Pheochromocytoma: A rare type of tumor that develops on one of the adrenal glands, typically causing high blood pressure and other symptoms due to excessive production of hormones such as epinephrine and norepinephrine.
5. Adrenal insufficiency: A condition in which the adrenal glands do not produce enough cortisol and aldosterone hormones, often caused by a autoimmune response or a viral infection. This can lead to symptoms such as fatigue, weight loss, and skin changes.
6. Primary aldosteronism: A condition in which the adrenal glands produce too much aldosterone hormone, leading to high blood pressure and other symptoms.
7. Adrenal incidentalomas: Tumors that are found on the adrenal glands, but do not produce excessive hormones or cause symptoms. These tumors can be benign or malignant.
8. Adrenal metastases: Tumors that have spread to the adrenal glands from another part of the body, often causing symptoms such as high blood pressure and abdominal pain.
9. Adrenal cysts: Fluid-filled sacs that form on the adrenal glands, which can cause symptoms such as abdominal pain and weight loss.
10. Adrenal hemorrhage: Bleeding in the adrenal glands, often caused by trauma or a blood clotting disorder. This can lead to symptoms such as severe abdominal pain and shock.
It is important to note that this list is not exhaustive and there may be other rare conditions that affect the adrenal glands not included here. If you suspect you have any of these conditions, it is important to seek medical attention from a qualified healthcare professional for proper diagnosis and treatment.
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- Perfecting experimentation that began in the late 1800s, the prohormone and testosterone precursor androstenedione was synthesized in 1938when the first of it was synthesized from testosterone. (link2learnint.org)
- Testosterone, androstenedione and luteinizing hormone levels in the serum were measured 24 h before supplementation (clear probe), and at 24, 72, 240, 408 and 576 h from the beginning of the supplementation. (nih.gov)
- DHEA and androstenedione are androgens and are precursors of testosterone. (globalrph.com)
- To quantify the magnitude of the effects of atorvastatin on free testosterone, sex hormone binding globin (SHBG), androstenedione, dehydroepiandrosterone sulphate (DHEAS) concentrations, free androgen index (FAI), and withdrawal due to adverse effects (WDAEs) in both males and females, compared to placebo or no treatment. (cochrane.org)
- Results of adrenal hormonal analyses revealed considerable increases in serum concentrations of androstenedione and testosterone. (avma.org)
- CRPC cells are able to metabolise the C19 adrenal steroids DHEA(S) and androstenedione (A4) to DHT, while bypassing testosterone completely. (sun.ac.za)
- Depending on the tissue type, androstenedione can serve as a precursor to TESTOSTERONE as well as ESTRONE and ESTRADIOL . (nih.gov)
- Besides being a precursor for estradiol and estrone synthesis, androstenedione is also converted into testosterone. (ndnr.com)
- Since the sources of precursors for estrogens and testosterone (androstenedione and DHEA) and progesterone are produced by the adrenal glands in postmenopausal women, it seems reasonable to assume that optimal adrenal gland function is needed for a smooth menopausal transition and to remain symptom free during postmenopausal years. (ndnr.com)
- We also offer measurement data on additional steroid hormone levels (17α-hydroxyprogesterone, 17α-hydroxyprogesterone [17-OHP], androstenedione, progesterone, testosterone, estrone, 17β-estradiol, estrone sulfate, and dehydroepiandrosterone sulfate) and 24,25-dihydroxyvitamin D. Customization is available on request. (cdc.gov)
- CYP17 catalyzes two sequential reactions: 1) the conversion of pregnenolone and progesterone to their 17a-hydroxy derivatives by 17α-hydroxylase activity and 2) the subsequent formation of dehydroepiandrosterone (DHEA) and androstenedione, respectively, by C17, 20 lyase activity. (globalrph.com)
- The adrenal androgens are dehydroepiandrosterone (DHEA), androstenedione and 11-hydroxyandrostenedione. (dermnetnz.org)
- 5. Production of estrone and fractional conversion of circulating androstenedione to estrone in women with endometrial carcinoma. (nih.gov)
- 18. The effect of chronic and acyclic elevation of circulating androstenedione or estrone concentrations on ovarian function in the rhesus monkey. (nih.gov)
- 20. Effect of obesity on conversion of plasma androstenedione to estrone in postmenopausal women with and without endometrial cancer. (nih.gov)
- After menopause, the adrenal glands produce androstenedione, which is converted peripherally into estrone by the aromatase enzyme found mainly in adipose tissue. (ndnr.com)
- It came into popular use as the progesterone analogue, androstenedione, androstenedione and sibutramine, but its progestin-like properties led to it being renamed androstenedione-beta-hydroxamic acid (androstanolone), which was then marketed as 'estrogen-containing' androstenedione for use as a hormone for the treatment of female conditions, androstenedione spray. (link2learnint.org)
- A study by Adriaansen et al suggested that salivary samples of the 17-ketosteroid androstenedione as well as of another steroid, 17-hydroxyprogesterone, can be used to monitor the efficacy of treatment in congenital adrenal hyperplasia. (medscape.com)
- Diurnal salivary androstenedione and 17-hydroxyprogesterone levels in healthy volunteers for monitoring treatment efficacy of patients with congenital adrenal hyperplasia. (medscape.com)
- An overview of Genetic Toxicology Micronucleus Rats study conclusions related to Androstenedione (63-05-8). (nih.gov)
- 14. Androstenedione metabolism in patients with endometrial cancer. (nih.gov)
- Genetic Toxicity Evaluation of Androstenedione in Salmonella/E.coli Mutagenicity Test or Ames Test. (nih.gov)
- Before and after 12 weeks' treatment, patients were infused with 3H-Delta4 androstenedione (20 MBq) and 14C-oestrone (E1) (1 MBq) for 18 h. (nih.gov)
- This project includes 90-day and 2-year studies of Chromium Picollinate, Goldenseal, Milk Thistle, Thujone, and Androstenedione. (nih.gov)
- Effects from prescription drugs androstenedione and 19-nortestosterone subjective and objective assessments of hair growth and density (23). (hatchchilefest.com)
- In this study, we synthesized androsta-4,14-diene-3,16-dione, 12ß-hydroxyandrosta-4,14-diene-3,16-dione, and other 3,16- androstenedione derivatives from commercially available dehydroepiandrosterone as a starting material in 9-13 steps with high yields. (bvsalud.org)
- The positive associations between serum testosterone and androstenedione and AMH in premenopausal women is consistent with androgens directly or indirectly influencing AMH production during follicular development. (medscape.com)
- Androstenedione is a C-19 (19 carbon atoms) steroid hormone found in men as well as in premenopausal women. (medscape.com)
- Each laboratory has its own reference range for androstenedione, depending on the assay. (medscape.com)
- The role of androstenedione as an estrogen precursor in postmenopausal women with endometrial carcinoma. (nih.gov)
- Androstenedione production in the adrenal glands is under effect of the adrenocorticotropic hormone (ATCH), whereas in the gonads it is controlled by the luteinizing hormone/follicle-stimulating hormone (LH/FSH). (medscape.com)