An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.
Compounds that inhibit AROMATASE in order to reduce production of estrogenic steroid hormones.
An analog of desoxycorticosterone which is substituted by a hydroxyl group at the C-18 position.
The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.
A delta-4 C19 steroid that is produced not only in the TESTIS, but also in the OVARY and the ADRENAL CORTEX. Depending on the tissue type, androstenedione can serve as a precursor to TESTOSTERONE as well as ESTRONE and ESTRADIOL.
One of the SELECTIVE ESTROGEN RECEPTOR MODULATORS with tissue-specific activities. Tamoxifen acts as an anti-estrogen (inhibiting agent) in the mammary tissue, but as an estrogen (stimulating agent) in cholesterol metabolism, bone density, and cell proliferation in the ENDOMETRIUM.
The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.
Periods of sleep manifested by changes in EEG activity and certain behavioral correlates; includes Stage 1: sleep onset, drowsy sleep; Stage 2: light sleep; Stages 3 and 4: delta sleep, light sleep, deep sleep, telencephalic sleep.
A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.
Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.
Unsaturated androstane derivatives which are substituted with two hydroxy groups in any position in the ring system.
An aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone, a major mammalian estrogen. It is converted from ANDROSTENEDIONE directly, or from TESTOSTERONE via ESTRADIOL. In humans, it is produced primarily by the cyclic ovaries, PLACENTA, and the ADIPOSE TISSUE of men and postmenopausal women.
Tumors or cancer of the human BREAST.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).
An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.
Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.
A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)
Certain tumors that 1, arise in organs that are normally dependent on specific hormones and 2, are stimulated or caused to regress by manipulation of the endocrine environment.
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
An enzyme that catalyzes the desaturation (aromatization) of the ring A of C19 androgens and converts them to C18 estrogens. In this process, the 19-methyl is removed. This enzyme is membrane-bound, located in the endoplasmic reticulum of estrogen-producing cells of ovaries, placenta, testes, adipose, and brain tissues. Aromatase is encoded by the CYP19 gene, and functions in complex with NADPH-FERRIHEMOPROTEIN REDUCTASE in the cytochrome P-450 system.
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.
These compounds stimulate anabolism and inhibit catabolism. They stimulate the development of muscle mass, strength, and power.
A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.

A proposed sequence of hormones controlling the induction of luteal 20alpha-hydroxy steroid dehydrogenase and progesterone withdrawal in the late-pregnant rat. (1/183)

1. The previously reported induction of luteal 20alpha-hydroxy steroid dehydrogenase by administration of aminoglutethimide to late-pregnant rats was shown to be unaffected by prior removal of the foetuses. Aminoglutethimide therefore does not act via the foetuses in this context. 2. The ability of injected oestrogen to prevent the above induction was lost by delaying the injection for 12h after aminoglutethimide, although the increase in enzyme activity begins only after 24h. 3. Induction of 20alpha-hydroxy steroid dehydrogenase by foetoplacental removal on day 18 of pregnancy was inhibited by human choriogonadotropin, lutropin (luteinizing hormone) and pregnant-mare serum gonadotropin, but not by somatotropin (growth hormone), thyrotropin or follitropin (follicle-stimulating hormone) 4. Indomethacin blocked the normal induction of 20alpha-hydroxy steroid dehydrogenase in late pregnancy and that caused by aminoglutethimide. It partially blocked that caused by human choriogonadotropin given on days 19-20 and that caused by 2-bromo-alpha-ergocryptine on days 5-6, but failed to block that caused by human choriogonadotropin on days 15-16 or by foetoplacental removal on day 18 of pregnancy. 5. These findings, and the control of progesterone synthesis in late pregnancy, are interpreted in terms of a sequence of hormonal or enzymic syntheses, each of which is inhibited by the product of the preceding synthesis.  (+info)

Product of side-chain cleavage of cholesterol, isocaproaldehyde, is an endogenous specific substrate of mouse vas deferens protein, an aldose reductase-like protein in adrenocortical cells. (2/183)

Mouse vas deferens protein (MVDP) is an aldose reductase-like protein that is highly expressed in the vas deferens and adrenal glands and whose physiological functions were unknown. We hereby describe the enzymatic characteristics of MVDP and its role in murine adrenocortical Y1 cells. The murine aldose reductase (AR) and MVDP cDNAs were expressed in bacteria to obtain recombinant proteins and to compare their enzymatic activities. Recombinant MVDP was functional and displayed kinetic properties distinct from those of murine AR toward various substrates, a preference for NADH, and insensitivity to AR inhibitors. For MVDP, isocaproaldehyde, a product of side-chain cleavage of cholesterol generated during steroidogenesis, is the best natural substrate identified so far. In Y1 cells, we found that NADH-linked isocaproaldehyde reductase (ICR) activity was much higher than NADPH-linked ICR activity and was not abolished by AR inhibitors. We demonstrate that in Y1 cells, forskolin-induced MVDP expression enhanced NADH-linked ICR activity by 5-6-fold, whereas no variation in ICR-linked NADPH activity was observed in the same experiment. In cells stably transfected with MVDP antisense cDNA, NADH-linked ICR activity was abolished even in the presence of forskolin, and the isocaproaldehyde toxicity was increased compared with that of intact Y1 cells, as measured by isocaproaldehyde LD(50). In Y1 cells transfected with MVDP antisense cDNA, forskolin-induced toxicity was abolished by aminoglutethimide. These results indicate that in adrenocortical cells, MVDP is responsible for detoxifying isocaproaldehyde generated by steroidogenesis.  (+info)

Decreased progesterone levels and progesterone receptor antagonists promote apoptotic cell death in bovine luteal cells. (3/183)

We tested the hypothesis that progesterone (P(4)) acts at a local level to inhibit luteal apoptosis. Initial experiments employed aminoglutethimide, a P450 cholesterol side-chain cleavage inhibitor, to inhibit steroid synthesis. Cultured bovine luteal cells were treated with aminoglutethimide (0.15 mM) +/- P(4) (500 ng/ml) for 48 h. Luteal cells were recovered and snap frozen for isolation and analysis of oligonucleosomal DNA fragmentation or fixed for morphological analysis. Medium was collected for analysis of P(4) levels by RIA. Aminoglutethimide inhibited P(4) synthesis by > 95% and increased the level of apoptosis as evidenced by (32)P-labeled oligonucleosomal DNA fragmentation (> 40%). P(4) supplementation inhibited the onset of apoptosis that was induced by aminoglutethimide. These data were further supported by morphological assessment of apoptotic cells utilizing a Hoechst staining technique and together strongly suggest that P(4) has anti-apoptotic capacity. Using reverse transcription-polymerase chain reaction, we were able to isolate a 380-base pair cDNA from the bovine corpus luteum (CL) that was 100% homologous to the progesterone receptor (PR) previously found in bovine oviductal tissue. Furthermore, PR transcripts were present in large and small luteal cells. Immunohistochemistry also revealed that PR protein was present in both large and small luteal cells. To determine whether the anti-apoptotic effect of P(4) was regulated at the receptor level, luteal cells were cultured in the presence of PR antagonists, RU-486 and onapristone, for 48 h. Both antagonists caused approximately a 40% increase in (32)P-labeled oligonucleosomal DNA fragmentation. Interestingly, there was no difference (P >/= 0.05) in P(4) levels after treatment with PR antagonists. These observations support the concept that P(4) represses the onset of apoptosis in the CL by a PR-dependent mechanism.  (+info)

Status of aromatase inhibitors in relation to other breast cancer treatment modalities. (4/183)

Aromatase is one of the key enzymes possibly linked with the perpetuation or even initiation of breast cancer. Modulation of its activity by the new generation inhibitors has resulted in increased responses and improved therapeutic ratio compared with those of parent aromatase inhibitors. More recent trials have shown promising results with regard to improved therapeutic ratio compared with what is seen with presently accepted second-line hormonal approaches. Present data and laboratory research indicate that new aromatase inhibitors have the potential to play an important role as adjuvants, and possibly in the prevention of human breast cancer. It is probable that it may be as adjuvants that their real therapeutic strength in terms of a beneficial impact on survival may be realized. The absence of estrogen agonist activity of new aromatase inhibitors on lipid and bone metabolism calls for more clinical studies having late mortality in breast cancer survivors as the ultimate outcome objective; in this regard, interaction of new aromatase inhibitors with new selective estrogen receptor modulators looks promising. Achievement of these outcomes, and understanding of interactions with other therapies, await the termination of present trials and the start of new initiatives.  (+info)

Use of aromatase inhibitors in breast carcinoma. (5/183)

Aromatase, a cytochrome P-450 enzyme that catalyzes the conversion of androgens to estrogens, is the major mechanism of estrogen synthesis in the post-menopausal woman. We review some of the recent scientific advances which shed light on the biologic significance, physiology, expression and regulation of aromatase in breast tissue. Inhibition of aromatase, the terminal step in estrogen biosynthesis, provides a way of treating hormone-dependent breast cancer in older patients. Aminoglutethimide was the first widely used aromatase inhibitor but had several clinical drawbacks. Newer agents are considerably more selective, more potent, less toxic and easier to use in the clinical setting. This article reviews the clinical data supporting the use of the potent, oral competitive aromatase inhibitors anastrozole, letrozole and vorozole and the irreversible inhibitors 4-OH androstenedione and exemestane. The more potent compounds inhibit both peripheral and intra-tumoral aromatase. We discuss the evidence supporting the notion that aromatase inhibitors lack cross-resistance with antiestrogens and suggest that the newer, more potent compounds may have a particular application in breast cancer treatment in a setting of adaptive hypersensitivity to estrogens. Currently available aromatase inhibitors are safe and effective in the management of hormone-dependent breast cancer in post-menopausal women failing antiestrogen therapy and should now be used before progestational agents. There is abundant evidence to support testing these compounds as first-line hormonal therapy for metastatic breast cancer as well as part of adjuvant regimens in older patients and quite possibly in chemoprevention trials of breast cancer.  (+info)

Lipoproteins regulate expression of the steroidogenic acute regulatory protein (StAR) in mouse adrenocortical cells. (6/183)

The steroidogenic acute regulatory protein (StAR) is required for the movement of cholesterol from the outer to the inner mitochondrial membrane, the site of cholesterol side chain cleavage. Here we describe a novel form of regulation of StAR gene expression in steroidogenic cells. Treatment of Y-1 BS1 adrenocortical cells with either low density lipoprotein (LDL) or high density lipoprotein (HDL) increases expression of endogenous StAR mRNA and protein in a dose-dependent manner. Induction of StAR mRNA by lipoprotein requires basal cAMP-dependent protein kinase, since the inhibitor, R(p)-8-Br-cAMP, inhibited induction of StAR protein by LDL. Likewise, basal StAR expression or LDL induction of StAR protein was not detectable in Y-1 kin-8 cells which are deficient in cAMP-dependent protein kinase. Aminoglutethimide and ketoconazole were used to determine if side chain cleavage of lipoprotein-derived cholesterol is required for induction of StAR mRNA. Treatment with either drug alone induced StAR mRNA expression 1.5-3-fold, while induction of StAR in cells treated with either drug plus LDL, was equal to, or greater than, induction seen with either agent alone, suggesting that lipoprotein does not regulate StAR via generation of an oxysterol intermediate. Both LDL and HDL increased expression of a mouse -966 StAR promoter-reporter construct 1.5-2.5-fold, indicating that regulation occurs at the level of transcription. In contrast, neither lipoprotein was able to induce transcription from a -966 StAR promoter in which the steroidogenic factor-1 site at -135 was abolished, indicating that regulation of StAR transcription by lipoproteins requires steroidogenic factor-1. The regulation of StAR gene expression by lipoproteins may represent a positive feedback circuit which links cholesterol availability with steroidogenic output.  (+info)

Contribution of progesterone, follicle stimulating hormone and glucocorticoids in survival of serum-free cultured granulosa cell explants. (7/183)

To investigate the role of progesterone (P4) as a survival factor in quail granulosa cell explants, P4 content was determined under various conditions and correlated with apoptotic indexes (AIs) evaluated by 2',6'-diamidino-2-phenylindole (DAPI)-staining. Analysis of serum-free cultures from 24 to 96 h shows decreased P4 levels in the medium paralleled by increasing AI. Inhibiting apoptosis by gonadotropic support (FSH, 100 ng/ml) stimulates a 3-fold increase of the P4 level in the medium (83.49+/-8.69 vs 26.31+/-1.61 ng/ml in serum-free controls) together with a significant decrease in AI from 8.81+/-1.06% in serum-free controls to 3.50+/-0.72%. Substantial evidence for P4 as an autocrine/paracrine survival factor can be inferred from experiments with aminoglutethimide (AG, 1 mM) and RU486 (20 microM). Blocking P4 synthesis by AG causes a 2-fold increase in apoptosis from 6.08+/-0.67% in serum-free controls to 12.53+/-1.60%. Blocking P4 receptors by RU486 causes a similar increase in AI (3.02+/-0.98% in serum-free controls to 17.07+/-3.20%) and about a 50% decrease in P4. The effect of RU486 could be attenuated by exogenous P4 but not by dexamethasone indicating selective binding of P4 to the progesterone receptor. Dexamethasone treatment promotes survival without affecting P4 levels. In further support of an autocrine/paracrine action for P4 in the granulosa cells, both the A and B form of the avian P4 receptor (PR) are identified in vivo and in vitro by Western blotting. Exogenous administration of P4 only affects survival when endogenous P4 synthesis is blocked or after 48 h of serum-free culture when endogenous P4 production is very low. Because FSH also affects survival when its stimulatory effect on P4 synthesis is blocked by AG (AI decrease from 6.08+/-0.67% in serum-free controls to 1.64+/-0.71% in FSH+AG treated) it is proposed that (1) P4 is an autocrine/paracrine survival factor in the preovulatory granulosa and (2) FSH mediates both P4-dependent and P4-independent survival pathways.  (+info)

Aromatase inhibition by an 11,13-dihydroderivative of a sesquiterpene lactone. (8/183)

Compounds that inhibit aromatase activity are used for the treatment of breast cancer. A group of sesquiterpene lactones inhibit aromatase activity and also exert cytotoxicity through their reactive alpha-methylene-gamma-lactone group. To synthesize sesquiterpene lactones with greater specificity for aromatase inhibition and lower cytotoxicity, we chemically reduced the alpha-methylene-gamma-lactone group in the active aromatase inhibitor 10-epi-8-deoxycumambrin B (compound 1), to obtain the new compound 11betaH,13-dihydro-10-epi-8-deoxycumambrin B (compound 2). Reduction of the alpha-methylene-gamma-lactone group abrogated the cytotoxic activity of compound 1 against the JEG-3, HeLa, and COS-7 cell lines. Compound 2 had higher aromatase inhibitory activity than compound 1 (IC(50) = 2 +/- 0.5 microM versus 7 +/- 0.5 microM, K(i) = 1.5 microM versus 4.0 microM) and was a more potent type II ligand to the heme iron present in the cytochrome P450(arom) active site. Compound 2 inhibited aromatase activity in JEG-3 cells in a comparable manner to the inhibitor aminoglutethimide (AG) used clinically for the treatment of breast cancer. Additionally, compound 2 inhibited androstenedione-induced uterine hypertrophy in sexually immature mice (41% of uterine weight suppression for compound 2 versus 51% for AG). We conclude that the anti-aromatase activity of sesquiterpene lactones does not depend on the presence of the highly reactive alpha-methylene-gamma-lactone group, whereas their cytotoxicity does. These findings may facilitate the development of safer agents for breast cancer therapy.  (+info)

Aminoglutethimide is a medication that is primarily used to treat hormone-sensitive cancers such as breast cancer and prostate cancer. It works by blocking the production of certain hormones in the body, including estrogen and cortisol. Aminoglutethimide is an inhibitor of steroid synthesis, specifically targeting the enzymes involved in the conversion of cholesterol to steroid hormones.

The medication is available in oral form and is typically taken 2-3 times a day. Common side effects include drowsiness, dizziness, dry mouth, skin rash, and changes in appetite or weight. More serious side effects may include liver damage, severe allergic reactions, and changes in heart rhythm.

It's important to note that aminoglutethimide can interact with other medications, so it's crucial to inform your healthcare provider about all the drugs you are currently taking before starting this medication. Additionally, regular monitoring of liver function and hormone levels may be necessary during treatment with aminoglutethimide.

Aromatase inhibitors (AIs) are a class of drugs that are primarily used in the treatment of hormone-sensitive breast cancer in postmenopausal women. They work by inhibiting the enzyme aromatase, which is responsible for converting androgens into estrogens. By blocking this conversion, AIs decrease the amount of estrogen in the body, thereby depriving hormone-sensitive breast cancer cells of the estrogen they need to grow and multiply.

There are three main types of aromatase inhibitors:

1. Letrozole (Femara) - a non-steroidal AI that is taken orally once a day.
2. Anastrozole (Arimidex) - another non-steroidal AI that is also taken orally once a day.
3. Exemestane (Aromasin) - a steroidal AI that is taken orally once a day.

In addition to their use in breast cancer treatment, AIs are also sometimes used off-label for the treatment of estrogen-dependent conditions such as endometriosis and uterine fibroids. However, it's important to note that the use of aromatase inhibitors can have significant side effects, including hot flashes, joint pain, and bone loss, so they should only be used under the close supervision of a healthcare provider.

18-Hydroxydesoxycorticosterone is a steroid hormone that is produced by the adrenal gland. It is an intermediate in the biosynthesis of aldosterone, which is the major hormone responsible for regulating sodium and potassium balance in the body. 18-Hydroxydesoxycorticosterone itself has minimal biological activity, but it is converted to aldosterone by the enzyme aldosterone synthase.

The medical relevance of 18-Hydroxydesoxycorticosterone lies in its role as a precursor to aldosterone and its potential use as a marker for certain adrenal gland disorders. For example, increased production of 18-Hydroxydesoxycorticosterone has been observed in some cases of primary hyperaldosteronism, which is a condition characterized by excessive aldosterone production leading to high blood pressure and low potassium levels. Measuring the levels of this hormone can help diagnose and manage such conditions.

Menopause is a natural biological process that typically occurs in women in their mid-40s to mid-50s. It marks the end of menstrual cycles and fertility, defined as the absence of menstruation for 12 consecutive months. This transition period can last several years and is often accompanied by various physical and emotional symptoms such as hot flashes, night sweats, mood changes, sleep disturbances, and vaginal dryness. The hormonal fluctuations during this time, particularly the decrease in estrogen levels, contribute to these symptoms. It's essential to monitor and manage these symptoms to maintain overall health and well-being during this phase of life.

Androstenedione is a steroid hormone produced by the adrenal glands, ovaries, and testes. It is a precursor to both male and female sex hormones, including testosterone and estrogen. In the adrenal glands, it is produced from cholesterol through a series of biochemical reactions involving several enzymes. Androstenedione can also be converted into other steroid hormones, such as dehydroepiandrosterone (DHEA) and estrone.

In the body, androstenedione plays an important role in the development and maintenance of secondary sexual characteristics, such as facial hair and a deep voice in men, and breast development and menstrual cycles in women. It also contributes to bone density, muscle mass, and overall physical strength.

Androstenedione is available as a dietary supplement and has been marketed as a way to boost athletic performance and increase muscle mass. However, its effectiveness for these purposes is not supported by scientific evidence, and it may have harmful side effects when taken in high doses or for extended periods of time. Additionally, the use of androstenedione as a dietary supplement is banned by many sports organizations, including the International Olympic Committee and the National Collegiate Athletic Association.

Tamoxifen is a selective estrogen receptor modulator (SERM) medication that is primarily used in the treatment and prevention of breast cancer. It works by blocking the action of estrogen in the body, particularly in breast tissue. This can help to stop or slow the growth of hormone-sensitive tumors.

Tamoxifen has been approved by the U.S. Food and Drug Administration (FDA) for use in both men and women. It is often used as a part of adjuvant therapy, which is treatment given after surgery to reduce the risk of cancer recurrence. Tamoxifen may also be used to treat metastatic breast cancer that has spread to other parts of the body.

Common side effects of tamoxifen include hot flashes, vaginal discharge, and changes in mood or vision. Less commonly, tamoxifen can increase the risk of blood clots, stroke, and endometrial cancer (cancer of the lining of the uterus). However, for many women with breast cancer, the benefits of taking tamoxifen outweigh the risks.

It's important to note that while tamoxifen can be an effective treatment option for some types of breast cancer, it is not appropriate for all patients. A healthcare professional will consider a variety of factors when determining whether tamoxifen is the right choice for an individual patient.

Hydrocortisone is a synthetic glucocorticoid, which is a class of steroid hormones. It is identical to the naturally occurring cortisol, a hormone produced by the adrenal gland that helps regulate metabolism and helps your body respond to stress. Hydrocortisone has anti-inflammatory effects and is used to treat various inflammatory conditions such as allergies, skin disorders, and autoimmune diseases. It works by suppressing the immune system's response to reduce swelling, redness, itching, and other symptoms caused by inflammation.

Hydrocortisone is available in different forms, including oral tablets, topical creams, lotions, gels, and ointments, as well as injectable solutions. The specific use and dosage depend on the condition being treated and the individual patient's medical history and current health status.

As with any medication, hydrocortisone can have side effects, especially when used in high doses or for extended periods. Common side effects include increased appetite, weight gain, mood changes, insomnia, and skin thinning. Long-term use of hydrocortisone may also increase the risk of developing osteoporosis, diabetes, cataracts, and other health problems. Therefore, it is essential to follow your healthcare provider's instructions carefully when using this medication.

Sleep stages are distinct patterns of brain activity that occur during sleep, as measured by an electroencephalogram (EEG). They are part of the sleep cycle and are used to describe the different types of sleep that humans go through during a normal night's rest. The sleep cycle includes several repeating stages:

1. Stage 1 (N1): This is the lightest stage of sleep, where you transition from wakefulness to sleep. During this stage, muscle activity and brain waves begin to slow down.
2. Stage 2 (N2): In this stage, your heart rate slows, body temperature decreases, and eye movements stop. Brain wave activity becomes slower, with occasional bursts of electrical activity called sleep spindles.
3. Stage 3 (N3): Also known as deep non-REM sleep, this stage is characterized by slow delta waves. It is during this stage that the body undergoes restorative processes such as tissue repair, growth, and immune function enhancement.
4. REM (Rapid Eye Movement) sleep: This is the stage where dreaming typically occurs. Your eyes move rapidly beneath closed eyelids, heart rate and respiration become irregular, and brain wave activity increases to levels similar to wakefulness. REM sleep is important for memory consolidation and learning.

The sleep cycle progresses through these stages multiple times during the night, with REM sleep periods becoming longer towards morning. Understanding sleep stages is crucial in diagnosing and treating various sleep disorders.

Dehydroepiandrosterone (DHEA) is a steroid hormone produced by the adrenal glands. It serves as a precursor to other hormones, including androgens such as testosterone and estrogens such as estradiol. DHEA levels typically peak during early adulthood and then gradually decline with age.

DHEA has been studied for its potential effects on various health conditions, including aging, cognitive function, sexual dysfunction, and certain chronic diseases. However, the evidence supporting its use for these purposes is generally limited and inconclusive. As with any supplement or medication, it's important to consult with a healthcare provider before taking DHEA to ensure safety and effectiveness.

Adrenergic agents are a class of drugs that bind to and activate adrenergic receptors, which are cell surface receptors found in the nervous system and other tissues. These receptors are activated by neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline), which are released by the sympathetic nervous system in response to stress or excitement.

Adrenergic agents can be classified based on their mechanism of action and the specific receptors they bind to. There are two main types of adrenergic receptors: alpha and beta receptors, each with several subtypes. Some adrenergic agents bind to both alpha and beta receptors, while others are selective for one or the other.

Adrenergic agents have a wide range of therapeutic uses, including the treatment of asthma, cardiovascular diseases, glaucoma, and neurological disorders. They can also be used as diagnostic tools to test the function of the sympathetic nervous system. Some examples of adrenergic agents include:

* Alpha-agonists: These drugs bind to alpha receptors and cause vasoconstriction (narrowing of blood vessels), which can be useful in the treatment of hypotension (low blood pressure) or nasal congestion. Examples include phenylephrine and oxymetazoline.
* Alpha-antagonists: These drugs block the action of alpha receptors, leading to vasodilation (widening of blood vessels) and a decrease in blood pressure. Examples include prazosin and doxazosin.
* Beta-agonists: These drugs bind to beta receptors and cause bronchodilation (opening of the airways), increased heart rate, and increased force of heart contractions. They are used in the treatment of asthma, chronic obstructive pulmonary disease (COPD), and other respiratory disorders. Examples include albuterol and salmeterol.
* Beta-antagonists: These drugs block the action of beta receptors, leading to a decrease in heart rate, blood pressure, and bronchodilation. They are used in the treatment of hypertension, angina (chest pain), and heart failure. Examples include metoprolol and atenolol.
* Nonselective alpha- and beta-antagonists: These drugs block both alpha and beta receptors and are used in the treatment of hypertension, angina, and heart failure. Examples include labetalol and carvedilol.

Androstenediols are endogenous steroid hormones that are produced in the body from dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS), which are secreted by the adrenal glands. There are two major types of androstenediols: 5-androstenediol and 4-androstenediol. These hormones can be further metabolized into testosterone and estrogens, making them important intermediates in steroid hormone synthesis.

5-androstenediol is a weak androgen that can be converted to testosterone in peripheral tissues, while 4-androstenediol has little known biological activity. Both of these compounds have been studied for their potential role in various physiological processes, including sexual differentiation, bone metabolism, and aging. However, more research is needed to fully understand their functions and clinical significance.

It's worth noting that androstenediols are also sometimes referred to as "prohormones" because they can be converted into active steroid hormones in the body. Some athletes and bodybuilders have used synthetic forms of these compounds as performance-enhancing drugs, although their use is banned by many sports organizations due to concerns about potential health risks and unfair advantages in competition.

Estrone is a type of estrogen, which is a female sex hormone. It's one of the three major naturally occurring estrogens in women, along with estradiol and estriol. Estrone is weaker than estradiol but has a longer half-life, meaning it remains active in the body for a longer period of time.

Estrone is produced primarily in the ovaries, adrenal glands, and fat tissue. In postmenopausal women, when the ovaries stop producing estradiol, estrone becomes the dominant form of estrogen. It plays a role in maintaining bone density, regulating the menstrual cycle, and supporting the development and maintenance of female sexual characteristics.

Like other forms of estrogen, estrone can also have effects on various tissues throughout the body, including the brain, heart, and breast tissue. Abnormal levels of estrone, either too high or too low, can contribute to a variety of health issues, such as osteoporosis, menstrual irregularities, and increased risk of certain types of cancer.

Breast neoplasms refer to abnormal growths in the breast tissue that can be benign or malignant. Benign breast neoplasms are non-cancerous tumors or growths, while malignant breast neoplasms are cancerous tumors that can invade surrounding tissues and spread to other parts of the body.

Breast neoplasms can arise from different types of cells in the breast, including milk ducts, milk sacs (lobules), or connective tissue. The most common type of breast cancer is ductal carcinoma, which starts in the milk ducts and can spread to other parts of the breast and nearby structures.

Breast neoplasms are usually detected through screening methods such as mammography, ultrasound, or MRI, or through self-examination or clinical examination. Treatment options for breast neoplasms depend on several factors, including the type and stage of the tumor, the patient's age and overall health, and personal preferences. Treatment may include surgery, radiation therapy, chemotherapy, hormone therapy, or targeted therapy.

The adrenal cortex is the outer portion of the adrenal gland, which is located on top of the kidneys. It plays a crucial role in producing hormones that are essential for various bodily functions. The adrenal cortex is divided into three zones:

1. Zona glomerulosa: This outermost zone produces mineralocorticoids, primarily aldosterone. Aldosterone helps regulate sodium and potassium balance and thus influences blood pressure by controlling the amount of fluid in the body.
2. Zona fasciculata: The middle layer is responsible for producing glucocorticoids, with cortisol being the most important one. Cortisol regulates metabolism, helps manage stress responses, and has anti-inflammatory properties. It also plays a role in blood sugar regulation and maintaining the body's response to injury and illness.
3. Zona reticularis: The innermost zone produces androgens, primarily dehydroepiandrosterone (DHEA) and its sulfate form (DHEAS). These androgens are weak compared to those produced by the gonads (ovaries or testes), but they can be converted into more potent androgens or estrogens in peripheral tissues.

Disorders related to the adrenal cortex can lead to hormonal imbalances, affecting various bodily functions. Examples include Addison's disease (insufficient adrenal cortical hormone production) and Cushing's syndrome (excessive glucocorticoid levels).

Adrenocorticotropic Hormone (ACTH) is a hormone produced and released by the anterior pituitary gland, a small endocrine gland located at the base of the brain. ACTH plays a crucial role in the regulation of the body's stress response and has significant effects on various physiological processes.

The primary function of ACTH is to stimulate the adrenal glands, which are triangular-shaped glands situated on top of the kidneys. The adrenal glands consist of two parts: the outer cortex and the inner medulla. ACTH specifically targets the adrenal cortex, where it binds to specific receptors and initiates a series of biochemical reactions leading to the production and release of steroid hormones, primarily cortisol (a glucocorticoid) and aldosterone (a mineralocorticoid).

Cortisol is involved in various metabolic processes, such as regulating blood sugar levels, modulating the immune response, and helping the body respond to stress. Aldosterone plays a vital role in maintaining electrolyte and fluid balance by promoting sodium reabsorption and potassium excretion in the kidneys.

ACTH release is controlled by the hypothalamus, another part of the brain, which produces corticotropin-releasing hormone (CRH). CRH stimulates the anterior pituitary gland to secrete ACTH, which in turn triggers cortisol production in the adrenal glands. This complex feedback system helps maintain homeostasis and ensures that appropriate amounts of cortisol are released in response to various physiological and psychological stressors.

Disorders related to ACTH can lead to hormonal imbalances, resulting in conditions such as Cushing's syndrome (excessive cortisol production) or Addison's disease (insufficient cortisol production). Proper diagnosis and management of these disorders typically involve assessing the function of the hypothalamic-pituitary-adrenal axis and addressing any underlying issues affecting ACTH secretion.

Metyrapone is a medication that is primarily used in the diagnosis and treatment of Cushing's syndrome, a condition characterized by excessive levels of cortisol hormone in the body. It works as an inhibitor of steroidogenesis, specifically blocking the enzyme 11-beta-hydroxylase, which is involved in the production of cortisol in the adrenal gland.

By inhibiting this enzyme, metyrapone prevents the formation of cortisol and leads to an accumulation of its precursor, 11-deoxycortisol. This can help restore the balance of hormones in the body and alleviate symptoms associated with Cushing's syndrome.

It is important to note that metyrapone should only be used under the supervision of a healthcare professional, as it can have significant side effects and interactions with other medications.

Steroids, also known as corticosteroids, are a type of hormone that the adrenal gland produces in your body. They have many functions, such as controlling the balance of salt and water in your body and helping to reduce inflammation. Steroids can also be synthetically produced and used as medications to treat a variety of conditions, including allergies, asthma, skin conditions, and autoimmune disorders.

Steroid medications are available in various forms, such as oral pills, injections, creams, and inhalers. They work by mimicking the effects of natural hormones produced by your body, reducing inflammation and suppressing the immune system's response to prevent or reduce symptoms. However, long-term use of steroids can have significant side effects, including weight gain, high blood pressure, osteoporosis, and increased risk of infections.

It is important to note that anabolic steroids are a different class of drugs that are sometimes abused for their muscle-building properties. These steroids are synthetic versions of the male hormone testosterone and can have serious health consequences when taken in large doses or without medical supervision.

Danazol is a synthetic, orally active androgenic steroid with antigonadotropic properties. It is used primarily in the treatment of endometriosis, fibrocystic breast disease, and hereditary angioedema. Danazol works by suppressing the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary gland, which in turn inhibits the growth of ovarian tissue and reduces the production of estrogen and progesterone. This leads to a decrease in the symptoms associated with endometriosis and fibrocystic breast disease. In the case of hereditary angioedema, danazol helps prevent attacks by increasing the levels of a protein called C1 esterase inhibitor, which is necessary for regulating the immune system and preventing inflammation.

The common side effects of danazol include weight gain, acne, oily skin, increased hair growth, changes in menstrual cycle, decreased breast size, deepening of the voice, and emotional lability. Rare but serious side effects may include liver damage, blood clots, and adrenal gland problems. Danazol is contraindicated in pregnancy due to its potential virilizing effects on the fetus. It should be used with caution in individuals with a history of liver disease, heart disease, or seizure disorders.

The medical definition of danazol can be summarized as follows:

Danazol (dan-a-zole)

A synthetic androgenic steroid with antigonadotropic properties, used primarily in the treatment of endometriosis, fibrocystic breast disease, and hereditary angioedema. Danazol suppresses the release of FSH and LH from the pituitary gland, inhibiting ovarian tissue growth and reducing estrogen and progesterone production. In hereditary angioedema, danazol increases C1 esterase inhibitor levels to prevent attacks. Common side effects include weight gain, acne, increased hair growth, menstrual changes, decreased breast size, deepened voice, and emotional lability. Rare but serious side effects may involve liver damage, blood clots, or adrenal gland problems. Danazol is contraindicated in pregnancy due to potential virilizing effects on the fetus and should be used with caution in individuals with a history of liver disease, heart disease, or seizure disorders.

Estrogens are a group of steroid hormones that are primarily responsible for the development and regulation of female sexual characteristics and reproductive functions. They are also present in lower levels in males. The main estrogen hormone is estradiol, which plays a key role in promoting the growth and development of the female reproductive system, including the uterus, fallopian tubes, and breasts. Estrogens also help regulate the menstrual cycle, maintain bone density, and have important effects on the cardiovascular system, skin, hair, and cognitive function.

Estrogens are produced primarily by the ovaries in women, but they can also be produced in smaller amounts by the adrenal glands and fat cells. In men, estrogens are produced from the conversion of testosterone, the primary male sex hormone, through a process called aromatization.

Estrogen levels vary throughout a woman's life, with higher levels during reproductive years and lower levels after menopause. Estrogen therapy is sometimes used to treat symptoms of menopause, such as hot flashes and vaginal dryness, or to prevent osteoporosis in postmenopausal women. However, estrogen therapy also carries risks, including an increased risk of certain cancers, blood clots, and stroke, so it is typically recommended only for women who have a high risk of these conditions.

Cortisone is a type of corticosteroid hormone that is produced naturally in the body by the adrenal gland. It is released in response to stress and helps to regulate metabolism, reduce inflammation, and suppress the immune system. Cortisone can also be synthetically produced and is often used as a medication to treat a variety of conditions such as arthritis, asthma, and skin disorders. It works by mimicking the effects of the natural hormone in the body and reducing inflammation and suppressing the immune system. Cortisone can be administered through various routes, including oral, injectable, topical, and inhalational.

Hormone-dependent neoplasms are a type of tumor that requires the presence of specific hormones to grow and multiply. These neoplasms have receptors on their cell surfaces that bind to the hormones, leading to the activation of signaling pathways that promote cell division and growth.

Examples of hormone-dependent neoplasms include breast cancer, prostate cancer, and endometrial cancer. In breast cancer, for instance, estrogen and/or progesterone can bind to their respective receptors on the surface of cancer cells, leading to the activation of signaling pathways that promote tumor growth. Similarly, in prostate cancer, androgens such as testosterone can bind to androgen receptors on the surface of cancer cells, promoting cell division and tumor growth.

Hormone-dependent neoplasms are often treated with hormonal therapies that aim to reduce or block the production of the relevant hormones or interfere with their ability to bind to their respective receptors. This can help slow down or stop the growth of the tumor and improve outcomes for patients.

The adrenal glands are a pair of endocrine glands that are located on top of the kidneys. Each gland has two parts: the outer cortex and the inner medulla. The adrenal cortex produces hormones such as cortisol, aldosterone, and androgens, which regulate metabolism, blood pressure, and other vital functions. The adrenal medulla produces catecholamines, including epinephrine (adrenaline) and norepinephrine (noradrenaline), which help the body respond to stress by increasing heart rate, blood pressure, and alertness.

Aromatase is a enzyme that belongs to the cytochrome P450 superfamily, and it is responsible for converting androgens into estrogens through a process called aromatization. This enzyme plays a crucial role in the steroid hormone biosynthesis pathway, particularly in females where it is primarily expressed in adipose tissue, ovaries, brain, and breast tissue.

Aromatase inhibitors are used as a treatment for estrogen receptor-positive breast cancer in postmenopausal women, as they work by blocking the activity of aromatase and reducing the levels of circulating estrogens in the body.

Nausea is a subjective, unpleasant sensation of discomfort in the stomach and upper gastrointestinal tract that may precede vomiting. It's often described as a feeling of queasiness or the need to vomit. Nausea can be caused by various factors, including motion sickness, pregnancy, gastrointestinal disorders, infections, certain medications, and emotional stress. While nausea is not a disease itself, it can be a symptom of an underlying medical condition that requires attention and treatment.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Cushing syndrome is a hormonal disorder that occurs when your body is exposed to high levels of the hormone cortisol for a long time. This can happen due to various reasons such as taking high doses of corticosteroid medications or tumors that produce cortisol or adrenocorticotropic hormone (ACTH).

The symptoms of Cushing syndrome may include:

* Obesity, particularly around the trunk and upper body
* Thinning of the skin, easy bruising, and purple or red stretch marks on the abdomen, thighs, breasts, and arms
* Weakened bones, leading to fractures
* High blood pressure
* High blood sugar
* Mental changes such as depression, anxiety, and irritability
* Increased fatigue and weakness
* Menstrual irregularities in women
* Decreased fertility in men

Cushing syndrome can be diagnosed through various tests, including urine and blood tests to measure cortisol levels, saliva tests, and imaging tests to locate any tumors. Treatment depends on the cause of the condition but may include surgery, radiation therapy, chemotherapy, or adjusting medication dosages.

Anabolic agents are a class of drugs that promote anabolism, the building up of body tissues. These agents are often used medically to help people with certain medical conditions such as muscle wasting diseases, osteoporosis, and delayed puberty. Anabolic steroids are one type of anabolic agent. They mimic the effects of testosterone, the male sex hormone, leading to increased muscle mass and strength. However, anabolic steroids also have significant side effects and can be addictive. Therefore, their use is regulated and they are only available by prescription in many countries. Abuse of anabolic steroids for non-medical purposes, such as to improve athletic performance or appearance, is illegal and can lead to serious health consequences.

Hypothyroidism is a medical condition where the thyroid gland, which is a small butterfly-shaped gland located in the front of your neck, does not produce enough thyroid hormones. This results in a slowing down of the body's metabolic processes, leading to various symptoms such as fatigue, weight gain, constipation, cold intolerance, dry skin, hair loss, muscle weakness, and depression.

The two main thyroid hormones produced by the thyroid gland are triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating various bodily functions, including heart rate, body temperature, and energy levels. In hypothyroidism, the production of these hormones is insufficient, leading to a range of symptoms that can affect multiple organ systems.

Hypothyroidism can be caused by several factors, including autoimmune disorders (such as Hashimoto's thyroiditis), surgical removal of the thyroid gland, radiation therapy for neck cancer, certain medications, and congenital defects. Hypothyroidism is typically diagnosed through blood tests that measure levels of TSH (thyroid-stimulating hormone), T3, and T4. Treatment usually involves taking synthetic thyroid hormones to replace the missing hormones and alleviate symptoms.

... (AG), sold under the brand names Elipten, Cytadren, and Orimeten among others, is a medication which has been ... Aminoglutethimide is the generic name of the drug and its INNTooltip International Nonproprietary Name, USANTooltip United ... ISBN 978-1-56363-429-1. Siraki AG, Bonini MG, Jiang J, Ehrenshaft M, Mason RP (July 2007). "Aminoglutethimide-induced protein ...
Cash, Ralph; Brough, A. Joseph; Margo, N.P.Cohen; Satoh, Paul S. (1967). "Aminoglutethimide as an inhibitor of adrenal ... Cohen, Margo P. (1968). "Aminoglutethimide inhibition of adrenal desmolase activity". Proc Soc Exp Biol Med. 127 (4): 1086-1090 ...
Aminoglutethimide has an oral administration and a usual dosage range between 250 and 100 mg/day. The drug has good oral ... Aminoglutethimide is an NSAIs and therefore inhibits aromatase among other biosynthesis and is for example used to treat ... Aminoglutethimide has a good distribution around the body and is partly metabolized in the liver by acetylation. The ... In 1960 aminoglutethimide was marketed as an anticonvulsant. Later in 1963, a doctor at the Sinai Hospital in Detroit ...
These drugs include aminoglutethimide, ketoconazole, and abiraterone acetate. Aminoglutethimide inhibits cholesterol side-chain ... The earlier androgen synthesis inhibitors aminoglutethimide and ketoconazole have only limitedly been used in the treatment of ... The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960 and 1977, respectively, and ... These include, to varying extents, cyproterone acetate, flutamide, nilutamide, bicalutamide, aminoglutethimide, and ...
Aminoglutethimide Piperidione Methyprylone Pyrithyldione Anvisa (2023-03-31). "RDC Nº 784 - Listas de Substâncias Entorpecentes ...
Analogues of mitotane include aminoglutethimide, amphenone B, and metyrapone. Mitotane was introduced in 1960 for the treatment ...
The aromatase inhibitor aminoglutethimide induces the metabolism of tamoxifen. Conversely, the aromatase inhibitor letrozole ...
Analogues of metyrapone include aminoglutethimide, amphenone B, and mitotane. Metyrapone has been found in early human trials ...
Some Piperidinediones include Glutethimide, Methyprylon, Pyrithyldione, Glutarimide, and Aminoglutethimide. The first 3 ( ...
... inhibitors include aminoglutethimide, ketoconazole, and mitotane, among others. ...
... aminoglutethimide, and sulfamethazine. NAT2 is involved in the metabolism of xenobiotics, which can lead to both the ...
Ketoconazole can cause liver damage with prolonged use, and aminoglutethimide can cause skin rashes. When hormonal treatment is ... Medications that block the production of adrenal androgens such as DHEA include ketoconazole and aminoglutethimide. Because the ...
This makes it potentially useful in the treatment of breast cancer, and with fewer side effects than aminoglutethimide, but its ... MacNeill FA, Jones AL, Jacobs S, Lønning PE, Powles TJ, Dowsett M (October 1992). "The influence of aminoglutethimide and its ... but instead has pharmacological activity as a selective aromatase inhibitor similar to the related drug aminoglutethimide and ...
Aminoglutethimide inhibits both aromatase and other enzymes critical for steroid hormone synthesis in the adrenal glands. It ...
Other steroidogenesis inhibitors besides ketoconazole and levoketoconazole include the nonsteroidal compound aminoglutethimide ...
... and aminoglutethimide. They are used to treat Cushing's syndrome. Antiglucocorticoids could be effective antidepressants for a ...
... s (AIs) include: Aminoglutethimide (Elipten, Cytadren, Orimeten) Testolactone (Teslac) Anastrozole (Arimidex ...
The combination of MPA with aminoglutethimide to treat metastases from breast cancer has been associated with an increase in ...
Abiraterone acetate Ketoconazole Seviteronel Aminoglutethimide Alfatradiol Dutasteride Epristeride Finasteride Saw palmetto ...
In the past, surgical adrenalectomy and early androgen biosynthesis inhibitors like ketoconazole and aminoglutethimide were ... However, adrenalectomy is an invasive procedure with high morbidity, ketoconazole and aminoglutethimide have relatively high ...
... aminoglutethimide, exemestane, formestane, and testolactone are banned. Selective estrogen receptor modulators, including ...
Cholesterol side-chain cleavage enzyme (P450scc, CYP11A1) inhibitors such as aminoglutethimide, ketoconazole, and mitotane ... Aromatase inhibitors (AIs) such as aminoglutethimide, anastrozole, exemestane, letrozole, and testolactone inhibit the ...
... proven with the blockade of aminoglutethimide (AG, known to block P450-mediated enzymes. Harry Brodie, a chemist, joined the ...
List of corticosteroids List of corticosteroid cyclic ketals List of corticosteroid esters Aminoglutethimide blocks ...
... and aminoglutethimide, have corticotropic or procorticotropic effects. Anticorticotropins are analogous to antigonadotropins ...
... aminoglutethimide MeSH D03.383.621.808.800 - thalidomide MeSH D03.383.621.808.930 - triacetoneamine-n-oxyl MeSH D03.383.621.815 ...
... aminoglutethimide, fadrozole, finrozole, letrozole, liarozole, norendoxifen, rogletimide (pyridoglutethimide), vorozole Other ... steroidogenesis inhibitors: aminoglutethimide, ketoconazole, orteronel, seviteronel, others Miscellaneous: tanaproget ( ...
Aminoglutethimide (3-(4-aminophenyl)-3-ethylpiperidine-2,6-dione), which was originally introduced as an anticonvulsant in 1960 ...
They include: Antiglucocorticoids - e.g., mifepristone, ketoconazole, aminoglutethimide Antimineralocorticoids - e.g., ...
Inhibitors of cholesterol side-chain cleavage enzyme (P450scc), such as aminoglutethimide and ketoconazole, may block ...
Aminoglutethimide (AG), sold under the brand names Elipten, Cytadren, and Orimeten among others, is a medication which has been ... Aminoglutethimide is the generic name of the drug and its INNTooltip International Nonproprietary Name, USANTooltip United ... ISBN 978-1-56363-429-1. Siraki AG, Bonini MG, Jiang J, Ehrenshaft M, Mason RP (July 2007). "Aminoglutethimide-induced protein ...
Detailed drug Information for Jantoven. Includes common brand names, drug descriptions, warnings, side effects and dosing information.
Exfoliative dermatitis (ED) is a definitive term that refers to a scaling erythematous dermatitis involving 90% or more of the cutaneous surface. Exfoliative dermatitis is characterized by erythema and scaling involving the skins surface and often obscures the primary lesions that are important clues to understanding the evolution of the dis...
Aminoglutethimide: Aminoglutethimide may diminish adrenal suppression by corticosteroids. Amphotericin B injection and ...
Aminoglutethimide. *Anastrozole. *Androsta-1,4,6-triene-3,17-dione (androstatrienedione). *Androsta-3,5-diene-7,17-dione ( ...
Be sure to mention any of the following: aminoglutethimide (Cytadren; no longer available in U.S.); amphotericin B (Abelcet, ...
229960003437 aminoglutethimide Drugs 0.000 description 1 * ROBVIMPUHSLWNV-UHFFFAOYSA-N aminoglutethimide Chemical compound C=1C ... aminoglutethimide; hormones (i.e. estrogen); anticoagulants (heparin, synthetic heparin salts and other inhibitors of thrombin ...
Aminoglutethimide (Cytadren). *Amphotericin B (Amphocin, Fungizone Intravenous). *Cholesterol-lowering drugs. *Anticoagulants ...
Aminoglutethimide, sometimes used in Cushings Syndrome. *Ciclosporin. *Non-steroidal anti-inflammatory drugs for treating ...
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Aktuelle API Auditberichte • GMP-Audits der Herstelung pharmazeutischer Ausgangs- und Wirkstoffe nach ICH Q7 / EU GMP Guide Part II • Diapharm
Aminoglutethimide. *Ketoconazole. *Mifepristone. *Mitotane. Radiation therapy usually does not work for cancerous adrenal ...
Rifampicin, rifabutin, ephedrine, carbamazepine, phenylbutazone, phenobarbital, phenytoin, primidone, and aminoglutethimide ...
Aminoglutethimide Drug Info. T65197. Target Info. Target Name. Erythropoietin Receptor (EPOR). Target type. Successful Target. ...
You must have JavaScript enabled in your browser to utilize the functionality of this website. ...
... reflist Androgen Aminoglutethimide 125-84-8 1.00E+00 1.00E+01 1.00E+02 NA Decrease 78 Aminoglutethimide DTXSID8022589 ...
AMINOGLUTETHIMIDE 50205 AMINOHIPPURATE SODIUM 50210 AMINOPHYLLINE 50216 AMINOPYRINE 50220 AMINOSALICYLIC ACID 50223 AMIODARONE ...
aminoglutethimide. Cytadren. anagrelide. Agrylin. arsenic trioxide. Trisenox. asparaginase. Elspar, Erwinase, Kidrolase, ...
Inhibition of aldosterone synthase is currently being investigated as a medical treatment for hypertension, heart failure, and renal disorders.[15] Deactivation of enzymatic activity reduces aldosterone concentrations in plasma and tissues which decreases mineralocorticoid receptor-dependent and independent effects in cardiac vascular and renal target organs.[15] Inhibition has shown to decrease plasma and urinary aldosterone concentrations by 70 - 80%, rapid hypokalaemia correction, moderate decrease of blood pressure, and an increase plasma renin activity in patients who are on a low-sodium diet.[15] Ongoing medical research is focusing on the synthesis of second-generation aldosterone synthase inhibitors to create an ideally selective inhibitor as the current, orally delivered, LCl699 has shown to be non-specific to aldosterone synthase.[15]. ...
DL-Aminoglutethimide. Aminoglutethimide is an adrenal steroid inhibitor. It works by blocking the production of a variety of ...
aminoglutethimide (Cytadren). *amphotericin B (Amphocin, Fungizone Intravenous). *cholesterol-lowering drugs. *anticoagulants ...
Hereditary coproporphyria is one of the porphyrias, a group of diseases that involves defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. Inheritance is autosomal (usually autosomal dominant, but sometimes autosomal recessive).
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
... such as mitotane and aminoglutethimide). ...
Loss of corticosteroid-induced adrenal suppression w/ aminoglutethimide. Development of hypokalemia w/ K-depleting agents. ...
aromatase inhibitors like aminoglutethimide, anastrozole, exemestane, letrozole, testolactone. Estrace may also interact with ...
Example inducers include aminoglutethimide, carbamazepine, phenytoin, and rifampin.. Iron salts: Proton pump inhibitors may ... Example inducers include aminoglutethimide, carbamazepine, phenytoin, and rifampin.. CYP2C19 substrates: Rabeprazole may ... Example inducers include aminoglutethimide, carbamazepine, nafcillin, nevirapine, phenobarbital, phenytoin, and rifamycins.. ...
Aminoglutethimide or rifampin because they may decrease Proveras effectiveness.. This may not be a complete list of all ...
  • Aminoglutethimide (AG), sold under the brand names Elipten, Cytadren, and Orimeten among others, is a medication which has been used in the treatment of seizures, Cushing's syndrome, breast cancer, and prostate cancer, among other indications. (wikipedia.org)
  • 7. Endocrine effects of low dose aminoglutethimide as an aromatase inhibitor in the treatment of breast cancer. (nih.gov)
  • Aromatase inhibitors, such as aminoglutethimide and anastrozole, work in a different way to lower estrogen levels. (cancer.org)
  • 16. Potency of the effect of D-stereoisomer of aminoglutethimide on adrenal and extraadrenal steroidogenesis. (nih.gov)
  • 20. Adrenal suppression with aminoglutethimide. (nih.gov)
  • induced a significant inhibition in the aromatase mRNA expression as compared to cells exposed to the same doses of aminoglutethimide, but without melatonin pretreatment. (supp.ai)
  • 8. Low-dose aminoglutethimide in treatment of advanced breast cancer. (nih.gov)
  • 11. Aminoglutethimide in the treatment of advanced breast cancer. (nih.gov)
  • 14. Alterations in the metabolism of oestrogens during treatment with aminoglutethimide in breast cancer patients. (nih.gov)
  • 1. Aminoglutethimide dose and hormone suppression in advanced breast cancer. (nih.gov)
  • 2. Hydrocortisone alone vs hydrocortisone plus aminoglutethimide: a comparison of the endocrine effects in postmenopausal breast cancer. (nih.gov)
  • 3. A comparison of the endocrine effects of low dose aminoglutethimide with and without hydrocortisone in postmenopausal breast cancer patients. (nih.gov)
  • 4. Endocrine effects of low dose aminoglutethimide alone in advanced postmenopausal breast cancer. (nih.gov)
  • 6. Endocrine effects of aminoglutethimide plus hydrocortisone versus effects of high dose of hydrocortisone alone in postmenopausal metastatic breast cancer. (nih.gov)
  • 9. Endocrine and therapeutic effects of aminoglutethimide in premenopausal patients with breast cancer. (nih.gov)
  • 12. Preliminary study of hormone determinations during aminoglutethimide therapy for advanced breast cancer. (nih.gov)
  • 13. Role of aminoglutethimide in male breast cancer. (nih.gov)
  • 15. Kinetic, hormonal and clinical studies with aminoglutethimide in breast cancer. (nih.gov)
  • 17. Endocrine changes associated with relapse in advanced breast cancer patients on aminoglutethimide therapy. (nih.gov)
  • 18. Adjuvant aminoglutethimide therapy for postmenopausal patients with primary breast cancer: progress report. (nih.gov)