Adrenal Hyperplasia, Congenital
Polycystic Ovary Syndrome
The treatment of insulin resistance does not improve adrenal cytochrome P450c17alpha enzyme dysregulation in polycystic ovary syndrome. (1/235)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)
Congenital adrenal hyperplasia: not really a zebra. (2/235)Congenital adrenal hyperplasia was once considered a rare inherited disorder with severe manifestations. Mild congenital adrenal hyperplasia, however, is common, affecting one in 100 to 1,000 persons in the United States and frequently eluding diagnosis. Both classic and nonclassic forms of the disease are caused by deficiencies in the adrenal enzymes that are used to synthesize glucocorticoids. The net result is increased production from the adrenal gland of cortisol precursors and androgens. Even mild congenital adrenal hyperplasia can result in life-threatening sinus or pulmonary infections, orthostatic syncope, shortened stature and severe acne. Women with mild congenital adrenal hyperplasia often present with hirsutism, oligomenorrhea or infertility. Congenital adrenal hyperplasia is diagnosed by demonstration of excess cortisol precursors in the serum during an adrenal corticotropic hormone challenge. Diagnosis of congenital adrenal hyerplasia in fetuses that are at risk for congenital adrenal hyperplasia can be determined using human leukocyte antigen haplotype or by demonstration of excess cortisol precursors in amniotic fluid. Treatment includes carefully monitored hormone replacement therapy. Recognition of the problem and timely replacement therapy can reduce morbidity and enhance quality of life in patients that are affected by congenital adrenal hyperplasia. (+info)
The effect of chronic treatment with GH on gonadal function in men with isolated GH deficiency. (3/235)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)
Ovulatory and metabolic effects of D-chiro-inositol in the polycystic ovary syndrome. (4/235)BACKGROUND: Women with the polycystic ovary syndrome have insulin resistance and hyperinsulinemia, possibly because of a deficiency of a D-chiro-inositol-containing phosphoglycan that mediates the action of insulin. We hypothesized that the administration of D-chiro-inositol would replenish stores of the mediator and improve insulin sensitivity. METHODS: We measured steroids in serum and performed oral glucose-tolerance tests before and after the oral administration of 1200 mg of D-chiro-inositol or placebo once daily for six to eight weeks in 44 obese women with the polycystic ovary syndrome. The serum progesterone concentration was measured weekly to monitor for ovulation. RESULTS: In the 22 women given D-chiro-inositol, the mean (+/-SD) area under the plasma insulin curve after the oral administration of glucose decreased from 13,417+/-11,572 to 5158+/-6714 microU per milliliter per minute (81+/-69 to 31+/-40 nmol per liter per minute) (P=0.007; P=0.07 for the comparison of this change with the change in the placebo group); glucose tolerance did not change significantly. The serum free testosterone concentration in these 22 women decreased from 1.1+/-0.8 to 0.5+/-0.5 ng per deciliter (38+/-7 to 17+/-3 pmol per liter) (P=0.006 for the comparison with the change in the placebo group). The women's diastolic and systolic blood pressure decreased by 4 mm Hg (P<0.001 and P=0.05, respectively, for the comparisons with the changes in the placebo group), and their plasma triglyceride concentrations decreased from 184+/-88 to 110+/-61 mg per deciliter (2.1+/-0.2 to 1.2+/-0.1 mmol per liter) (P=0.002 for the comparison with the change in the placebo group). None of these variables changed appreciably in the placebo group. Nineteen of the 22 women who received D-chiro-inositol ovulated, as compared with 6 of the 22 women in the placebo group (P<0.001). CONCLUSIONS: D-Chiro-inositol increases the action of insulin in patients with the polycystic ovary syndrome, thereby improving ovulatory function and decreasing serum androgen concentrations, blood pressure, and plasma triglyceride concentrations. (+info)
Adrenal 21-hydroxylase gene mutations in Slovenian hyperandrogenic women: evaluation of corticotrophin stimulation and HLA polymorphisms in screening for carrier status. (5/235)OBJECTIVE: To study the incidence of 21-hydroxylase deficiency in Slovenian hyperandrogenic women, at the gene level. Previous endocrine studies indicated large differences in the incidence of 21-hydroxylase deficiency in hyperandrogenic women. The predictive values of the 17-hydroxyprogesterone (17-OHP) response to ACTH stimulation and of HLA typing in screening for carrier status were re-evaluated. DESIGN: Molecular analysis of CYP21 gene, ACTH stimulation and human leucocyte antigen (HLA) typing were performed in 83 consecutive Slovenian hyperandrogenic women. MEASUREMENTS: Cortisol and 17-OHP concentrations were measured at baseline and 60 min after ACTH stimulation. Basal adrenal androgen concentrations were also measured. RESULTS: None of 83 hyperandrogenic patients was affected with non-classical 21-hydroxylase deficiency, but 12 of 81 patients (14.8%) had high concentrations of 17-OHP after stimulation, indicative of carrier status. The increase in 17-OHP concentrations could be explained by a carrier status for CYP21 gene mutations in only three of 12 patients (25%), whereas seven of 69 patients (10. 1%) with normal concentrations of 17-OHP after stimulation were found to be carriers of CYP21 gene mutations, indicating low positive predictive values of ACTH stimulation as a screening test for carriers of 21-hydroxylase deficiency. In total, 11 carriers were identified among 83 patients: seven CYP21 gene deletions/conversions, two Gln(318)Stop and one Val(281)Leu mutation and one gene conversion extending from exon 4 to exon 7 were found. The association between Val(281)Leu mutation and HLA-B14 antigen was confirmed in this Slovenian population. CONCLUSIONS: Basal or ACTH-stimulated 17-OHP concentrations are not a good indicator of the carrier status for 21-hydroxylase deficiency among Slovenian hyperandrogenic patients. Reliable screening for carriers of 21-hydroxylase deficiency is possible only by molecular analysis of the CYP21 gene. (+info)
Alterations in cardiac flow parameters in patients with polycystic ovarian syndrome. (6/235)The aim of this study was to examine the echocardiographic profiles of patients with polycystic ovarian syndrome (PCOS). Serum concentrations of follicle stimulating hormone, luteinizing hormone, androstenedione, free testosterone, prolactin, DHEA-SO(4) and 17-OH-progesterone, lipid profile (high and low density lipoproteins, triglyceride and total cholesterol) and basal and total insulin after a glucose tolerance test were measured in 35 patients with PCOS and 35 healthy controls matched for body mass index. Doppler, two dimensional M mode echocardiography was performed for the following indices: isovolumetric relaxation time (IVRT), E wave duration time (EVT), A wave duration time (AVT), E wave deceleration time (DT), peak early diastolic flow velocity (PEV), peak late diastolic flow velocity (PAV), E wave velocity time integral (FVI-E), A wave velocity time integral (FVI-A), atrial filling fraction (AFF), ejection fraction (EF), pre-ejection time (PEP), ejection time (ET) and aortic flow velocity time integral (FVI). Androstenedione, free testosterone, low density lipoproteins and cholesterol concentrations were significantly higher in patients with PCOS. There was no difference in basal and total insulin concentrations. IVRT, AVT, FVI-A, AFF, and PEP were higher in patients with PCOS, while PEV, FVI-E, EF, ET, EVT and EVT/AVT were higher in the control group. There was a positive correlation between basal insulin values and IVRT, and between total insulin values and EF. These changes are consistent with a non-restrictive type of diastolic dysfunction and left ventricular stiffness. PCOS may lead to diastolic dysfunction via hyperinsulinaemia and male type dyslipidaemia. (+info)
Aortic plaque size and endometrial response in cholesterol-fed rabbits treated with estrogen plus continuous or sequential progestin. (7/235)ERT is associated with a reduced incidence of coronary risk and cardiac events in postmenopausal women, but increases the risk of endometrial hyperplasia and carcinoma. Combined estrogen and progestin therapy protects the endometrium; however, its effects on heart disease risk factors are not completely known. In our study, 56 ovariectomized New Zealand White rabbits in 7 groups received a 0.5% cholesterol diet for 12 weeks. Controls were not treated with hormones. All other animals received (per kilogram body weight per week) intramuscular injections of either 0.3 mg estrogen (estradiol valerate) alone, 8.3 mg progestin (hydroxyprogesterone caproate) alone, estrogen and progestin continuously in 3 different dosages (0.3 and 8.3 mg; 1 and 8.3 mg; or 1 and 2.8 mg; estrogen and progestin, respectively), or 1 mg estrogen with 25 mg progestin sequentially in 2-week cycles. Eight non-ovariectomized animals served as further controls for endometrial analysis. Morphometric analysis of plaque size in the aortic arch showed that estrogen monotherapy, and the 3 combined therapies with 1 mg estrogen, significantly reduced intimal thickening (P<0.05). The application of progestin alone had no effect on plaque size. The endometrium was enlarged by 3-fold after estrogen treatment, and was decreased by half after progestin treatment, compared with control uteri (P<0.05). In all groups with combined hormone regimens, endometrial size was not significantly different from control uteri. However, these uteri showed more inflammatory reactions, especially when higher doses of hormones were given. In this animal model, doses of progestin that are able to successfully reduce the proliferative effect of estrogen on endometrium do not diminish the desirable antiatherosclerotic properties of estrogen. (+info)
Longitudinal measurements of 17alpha-hydroxyprogesterone in premature infants during the first three months of life. (8/235)AIMS: To determine normal concentrations of 17alpha-hydroxyprogesterone (17OHP) for premature infants. METHODS: 17OHP was measured in 66 consecutive premature infants once a week during the first month, and once every two weeks thereafter, until the age of 3 months. The 17OHP values in 100 full term healthy neonates on the third day of life served as controls. Blood was sampled on filter paper using a neonatal radioimmunoassay kit. Findings were correlated with gestational age, birthweight, mode of delivery, Apgar scores, presence of respiratory distress syndrome and intake of maternal steroids. RESULTS: Mean 17OHP was raised at 7 days of age (138.9, 46.3, 53.3, 29.9 nmol/l, respectively, for infants whose gestational age was under 29 weeks, 29 to 30 weeks, 31 to 32 weeks, and 33 weeks and above). It fell sharply in the first two weeks after which it gradually decreased further, reaching 32.7, 23.6, 16.9, and 13.0 nmol/l, respectively, by the age of 90 days. The mean (SEM) 17OHP concentration in full term infants on day 3 of life was 17.8 (8.9) nmol/l. These values were independent of the presence and severity of respiratory distress syndrome and of prenatal maternal steroids. CONCLUSIONS: The increased 17OHP concentrations found at birth fell to those found in term infants during the first three months of life in infants over 31 weeks of gestation. Postconceptional age is the most important factor determining 17OHP concentration. (+info)
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.
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.
Adrenocortical hyperfunction can be caused by a variety of factors, including:
1. Cushing's syndrome: This is a rare hormonal disorder caused by excessive production of cortisol by the adrenal glands. It can be caused by a benign tumor in the pituitary gland or an adrenal gland, or by taking too much corticosteroid medication.
2. Adrenocortical carcinoma: This is a rare and aggressive type of cancer that affects the adrenal glands. It can cause excessive production of cortisol and other hormones.
3. Familial Cushing's syndrome: This is a genetic disorder that causes excessive production of cortisol by the adrenal glands.
4. Glucocorticoid-remediable aldosteronism (GRA): This is a rare genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive production of cortisol and aldosterone.
5. Licorice ingestion: Consuming large amounts of licorice can cause an increase in the production of cortisol and other hormones by the adrenal glands.
6. Primary aldosteronism (PA): This is a group of rare genetic disorders that affect the production of hormones by the adrenal glands, leading to excessive production of aldosterone and cortisol.
7. Secondary adrenocortical hyperfunction: This can occur due to various conditions such as thyroid disorders, pituitary tumors, or other endocrine disorders that affect the regulation of hormone production by the adrenal glands.
Symptoms of adrenocortical hyperfunction may include:
1. Weight gain and central obesity
2. Increased appetite and food cravings
3. Fatigue and weakness
4. Mood changes, such as anxiety or depression
5. Insomnia and sleep disturbances
6. High blood pressure and cardiovascular risk factors
7. Easy bruising and poor wound healing
8. Muscle weakness and fatigue
9. Thinning of the skin and bones (osteoporosis)
10. Increased risk of infections and decreased immune function.
If you suspect that you or someone you know may have adrenocortical hyperfunction, it is essential to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform several tests, including:
1. Blood tests to measure hormone levels in the body, such as cortisol and aldosterone.
2. Saliva tests to measure cortisol levels throughout the day.
3. Urine tests to measure cortisol levels over a 24-hour period.
4. Imaging tests, such as CT scans or MRI scans, to examine the adrenal glands and look for any signs of tumors or other abnormalities.
5. Other tests to assess the body's response to stress, such as a corticotropin (ACTH) stimulation test.
Treatment options for adrenocortical hyperfunction depend on the underlying cause of the condition and may include:
1. Medications to reduce hormone production in the adrenal glands, such as metyrapone or ketoconazole.
2. Surgery to remove any tumors or cysts in the adrenal glands.
3. Radiation therapy to shrink tumors and reduce hormone production.
4. Lifestyle changes, such as weight loss, stress management techniques, and regular exercise.
5. Monitoring of hormone levels and other health markers to ensure that the condition is under control.
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.
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.
Precocious puberty is a condition wherein children under the age of 8 or 9 experience early onset of pubertal changes, such as breast development, menstruation, or enlargement of the testes and scrotum. It is also known as central precocious puberty (CPP) when it is caused by premature activation of the hypothalamic-pituitary-gonadal axis, resulting in early release of sex hormones.
Precocious Puberty: Causes
The exact cause of precocious puberty is not known; however, several factors have been implicated, including:
1. Genetics: In some cases, precocious puberty may be inherited, with a family history of early puberty or other hormonal disorders.
2. Brain tumors: Tumors in the hypothalamus or pituitary gland can cause early activation of the HPG axis and result in precocious puberty.
3. Congenital anomalies: Some children may be born with abnormalities in the HPG axis, leading to early puberty.
4. Trauma: Traumatic brain injury or stroke may trigger premature activation of the HPG axis and result in precocious puberty.
5. Infections: Certain infections, such as meningitis or encephalitis, can cause inflammation in the hypothalamus or pituitary gland, leading to early puberty.
6. Nutritional factors: Malnutrition or rapid weight gain may contribute to early puberty.
7. Hormonal imbalance: Some children may have an imbalance of sex hormones, such as estrogen or testosterone, which can lead to early puberty.
8. Thyroid disorders: Hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid) can cause early puberty.
9. Chronic diseases: Certain chronic diseases, such as type 1 diabetes mellitus or inflammatory bowel disease, may increase the risk of early puberty.
It is important to note that in many cases, the exact cause of precocious puberty cannot be determined. If you suspect that your child is experiencing early puberty, it is essential to consult with a healthcare professional for proper evaluation and treatment.
Pharmacodynamics of progesterone
Testosterone enantate benzilic acid hydrazone
List of MeSH codes (D04)
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Pharmacology of bicalutamide
Estrogen insensitivity syndrome
Membrane progesterone receptor
Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency
Late onset congenital adrenal hyperplasia
Pharmacology of cyproterone acetate
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- Previous investigators have examined the influence of a variety of factors on 17-alpha hydroxyprogesterone caproate response but have analyzed data that used a fixed outcome of term delivery to define progesterone response. (bvsalud.org)
- A metabolite of PROGESTERONE with a hydroxyl group at the 17-alpha position. (bvsalud.org)
- It is derived from progesterone via 17α-hydroxylase and is a chemical intermediate in the biosynthesis of several other steroids, including cortisol. (cdc.gov)
- Staff numbers and in men 15-hydroxyprogesterone from progesterone. (gatech.edu)
- Predictors of response to 17-alpha hydroxyprogesterone caproate for prevention of recurrent spontaneous preterm birth. (bvsalud.org)
- Intramuscular 17-alpha hydroxyprogesterone caproate injections reduce the risk of recurrent prematurity by approximately one third. (bvsalud.org)
- Unfortunately, prophylactic 17-alpha hydroxyprogesterone caproate is not always effective, and one-third of high- risk women will have a recurrent preterm birth , despite 17-alpha hydroxyprogesterone caproate therapy . (bvsalud.org)
- All women who were included in this analysis received 17-alpha hydroxyprogesterone caproate during the studied pregnancy . (bvsalud.org)
- We classified women as a 17-alpha hydroxyprogesterone caproate responder or nonresponder by calculating the difference in delivery gestational age between the 17-alpha hydroxyprogesterone caproate -treated pregnancy and her earliest spontaneous preterm birth . (bvsalud.org)
- Responders were defined as those with pregnancy that extended ≥3 weeks later with 17-alpha hydroxyprogesterone caproate , compared with the delivery gestational age of their earliest previous spontaneous preterm birth . (bvsalud.org)
- P = .024) were associated with response to 17-alpha hydroxyprogesterone caproate . (bvsalud.org)
- Because women with a penultimate preterm pregnancy were more likely to be 17-alpha hydroxyprogesterone caproate nonresponders, we performed an additional limited analysis examining only the 130 women whose penultimate pregnancy was preterm. (bvsalud.org)
- Several historic and current pregnancy characteristics define women who are at risk for recurrent preterm birth at a similar gestational age , despite 17-alpha hydroxyprogesterone caproate therapy . (bvsalud.org)
- A trial of 17 alpha-hydroxyprogesterone caproate to prevent prematurity in twins. (medscape.com)
- To evaluate whether the use of 17α-hydroxyprogesterone caproate for the prevention of recurrent preterm deliveries is cost-effective. (wustl.edu)
- Costs included those for 17α-hydroxyprogesterone caproate, hospital admissions, and complications from preterm deliveries. (wustl.edu)
- The use of 17α-hydroxyprogesterone caproate for the prevention of preterm deliveries result in cost-savings in women with prior preterm deliveries less than 32 weeks and 32-37 weeks. (wustl.edu)
- Within our baseline assumptions, 17α-hydroxyprogesterone caproate was associated with cost-savings when used for the prevention of preterm deliveries in women with prior preterm deliveries. (wustl.edu)
- Measurement of androstenedione is useful in the diagnosis of congenital adrenal hyperplasia, in conjunction with other androgenic precursors, such as 17α-hydroxyprogesterone. (cdc.gov)
- Treatment can be monitored non-invasively by measuring salivary androstenedione (A4) and 17-hydroxyprogesterone (17-OHP). (stemcellcharter.org)
- Normally, your adrenal glands use 17-OHP to make a hormone called cortisol. (medlineplus.gov)
- A 17-OHP test helps diagnose a group of uncommon, inherited genetic disorders that affect how well your adrenal glands make cortisol. (medlineplus.gov)
- 21-hydroxylase helps your adrenal glands use 17-OHP to make cortisol. (medlineplus.gov)
- Serum SHBG, cortisol, and 17-hydroxyprogesterone did not show significant variations under any treatment. (unifi.it)
- 17α-hydroxyprogesterone (17-OHP) is a steroid hormone that is primarily produced in the adrenal glands, as well as in ovaries, testes, and placenta. (cdc.gov)
- So, tests for male hormones, including testosterone , are often used with 17-OHP tests to help diagnose CAH. (medlineplus.gov)
- 17-OHP is a substance that your adrenal glands make. (medlineplus.gov)
- As the adrenal glands work harder to do their job, they become enlarged and make abnormally high levels of 17-OHP. (medlineplus.gov)
- The adrenal glands use the extra 17-OHP to make larger than normal amounts of male sex hormones. (medlineplus.gov)
- One to 2% of hyperandrogenic women demonstrate a 17-hydroxyprogesterone (17-HP) level greater than 36.3 nmol/L (1200 ng/dL) after acute ACTH-(1-24) adrenal stimulation, consistent with 21-hydroxylase (21-OH) deficient late-onset adrenal hyperplasia (LOAH). (unboundmedicine.com)
- Measurement of 17-OHP is useful in the diagnosis of congenital adrenal hyperplasia (CAH). (cdc.gov)
- PA), thyroid stimulating hormone that is optimal in terms of quality and (TSH), 17-hydroxyprogesterone and performance . (who.int)
- These high levels of 17-OHP are a sign of CAH with 21-hydroxylase deficiency. (medlineplus.gov)
- Classic CAH that is caused by a 21-hydroxylase deficiency can be diagnosed with 17-OHP testing. (medlineplus.gov)
- A 17-OHP test is used to help find and monitor the most common type of CAH, which is sometimes called 21-hydroxylase deficiency. (medlineplus.gov)
- Along with AIS, 5 alpha-reductase deficiency (5aRD) is another representative 46,XY disorder of sexual development (DSDs) that manifests with discrepancies between internal and external genitalia. (e-apem.org)
- If you don t feel like things might improve when the canadian passion for cricket allowed him to continue treatment with alpha agonistic drugs were chosen because they assist in appropriate settings. (gatech.edu)
- Seven patients or five separate families (1.8% of total) demonstrated poststimulation 17-HP levels consistent with LOAH. (unboundmedicine.com)
- Before and after treatments, plasma beta-endorphin levels were evaluated in response to three neuroendocrine tests: (a) clonidine, an alpha 2-presynaptic adrenergic agonist (1.25 mg i.v.) (b) naloxone, an opioid receptor antagonist (4 mg i.v.) and (c) fluoxetine, a serotonin selective reuptake inhibitor (30 mg p.o. (unifi.it)
- The following study was undertaken to endocrinologically and genetically define hyperandrogenic patients with an exaggerated 17-HP response to ACTH stimulation, and which do not represent LOAH. (unboundmedicine.com)
- Of the remaining 16 patients, the net increment in 17-HP (delta 17-HP0-30) was within normal limits in seven (2.6%) and these women were assumed to have a normal 17-HP adrenocortical response superimposed on an elevated basal level of nonadrenal (e.g. ovarian) origin. (unboundmedicine.com)
- Of 265 consecutive patients suffering from hirsutism and/or hyperandrogenic oligomenorrhea, 23 (8.7%) demonstrated a 17-HP level 30 min post stimulation greater than 9.6 nmol/L or 316 ng/dL (the upper 95th percentile in 41 eumenorrheic nonhirsute healthy control women). (unboundmedicine.com)
- If you give birth in a hospital , your baby will usually have a 17-OHP test before going home. (medlineplus.gov)
- It is almost always caused by a lack of 21-hydroxylase and can be found with a 17-OHP test. (medlineplus.gov)
- Investigators from the National Institutes of Child Health and Human Development Maternal-Fetal Medicine Units Network reported significant results treating women at high risk of preterm delivery with 17-alpha hydroxyprogesterone (17P). (medscape.com)
- PA), thyroid stimulating hormone that is optimal in terms of quality and (TSH), 17-hydroxyprogesterone and performance . (who.int)
- HN - 2019 MH - Aegilops UI - D000078065 MN - B1.650.940.800.575.912.250.822.17 MS - A genus of grasses known generally as goatgrasses, presumed to be wild ancestors of domestic WHEAT. (nih.gov)