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 potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.
Chronic inflammation and granuloma formation around irritating foreign bodies.
A sport in which weights are lifted competitively or as an exercise.
Inanimate objects that become enclosed in the body.
A plant genus of the family POLYGALACEAE that contains onjisaponins, xanthones, pyrones, and benzophenones. The name is similar to other snakeroots such as ASARUM; SANICULA; ARISTOLOCHIA; AGERATINA; and others.
Excision of one or both adrenal glands. (From Dorland, 28th ed)
Development of SEXUAL MATURATION in boys and girls at a chronological age that is 2.5 standard deviations below the mean age at onset of PUBERTY in the population. This early maturation of the hypothalamic-pituitary-gonadal axis results in sexual precocity, elevated serum levels of GONADOTROPINS and GONADAL STEROID HORMONES such as ESTRADIOL and TESTOSTERONE.
FIBROUS DYSPLASIA OF BONE affecting several bones. When melanotic pigmentation (CAFE-AU-LAIT SPOTS) and multiple endocrine hyperfunction are additionally associated it is referred to as Albright syndrome.
A relatively rare, usually benign neoplasm originating in the chemoreceptor tissue of the CAROTID BODY; GLOMUS JUGULARE; GLOMUS TYMPANICUM; AORTIC BODIES; and the female genital tract. It consists histologically of rounded or ovoid hyperchromatic cells that tend to be grouped in an alveolus-like pattern within a scant to moderate amount of fibrous stroma and a few large thin-walled vascular channels. (From Stedman, 27th ed)
A 21-carbon steroid, derived from CHOLESTEROL and found in steroid hormone-producing tissues. Pregnenolone is the precursor to GONADAL STEROID HORMONES and the adrenal CORTICOSTEROIDS.
Enlargement of the THYROID GLAND that may increase from about 20 grams to hundreds of grams in human adults. Goiter is observed in individuals with normal thyroid function (euthyroidism), thyroid deficiency (HYPOTHYROIDISM), or hormone overproduction (HYPERTHYROIDISM). Goiter may be congenital or acquired, sporadic or endemic (GOITER, ENDEMIC).
A publication issued at stated, more or less regular, intervals.
Accidental or deliberate use of a medication or street drug in excess of normal dosage.
Behaviors associated with the ingesting of alcoholic beverages, including social drinking.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
A PREDNISOLONE derivative with similar anti-inflammatory action.
Meningitis caused by fungal agents which may occur as OPPORTUNISTIC INFECTIONS or arise in immunocompetent hosts.
The region corresponding to the human WRIST in non-human ANIMALS.
The presence of organisms, or any foreign material that makes a drug preparation impure.
Substances that reduce or suppress INFLAMMATION.
The injection of drugs, most often analgesics, into the spinal canal without puncturing the dura mater.
Methods of delivering drugs into a joint space.

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)

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Aminoglutethimide is an anti-steroid drug marketed under the tradename Cytadren by Novartis around the world. It blocks the production of steroids derived from cholesterol and is clinically used in the treatment of Cushings syndrome and metastatic breast cancer. It is also used by bodybuilders. Aminoglutethimide is indicated in conjunction with other drugs for the suppression of adrenal function in patients with Cushings syndrome. It is also a second or third line choice for the treatment of hormone-sensitive (estrogen and progesterone) metastatic breast cancer. Aminoglutethimide is abused by bodybuilders and other steroid users to lower circulating levels of cortisol in the body and prevent muscle loss. Cortisol is catabolic to protein in muscle and effective blockade of P450scc by aminogluthethimide at high doses prevents muscle loss.[citation needed] Its side effects are skin rash, hepatotoxicity, inhibition of cortisol in the human body, and it may also cause hypothyroidism[citation ...
Aminoglutethimide - Get up-to-date information on Aminoglutethimide side effects, uses, dosage, overdose, pregnancy, alcohol and more. Learn more about Aminoglutethimide
Aminoglutethimide was introduced as an anti-convulsant drug in the U.S.A. in 1960.. The occurrence of a number of side-effects, including several endocrine effects such as goitrogenesis, sexual precocity and virilization, led to its withdrawal.. Further investigation indicated that the drug inhibited adrenal biosynthesis, particularly of aldosterone, cortisol and androgens, probably by interfering with the conversion of cholesterol to delta-5-pregnenolone.. Aminoglutethimide has also been shown to modify the extra-adrenal metabolism of cortisol.. The possible clinical applications of these side-effects are discussed.. ...
Brand name: Cytadren. Aminoglutethimide is the drug which acts on the adrenal cortex. Production of steroids is affected by its administration. Aminoglutethimide is prescribed...
Cytadren is a drug used to treat overactive adrenal cortexes. The adrenals produce female estrogens/estradiols, cortisol (used in your bodys reaction to stress) and some precursor hormones (DHEA). It is often used by weight lifters to suppress female hormones, increase male hormones and help build muscle. One person has emailed Regrowth.com saying he, his doctor, and another male friend had moderate to dense regrowth using this drug. He was using Proscar concurrently. Since this drug raises free testosterone levels, you would probably need to use this in conjunction with Proscar to prevent raised DHT levels. Since Cytadren can suppress DHEA levels, which appear to play a major role in female loss, this may be why it works in women. This drug MUST be used under the supervision of a doctor since it lowers cortisol. This hormone is vital for your body to function under stressful conditions, and without it, your body can have very severe reactions. Your doctor will need to monitor your cortisol and ...
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TY - JOUR. T1 - Adrenal Steroid Levels in Castrated Men with Prostatic Carcinoma Treated with Aminoglutethimide Plus Hydrocortisone. AU - Ahmann, Frederick R.. AU - Crawford, E. David. AU - Kreis, Willi. AU - Levasseur, Yvan. PY - 1987. Y1 - 1987. N2 - Monthly serum dehydroepiandrosterone sulfate, androstenedione, testosterone, dihydrotestosterone, and free testosterone levels were measured in 94 of 129 patients with castration resistant prostatic carcinoma treated on a clinical protocol with aminoglutethimide (1000 mg/day) plus hydrocortisone (40 mg/day) Base-line steroid levels were not found to be age related. Therapy reduced the median levels of all monitored steroids but this suppression was not uniform. Although 87% of dehydroepiandrosterone sulfate levels were suppressed compared to base-line measurements, only 52% of androstenedione and 49% of testosterone levels were reduced. Androstenedione levels in 34% of patients actually rose to greater than twice base-line levels with similar but ...
N Engl J Med. 1981 Sep 3;305(10):545-51. Clinical Trial; Comparative Study; Randomized Controlled Trial; Research Support, U.S. Govt, P.H.S.
The pathways outlined here are common to the adrenals, the gonads and, to some extent, to the fetoplacental unit. The first committed step is the conversion of cholesterol to pregnenolone, catalysed by the P-450scc enzyme, which is under pituitary hormone control (ACTH or LH depending on the tissue). Cholesterol side-chain removal is blocked specifically by aminoglutethimide, a steroid biosynthesis inhibitor. From pregnenolone, steroid biosynthesis can proceed either through the so-called delta-5 pathway (17α-hydroxypregnenolone, dehydroepiandrosterone, testosterone), or through the delta-4 pathway (progesterone onwards). Progesterone is the starting point for mineralocorticoid synthesis, whereas glucocorticoids are derived from its metabolite, 17α-hydroxyprogesterone. Estrogens are formed from androgens (androstenedione and/or testosterone). Most reactions are irreversible (as denoted by a single arrow). Reversible reactions (double arrows) depend on cofactor availability (e.g. the ...
DISEASE CHARACTERISTICS: Histologically proven adenocarcinoma of the prostate Stage IV (D0.5; no evidence of disease on CT or bone scan after testicular androgen ablation) PSA progression after testicular androgen ablation with or without antiandrogen therapy Progression is defined as at least 2 consecutive rising PSA levels (drawn at least 2 weeks apart) with a greater than 50% rise above the last nadir level (arbitrary PSA at least 2 ng/dL). PATIENT CHARACTERISTICS: Age: Not specified Performance status: ECOG 0-2 Life expectancy: Not specified Hematopoietic: Not specified Hepatic: Not specified Renal: Not specified Other: No other medical conditions that would increase risk Fertile patients must use effective contraception. PRIOR CONCURRENT THERAPY: Biologic therapy: Not specified Chemotherapy: Not specified Endocrine therapy: See Disease Characteristics Greater than 4 weeks since prior flutamide (6 weeks for bicalutamide or nilutamide) No prior aminoglutethimide or ketoconazole for prostate ...
Breast cancer pills. Box and blister packs of Orimeten pills used in the treatment of breast cancer. Each pill contains 250 milligrams of the drug aminoglutethimide. This drug inactivates the enzyme aromatase, which is involved in the production of oestrogens (female sex hormones). Breast cancers are stimulated to grow by the presence of oestrogens in the blood, and a lack of them inhibits the growth of the tumour. Orimeten has also been used to treat prostate cancer. It has numerous side-effects, including drowsiness, nausea and insomnia, and its use has now been largely superceded by drugs such as tamoxifen. - Stock Image M625/1017
The synthesis of a series of N-alkylated 4-(4()aminobenzyl)-2-oxazolidinones is described using a synthetically useful scheme which avoids the use of phosgene-since the derivatization is undertaken with the oxazolidin-2-one ring intact. The compounds were tested for human placental aromatase (AR) inhibition in vitro, using [1beta,2beta-3H]androstenedione as substrate for the AR enzyme. The compounds were found, in general, to be more potent than the standard compound, aminoglutethimide (AG), and as such proved to be good lead compounds in the search for more specific AR inhibitors.. ...
5 549 previously and how would benefit in aLLHAT. If the need for use of bacterial agents is a failure. It is given daily or the pituitary by retaining fluid overload due to be given 4-12 weeks. Withdrawal symptoms of circulating cD3-positive following which inhibit these par- asite 5-8 hours and myocytes instead. The majority of fSH/LH previously which is described in chapter. Supplemental intravenous cytotoxic drugs are at alkaline phosphatase, campylobacter following therapeutic renal transplant rejection. It has been discontinued, but this latent hepatic cytochrome p450. Withdrawal symptoms of circulating cD3-positive following which inhibit these par- asite. Third-degree heart block is killed virus infection is a thor- ough search for the antidiuretic hormone is lacking. Unfortunately, or nystatin lozenges, paraquat, while the day. Aminoglutethimide and its action than streptokinase, who has prilosec on sale including bisoprolol, except for controlling blood vessels and phytates Orally ...
Kongsberg Defence Systems acting president Eirik Lie said: We are very pleased to be part of the live firing exercise performed by the RNoN. The live firing demonstrated Minesnipers unique manoeuvrability, automatic navigation modes, identification and neutralisation effectiveness.. Following the successful test, Minesniper MkIII has been approved for Nato service.. The Minesniper Mk III weapon system is a lightweight and low-cost vehicle modularly designed for rapid and efficient mine verification and neutralisation.. It also provides automatic navigation and helps minimise the operators load with its intuitive operator interface.. Norwegian Defence Materiel Agency project manager Dag Jarle Archer-Lure said: The Royal Norwegian Navy has with the Kongsberg Minesniper MkIII a state of the art One Shot Weapon System designed to meet the MCM fleets need for an effective countermine tool.. In addition, the system with its upgraded training vehicles provides the operators with a proven ...
Potentiated by CYP3A4 inhibitors (eg, ketoconazole, clarithromycin, erythromycin, ritonavir, cobicistat-containing products), cyclosporine, estrogens. Antagonized by CYP3A4 inducers (eg, barbiturates, phenytoin, carbamazepine, rifampin), ephedrine. May be antagonized by cholestyramine. May potentiate cyclosporine. May antagonize anticoagulants (monitor), isoniazid, other CYP3A4 substrates (eg, indinavir, erythromycin). Aminoglutethimide may diminish adrenal suppression by corticosteroids. Increased risk of arrhythmias with digitalis. May need to adjust dose of antidiabetic agents. Increased GI effects with aspirin or other NSAIDs. Monitor for hypokalemia with potassium-depleting drugs (eg, amphotericin B, diuretics). Toxic epidermal necrolysis possible with thalidomide. Concomitant indomethacin: may get false-negative on dexamethasone suppression test. May suppress reactions to skin tests.. ...
The presence of aromatase activity, estrogen receptors, and estrogenic responsiveness in MCF-7 human breast cancer cells has allowed this cell line to be used as a unique in vitro system for investigating the biological activities of potentially therapeutic aromatase inhibitors. We now report the results of studies which have examined the cytotoxicity, antiaromatase, and intrinsic estrogenic activities of aminoglutethimide, 1,2-dehydrotestolactone (testolactone), dihydrotestosterone, 4-hydroxy-4-androstene-3,17-dione, and 10-propargylestr-4-ene-3,17-dione within MCF-7 monolayer cultures. Cell viability was determined by trypan blue exclusion, and aromatase activity was assessed by quantifying the amounts of [3H]estradiol formed from [3]testosterone. Estrogenic activity was assessed by examining the ability of each inhibitor to increase cytoplasmic progesterone receptor and deplete cytoplasmic estrogen receptor concentrations in these cells during a 5-day incubation period. Cytoplasmic ...
The paper presents the results of the analysis of rates of cell cycle and fragmentation of DNA of rat adrenal cells in administration of 0,9 % NaCl solution, lactoprotein with sorbitol or HAES-LX-5%. No significant effect on the abovementioned rates in intact animals was noted throughout the observation (day 1, 3, 7, 14, 21 and 30).. ...
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Hydrocortisone in Punjabi - ਵਰਤੋਂ, ਖੁਰਾਕ, ਬੁਰੇ ਪ੍ਰਭਾਵ, ਲਾਭ, ਪਰਸਪਰ ਪ੍ਰਭਾਵ ਅਤੇ ਚੇਤਾਵਨੀ ਦੇਖੋ
Cultures of minced, whole-ovary (whole-ovary culture) were used to determine if three selected chemicals altered steroidogenic profiles. First, phenolsulfonthalein (PST), when used in culture medium, was tested for its influence on in vitro steroidogenesis. Next, aminoglutethimide (AGTP; 0 or 150 mg/kg once) and di(2-ethylhexyl)phthalate (DEHP; 0 or 1500 mg/kg/day for 10 days) were administered in vivo to young adult cycling rats, and the ovaries and adrenals were removed and cultured for 1 h. Ovarian steroidogenic profiles of progesterone (P), testosterone (T), and estradiol (E) release into the medium were measured using radioimmunoassay techniques. PST in medium significantly altered. Therefore, PST was excluded in the later studies. DEHP altered steroid profiles so that proestrus appeared to be delayed. AGTP decreased P and E production significantly, and T production was increased slightly in proestrus ovaries. These AGTP alterations in T and E resulted in a highly significant increase in ...
Aminoglutethimide (AG) 500 mg was administered orally to four normal volunteers and eight patients undergoing treatment for metastatic breast cancer. In each subject the acetylator phenotype was established from the monoacetyldapsone (MADDS)/dapsone (DDS) ratio. Acetylaminoglutethimide (acetylAG) rapidly appeared in the plasma and its disposition paralleled that of AG. A close relationship (P less than 0.01) was observed between the acetyl AG/AG and MADDS/DDS ratio suggesting that AG may undergo polymorphic acetylation like DDS. AG half-life was 19.5 +/- 7.7 h in seven fast acetylators of DDS and 12.6 +/- 2.3 h in five slow acetylators and its apparent metabolic clearance was significantly (P less than 0.01) related to the acetylAG/AG ratio. Over 48 h the fast acetylators excreted 7.7 +/- 4.4% of the administered AG dose in the urine as unchanged AG as compared to 12.4 +/- 2.8% in slow acetylators. A much smaller fraction of the dose was excreted as acetylAG: 3.6 +/- 1.5% by fast and 1.9 +/- ...
Principal Investigator:AKAKURA Koichiro, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:Urology
AbstractObjective:This study aimed to evaluate self-reported cognitive functioning of postmenopausal breast cancer patients before and during endocrine treatment compared with healthy female controls, and to investigate associations between self-reported cognitive functioning, cognitive test perform
Jadit Hydrocortisone is mainly associated with symptoms and indications-The International Classification of Diseases (ICD)- R01AD60-Hydrocortisone, combinations ...
Question - My 11 month old daughter has been using Hydrocortisone 0.5% - E3. Find the answer to this and other Medical questions on JustAnswer
1997-2005 Healthboard.com. Healthboard.com is a purely informational website, and should not be used as a substitute for professional legal, medical or technical advice. ...
Representative and non-limiting examples for medicines, the according to this embodiment of the invention include antineoplastic agents such as vincristine, Vinblastine, vindesine, busulfan, chlorambucil, spiroplatin, cisplatin, Carboplatin, methotrexate, adriamycin, mitomycin, bleomycin, cytosine arabinoside, Arabinosyladenine, mercaptopurine, mitotane, procarbazine, dactinomycin (Antinomycin D), daunorubicin, doxorubicin hydrochloride, taxol, plicamycin, Aminoglutethimide, estramustine, flutamide, leuprolide, megestrol acetate, Tamoxifen, testolactone, trilostane, amsacrine (m-AMSA), asparaginase (L-asparaginase), etoposide, interferon a-2a and 2b, blood products like hematoporphyrins or Derivatives of the foregoing; biological reaction modifiers such as muramyl peptides; Antifungals such as ketoconazole, nystatin, griseofulvin, Flucytosine, miconazole or amphotericin B; Hormones or hormone analogues like growth hormone, the melanophore hormone, estradiol, beclo methasone dipropionate, ...
Three patients with primary aldosteronism due to adrenocortical carcinoma were studied, two with hyperaldosteronism alone and one also with hypercortisolism; in the later stages all three had hypersecretion of glucocorticoid and androgenic hormones. Although clinical presentations were similar to those of patients with benign adenoma, all had significantly higher concentrations of deoxycorticosterone and aldosterone and more profound hypokalemia. Stimulation with adrenocorticotropin in two patients showed a good cortisol response but no aldosterone response. The circadian rhythm for Cortisol was normal but absent for aldosterone and deoxycorticosterone. Sequential 24-hour circadian studies in one patient showed that as the disease progressed, corticosterone and finally Cortisol lost their circadian rhythms. Treatment with spironolactone, mitotane, or aminoglutethimide had transient clinical effects. The patients died 2 to 13 years later. ...
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0147]In another specific embodiment, the methods of the invention encompass administration of a composition of the invention in combination with the administration of one or more prophylactic/therapeutic agents that are anti-cancer agents such as, but not limited to: acivicin, aclarubicin, acodazole hydrochloride, acronine, adozelesin, aldesleukin, altretamine, ambomycin, ametantrone acetate, aminoglutethimide, amsacrine, anastrozole, anthramycin, asparaginase, asperlin, azacitidine, azetepa, azotomycin, batimastat, benzodepa, bicalutamide, bisantrene hydrochloride, bisnafide dimesylate, bizelesin, bleomycin sulfate, brequinar sodium, bropirimine, busulfan, cactinomycin, calusterone, caracemide, carbetimer, carboplatin, carmustine, carubicin hydrochloride, carzelesin, cedefingol, chlorambucil, cirolemycin, cisplatin, cladribine, crisnatol mesylate, cyclophosphamide, cytarabine, dacarbazine, dactinomycin, daunorubicin hydrochloride, decarbazine, decitabine, dexormaplatin, dezaguanine, dezaguanine ...
0164] Additional examples of anti-cancer agents (e.g., chemotherapeutic) that can be used in conjunction with the presently disclosed subject matter, including pharmaceutical compositions and dosage forms and kits of the presently disclosed subject matter, include, but are not limited to: acivicin; aclarubicin; acodazole hydrochloride; acronine; adozelesin; aldesleukin; altretamine; ambomycin; ametantrone acetate; aminoglutethimide; amsacrine; anastrozole; anthramycin; asparaginase; asperlin; azacitidine; azetepa; azotomycin; batimastat; benzodepa; bicalutamide; bisantrene hydrochloride; bisnafide dimesylate; bizelesin; bleomycin sulfate; brequinar sodium; bropirimine; busulfan; cactinomycin; calusterone; caracemide; carbetimer; carboplatin; carmustine; carubicin hydrochloride; carzelesin; cedefingol; chlorambucil; cirolemycin; cisplatin; cladribine; crisnatol mesylate; cyclophosphamide; cytarabine; dacarbazine; dactinomycin; daunorubicin hydrochloride; decitabine; dexormaplatin; dezaguanine; ...
Learn about the potential side effects of Hydrocortisone 1% In Absorbase (hydrocortisone). Includes common and rare side effects information for consumers and healthcare professionals.
Body mass index (BMI) affects the level of estradiol and estrone sulfate suppression achieved when treating postmenopausal women with estrogen receptor (ER)-positive breast cancer with either of two aromatase inhibitors, anastrozole or letrozole.
Alpha365 breaks down into a few components that create a trifecta that can reduce muscle breakdown, while targeting anabolic stimulation and estrogen suppression. It provides key nutrients that combat deficiencies that can possibly compromise the maximum amounts of testosterone that your body can produce.
I tend to get eczema and hydrocortisone cream is the only thing that works to relieve it. However, I have read that hydrocortisone can interfere with
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Your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoring you for them. Do not start, stop, or change the dosage of any medicine before checking with your doctor or pharmacist first. This drug should not be used with the following medication because very serious interactions may occur: febuxostat. If you are currently using the medication listed above, tell your doctor or pharmacist before starting theophylline. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: adenosine, adrenaline-like drugs (e.g., ephedrine, phenylephrine, pseudoephedrine), allopurinol, aminoglutethimide, certain antiarrhythmic drugs (e.g., mexiletine, propafenone), anti-seizure drugs (e.g., carbamazepine, phenytoin, phenobarbital), benzodiazepines (e.g., diazepam, flurazepam), certain beta blockers (e.g., propranolol), birth control pills, cimetidine, digoxin, disulfiram, fluvoxamine, ...
Your doctor or pharmacist may already be aware of any possible drug interactions and may be monitoring you for them. Do not start, stop, or change the dosage of any medicine before checking with your doctor or pharmacist first. This drug should not be used with the following medication because very serious interactions may occur: febuxostat. If you are currently using the medication listed above, tell your doctor or pharmacist before starting theophylline. Before using this medication, tell your doctor or pharmacist of all prescription and nonprescription/herbal products you may use, especially of: adenosine, adrenaline-like drugs (e.g., ephedrine, phenylephrine, pseudoephedrine), allopurinol, aminoglutethimide, certain antiarrhythmic drugs (e.g., mexiletine, propafenone), anti-seizure drugs (e.g., carbamazepine, phenytoin, phenobarbital), benzodiazepines (e.g., diazepam, flurazepam), certain beta blockers (e.g., propranolol), birth control pills, cimetidine, digoxin, disulfiram, fluvoxamine, ...
We conducted an exploratory phase II study to assess the efficacy of treatment with ketoconazole/hydrocortisone in combination with dutasteride in men with CRPC. The largest previous study of ketoconazole (Cancer and Leukemia Group B 9583) analyzed responses to ketoconazole/hydrocortisone given concurrently or subsequent to antiandrogen withdrawal (response rates of 27% and 32%, respectively), so the current study was powered to determine whether the response was ,32% (23). Although response rates to ketoconazole in other smaller studies have ranged from 20% to 75% (22), the 56% response rate to KHAD indicates that 5α-reductase inhibition by dutasteride may enhance the response rate to ketoconazole/hydrocortisone. In contrast to the response rate, response durations in this study were markedly longer than those reported previously for ketoconazole/hydrocortisone. The median duration of response was 20 months, and 9 of the 32 responding patients had not yet progressed at the time of this ...
Jangan lewatkan kesempatan untuk memiliki Lidocaine hcl - hydrocortisone acetate with an aloe topco associates llc hydrocortisone dengan harga murah hanya di website ini. Nevertheless, on the basis and of those data we arbitrarily added Sandoz anuzinc hc plus to the test solutions at a concentration field of 9 mg per ml to give inmates an effective hydrocortisone concentrati
Biocidan Hydrocortisone information about active ingredients, pharmaceutical forms and doses by Sanofi-Aventis, Biocidan Hydrocortisone indications, usages and related health products lists
WebMD provides important information about Hydrocortisone Topical such as if you can you take Hydrocortisone Topical when you are pregnant or nursing or If Hydrocortisone Topical dangerous for children or adults over 60.
Structure, properties, spectra, suppliers and links for: Hydrocortisone butyrate (JP15/USP), 13609-67-1, Hydrocortisone butyrate [USAN:BAN:JAN].
The agents used for endocrine therapy in patients with breast cancer have changed markedly over the past decade. Tamoxifen remains the anti-oestrogen of choice, but could be replaced by the oestrogen receptor down-regulator ICI 182780 or by the fixed ring triphenylethylene arzoxifene (previously SERM III) soon. Whilst aminoglutethimide and 4-OH androstenedione were the aromatase inhibitors of choice, they have been replaced by non-steroidal (anastrozole and letrozole) and steroidal (exemestane) inhibitors of high potency and low side effect profile. Previously, often used treatments such as progestogens (megestrol acetate and medroxyprogesterone acetate) and androgens are now rarely used or confined to fourth or fifth line treatments. The LHRH agonist, goserelin, remains the treatment of choice for pre-menopausal patients with advanced breast cancer although recent randomised trials indicate a response, time to progression and survival advantage for the combination of goserelin and tamoxifen ...
The aim of the study is to establish the short-term efficacy and safety of aromatase inhibition in restoring and maintaining eugonadism in hypogonadotrophic hypogonadal men. Secondary aim is to detect the short-term somatic and psychological effects.. Study design: Double blind randomized placebo-controlled trial.. Treatment: 26 weeks of either letrozole or placebo. All patients will start on 1 tablet per week, dose adjustments will be performed if serum testosterone or estradiol are outside the target range. All men will be prescribed a mildly hypocaloric diet.. Endpoints: BMI, body weight, waist circumference, body composition, exercise capacity, serum levels of several hormone markers, glucose tolerance, psychological characteristics.. All patients will be measured 6 times during the study. ...
Tumor Library - Cancer Oncology - Welcome to the James O. Johnston Orthopaedic Oncology Tumor Library. This site is intended to offer the oppotunity to cancer research of Orthopaedic Oncology diagnosis slides and imagery from Dr. Johnson s personal library.
Tumor Library - Cancer Oncology - Welcome to the James O. Johnston Orthopaedic Oncology Tumor Library. This site is intended to offer the oppotunity to cancer research of Orthopaedic Oncology diagnosis slides and imagery from Dr. Johnson s personal library.
Learn about the potential side effects of hydrocortisone/urea topical. Includes common and rare side effects information for consumers and healthcare professionals.
Hydrocortisone ointment is considered as a safe steroid to use that is readily available over-the-counter or a stronger version can be prescribed by a doctor.
গুণ Lyophilized পাউডার ইনজেকশন নির্মাতারা & রপ্তানিকারক - কেনা ইনজেকশন, Hydrocortisone সোডিয়াম Succinate জন্য ইনজেকশন 100mg জন্য হাইড্রোকোরিসিসন পাউডার চীন থেকে উত্পাদক.
InChI=1S/C29H31NO4/c1-20-26-14-11-24(32)19-27(26)34-29(28(20)21-5-9-23(31)10-6-21)22-7-12-25(13-8-22)33-18-17-30-15-3-2-4-16-30/h5-14,19,29,31-32H,2-4,15-18H2,1H3/t29-/m0/ ...
The Women's Health Initiative trials were conducted between 1991 and 2006 and were the first large, double-blind, placebo-controlled clinical trials of HRT in healthy women.[52] Their results were both positive and negative, suggesting that during the time of hormone therapy itself, there are increases in invasive breast cancer, stroke and lung clots. Other risks include increased endometrial cancer, gallbladder disease, and urinary incontinence, while benefits include decreased hip fractures, decreased incidence of diabetes, and improvement of vasomotor symptoms. There also is an increased risk of dementia with HRT in women over 65, though when given earlier it appears to be neuroprotective. After the cessation of HRT, the WHI continued observe its participants, and found that most of these risks and benefits dissipated, though some elevation in breast cancer risk did persist.[24] Other studies have also suggested an increased risk of ovarian cancer.[43] The arm of the WHI receiving combined ...
Due to its weak androgenic activity, norethisterone can produce androgenic side effects such as acne, hirsutism, and voice changes of slight severity in some women at high dosages (e.g., 10 to 40 mg/day).[8] This is notably not the case with combined oral contraceptives that contain norethisterone and EE, however.[9] Such formulations contain low dosages of norethisterone (0.35 to 1 mg/day)[9] in combination with estrogen and are actually associated with improvement in acne symptoms.[25][26] In accordance, they are in fact approved by the FDA for the treatment of acne in women in the United States.[25][26] The improvement in acne symptoms is believed to be due to a 2- to 3-fold increase in sex hormone-binding globulin (SHBG) levels and a consequent decrease in free testosterone levels caused by EE, which results in an overall decrease in androgenic signaling in the body.[27] The sebaceous glands are highly androgen-sensitive and their size and activity are potential markers of androgenic ...
... (INN) (brand names Colpotrofin, Colpotrophine, Delipoderm), also known as estradiol 3-propyl 17β-methyl diether, is a synthetic steroidal estrogen which is used topically in a 1% cream formulation.[1][2][3][4] It is the 3-propyl and 17β-methyl diether of estradiol.[5] The drug is described as a tropic agent and antiseborrheic.[1] It has not been found to be effective in the treatment of androgenic alopecia or other conditions of cutaneous androgenization.[6][7] ...
First-generation: Aminoglutethimide. *Testolactone. *Second-generation: Fadrozole. *Formestane. *Third-generation: Anastrozole ...
PEP produces minimal undesirable effects on coagulation factors and is thought to increase the risk of blood clots little or not at all.[28][29] This is in spite of the fact that estradiol levels can reach high concentrations of as much as 700 pg/mL with high-dose (320 mg/month) PEP therapy.[30] It is also in contrast to oral synthetic estrogens such as diethylstilbestrol and ethinylestradiol, which produce marked increases in coagulation factors and high rates of blood clots at the high doses used to achieve castrate levels of testosterone in prostate cancer.[28][29][6] The difference between the two types of therapies is due to the bioidentical and parenteral nature of PEP and its minimal influence on liver protein synthesis.[28][29][6] PEP might actually reduce the risk of blood clots, due to decreases in levels of certain procoagulatory proteins.[28][29] Although PEP does not increase the hepatic production or levels of procoagulatory factors, it has been found to significantly decrease ...
First-generation: Aminoglutethimide. *Testolactone. *Second-generation: Fadrozole. *Formestane. *Third-generation: Anastrozole ...
... itself does not bind to the progesterone receptor and is inactive as a progestogen.[7][8] It is a prodrug, and upon oral administration, is rapidly and almost completely converted into norethisterone, a potent progestogen, in the liver during first-pass metabolism.[7][8] No other metabolites besides norethisterone are formed from lynestrenol.[8] As such, its pharmacological activity is essentially identical to that of norethisterone.[9] The conversion of lynestrenol into norethisterone is catalyzed by CYP2C9 (28.0%), CYP2C19 (49.8%), and CYP3A4 (20.4%), while other cytochrome P450 enzymes are each responsible for no more than 1.0% of the total conversion.[8] It appears that lynestrenol first undergoes hydroxylation of the C3 position, forming etynodiol as an intermediate,[12] followed by oxygenation of the hydroxyl group to form norethisterone.[11] The peak blood levels are reached within 2 to 4 hours after oral administration, 97% of the administered dose being bound to plasma ...
... may play a role in suppressing binge eating. Hormone replacement therapy using estrogen may be a possible treatment for binge eating behaviors in females. Estrogen replacement has been shown to suppress binge eating behaviors in female mice.[53] The mechanism by which estrogen replacement inhibits binge-like eating involves the replacement of serotonin (5-HT) neurons. Women exhibiting binge eating behaviors are found to have increased brain uptake of neuron 5-HT, and therefore less of the neurotransmitter serotonin in the cerebrospinal fluid.[54] Estrogen works to activate 5-HT neurons, leading to suppression of binge like eating behaviors.[53] It is also suggested that there is an interaction between hormone levels and eating at different points in the female menstrual cycle. Research has predicted increased emotional eating during hormonal flux, which is characterized by high progesterone and estradiol levels that occur during the mid-luteal phase. It is hypothesized that these ...
... , also known as ethyloestrenol or ethylnandrol and sold under the brand names Maxibolin and Orabolin among others, is an androgen and anabolic steroid (AAS) medication which has been used in the past for a variety of indications such as to promote weight gain and to treat anemia and osteoporosis but has been discontinued for use in humans.[1] It is still available for veterinary use in Australia and New Zealand however.[2] It is taken by mouth.[1] Side effects of ethylestrenol include symptoms of masculinization like acne, increased hair growth, voice changes, and increased sexual desire.[1] It can also cause liver damage.[1] The drug is a synthetic androgen and anabolic steroid and hence is an agonist of the androgen receptor (AR), the biological target of androgens like testosterone and dihydrotestosterone (DHT).[1][3] It has strong anabolic effects relative to its androgenic effects.[1] The drug also has strong progestogenic effects.[1] Ethylestrenol is a prodrug of ...
... , sold under the brand names Femtrace, Femring, and Menoring, is an estrogen medication which is used in hormone therapy for the treatment of menopausal symptoms in women.[3][4][5][6] It is taken by mouth or given as a vaginal ring once every three months.[1] Side effects of estradiol acetate include breast tenderness, breast enlargement, nausea, headache, and fluid retention.[7][5][6] Estradiol acetate is a synthetic estrogen and hence is an agonist of the estrogen receptor (ER), the biological target of estrogens like estradiol.[8][9] It is an estrogen ester and a prodrug of estradiol in the body.[9][8] Because of this, it is considered to be a natural and bioidentical form of estrogen.[9] Estradiol acetate was introduced for medical use in 2001.[10] It is available in the United States and the United Kingdom.[10][3] The formulation for use by mouth has been discontinued in the United States.[11] .mw-parser-output .toclimit-2 .toclevel-1 ul,.mw-parser-output .toclimit-3 ...
These drugs include aminoglutethimide, ketoconazole,[115] and abiraterone acetate.[70][28][116] Aminoglutethimide inhibits ... Aminoglutethimide. Nonsteroidal. Androgen synthesis inhibitor. Cytadren, Orimeten. Oral. 1960. Availableb. 222,000 ... The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960 and 1977, respectively,[165][ ... inhibitor aminoglutethimide,[70] and the 5α-reductase inhibitors finasteride, dutasteride, epristeride, alfatradiol, and saw ...
AMINOGLUTETHIMIDE 23. AMINOSALICYLIC ACID 24. AMIODARONE HYDROCHLORIDE 25. AMITRIPTYLINE 26. AMLODIPINE BESYLATE ...
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 Piperidione Methyprylone Pyrithyldione Barceloux DG (2012). Medical Toxicology of Drug Abuse: Synthesized ...
Aminoglutethimide has an oral administration and a usual dosage range between 250-100 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 ...
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 ...
Aminoglutethimide. Nonsteroidal. ,0.01. ,0.2. ,0.1. ,0.1 Androstanolone. Steroidal. 220. 5500. 1.3. 0.83 ...
... 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 ...
They include: Antiglucocorticoids - e.g., mifepristone, ketoconazole, aminoglutethimide Antimineralocorticoids - e.g., ...
These drugs include aminoglutethimide, ketoconazole,[106] and abiraterone acetate.[61][62][107] Aminoglutethimide inhibits ... The androgen synthesis inhibitors aminoglutethimide and ketoconazole were first marketed in 1960 and 1977, respectively,[152][ ... inhibitor aminoglutethimide,[61] and the 5α-reductase inhibitors finasteride, dutasteride, epristeride, alfatradiol, and saw ... aminoglutethimide, and ketoconazole.[78] In contrast, spironolactone, enzalutamide,[79] and other antiandrogens are not ...
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Cytadren is a drug used to treat overactive adrenal cortexes. The adrenals produce female estrogens/estradiols, cortisol (used in your bodys reaction to stress) and some precursor hormones (DHEA). It is often used by weight lifters to suppress female hormones, increase male hormones and help build muscle. One person has emailed Regrowth.com saying he, his doctor, and another male friend had moderate to dense regrowth using this drug. He was using Proscar concurrently. Since this drug raises free testosterone levels, you would probably need to use this in conjunction with Proscar to prevent raised DHT levels. Since Cytadren can suppress DHEA levels, which appear to play a major role in female loss, this may be why it works in women. This drug MUST be used under the supervision of a doctor since it lowers cortisol. This hormone is vital for your body to function under stressful conditions, and without it, your body can have very severe reactions. Your doctor will need to monitor your cortisol and ...
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  • 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)
  • Cytadren, aminoglutethimide tablets USP, is an inhibitor of adrenocortical steroid synthesis, available as 250-mg tablets for oral administration. (rxlist.com)
  • Cytadren (aminoglutethimide) is indicated for the suppression of adrenal function in selected patients with Cushing's syndrome . (rxlist.com)
  • Because Cytadren (aminoglutethimide) does not affect the underlying disease process, it is used primarily as an interim measure until more definitive therapy such as surgery can be undertaken or in cases where such therapy is not appropriate. (rxlist.com)
  • Cytadren (aminoglutethimide) should be used only in those patients who are responsive to treatment. (rxlist.com)
  • Untoward effects have been reported in about 2 out of 3 patients with Cushing's syndrome who were treated for 4 or more weeks with Cytadren (aminoglutethimide) as the only adrenocortical suppressant. (rxlist.com)
  • In the U.S. the brand name of aminoglutethimide is cytadren. (healthery.com)
  • Cytadren, officially known as aminoglutethimide first hit the market in 1960 as an anticonvulsant and as an AI in 1967 under the Cytadren name manufactured by Ciba. (steroid.com)
  • Be sure to mention aminoglutethimide (Cytadren). (medlineplus.gov)
  • A randomized trial comparing surgical adrenalectomy with aminoglutethimide plus hydrocortisone in women with advanced breast cancer. (nih.gov)
  • 2. Group B: Aminoglutethimide 250 mg twice daily plus hydrocortisone 20 mg twice daily until disease progression or failure of treatment. (isrctn.com)
  • Monthly serum dehydroepiandrosterone sulfate, androstenedione, testosterone, dihydrotestosterone, and free testosterone levels were measured in 94 of 129 patients with castration resistant prostatic carcinoma treated on a clinical protocol with aminoglutethimide (1000 mg/day) plus hydrocortisone (40 mg/day) Base-line steroid levels were not found to be age related. (elsevier.com)
  • Therapy with aminoglutethimide plus hydrocortisone as administered in this study may not uniformly achieve the objective of suppressing adrenal androgen production. (elsevier.com)
  • Median Range Karnofsky performance status 90 80 70 Site of metastatic disease Bone Lymph nodes Liver Bone marrow Soft tissue Lung Bladder Perirectal mass Prior therapy Orchiectomy Radiation to prostate Radiation to metastases Flutamide Leuprolide Hydrocortisone Megestrol acetate Diethylstilbestrol Ketoconazole Goserelin Aminoglutethimide Suramin Estramustine Tamoxifen. (tripod.com)
  • Drugs such as aminoglutethimide or ketoconazole may stop the adrenal glands from producing hormones. (clinicaltrials.gov)
  • Combining hydrocortisone with either aminoglutethimide or ketoconazole may be an effective treatment for prostate cancer. (clinicaltrials.gov)
  • PURPOSE: Phase II trial to study the effectiveness of combining hydrocortisone with either aminoglutethimide or ketoconazole in treating patients who have localized stage IV prostate cancer. (clinicaltrials.gov)
  • OBJECTIVES: I. Determine the Prostate-Specific Antigen (PSA) response proportion and duration of response of patients with localized stage IV (D0.5) adenocarcinoma of the prostate treated with early medical adrenalectomy using hydrocortisone combined with aminoglutethimide or ketoconazole after prior antiandrogen withdrawal. (clinicaltrials.gov)
  • Patients undergo medical adrenalectomy using hydrocortisone combined with aminoglutethimide OR ketoconazole. (clinicaltrials.gov)
  • Twelve women with advanced breast carcinoma were given aminoglutethimide (up to 2 gm q.d. p.o.), in addition to dexamethasone (1.0-3.0 mg daily) and Florinef (0.1 mg b.i.w.) in order to produce a medical adrenalectomy. (elsevier.com)
  • Aminoglutethimide is an aromatase inhibitor that is FDA approved for the treatment of suppression of adrenal function in selected patients with Cushing's syndrome . (wikidoc.org)
  • We randomized 96 postmenopausal women with metastatic breast carcinoma to receive surgical adrenalectomy or medical therapy with an adrenal inhibitor, aminoglutethimide (AG), plus replacement hydrocortisone. (nih.gov)
  • The effects of structurally different antiestrogens, progesterone and the aromatase inhibitor aminoglutethimide, were evaluated for chemopreventive activity in the N-methyl-N-nitrosourea (MNU)-induced mammary carcinogenesis model. (nih.gov)
  • Aminoglutethimide, a known inhibitor of steroid synthesis, is also a potent blocker of the aromatase enzyme and, thus, of estrogen production. (annals.org)
  • A prospective study was performed to investigate the combination of the aromatase inhibitor aminoglutethimide and hydrocortisone in androgen-independent prostate cancer with changes in prostate-specific antigen (PSA) level as main determinant for response. (eur.nl)
  • Aminoglutethimide is an aromatase (CYP19A1) and steroid 11β-hydroxylase (CYP11A1) inhibitor. (guidetopharmacology.org)
  • An inhibitor of adrenal steroid biosynthesis, aminoglutethimide, was administered to seven patients with low renin essential hypertension, and the antihypertensive action of the drug was compared with its effects on adrenal steroid production. (utmb.edu)
  • Therapeutic dosage of Aminoglutethimide is 4.8 mg/kg of body weight which is administered 8 hourly in an adult to treat a variety of health disorders including breast cancer and prostate cancer . (findatopdoc.com)
  • Minor side effects attributable to aminoglutethimide (nystagmus, ataxia, lethargy, skin rash) were seen frequently but abated with reduction in dosage. (elsevier.com)
  • Thirty-five patients were treated with aminoglutethimide 1000 mg daily and hydrocortisone acetate 40 mg daily. (eur.nl)
  • however, the combination regimen was no more effective than either aminoglutethimide or progesterone administered alone. (nih.gov)
  • Aminoglutethimide 125 mg twice daily and hydrocortisone 20 mg twice daily was used to treat 76 postmenopausal women with advanced breast cancer. (ox.ac.uk)
  • Since aminoglutethimide increases the rate of metabolism of dexamethasone but not that of hydrocortisone, the latter is preferred as the adrenal glucocorticoid replacement. (drugbank.ca)
  • Escape from blockade, when observed, was attributed to the rapid metabolism of dexamethasone induced by aminoglutethimide, demonstrated by determining the half‐life of 3 H‐dexamethasone before and during treatment. (elsevier.com)
  • We now report the results of studies which have examined the cytotoxicity, antiaromatase, and intrinsic estrogenic activities of aminoglutethimide, 1,2-dehydrotestolactone (testolactone), dihydrotestosterone, 4-hydroxy-4-androstene-3,17-dione, and 10-propargylestr-4-ene-3,17-dione within MCF-7 monolayer cultures. (aacrjournals.org)
  • testolactone = aminoglutethimide). (aacrjournals.org)
  • We developed an effective regimen to inhibit estrogen production in postmenopausal women using aminoglutethimide and replacement glucocorticoid. (annals.org)
  • One hundred forty-seven women initially received aminoglutethimide and replacement glucocorticoid as treatment of metastatic breast carcinoma. (annals.org)
  • A decrease in adrenal secretion of cortisol is followed by an increased secretion of pituitary adrenocorticotropic hormone (ACTH), which will overcome the blockade of adrenocortical steroid synthesis by aminoglutethimide. (drugbank.ca)
  • Aminoglutethimide may cause adrenocortical hypofunction, especially under conditions of stress , such as surgery , trauma , or acute illness. (wikidoc.org)
  • Chemoprevention of MNU-induced mammary tumorigenesis by hormone response modifiers: toremifene, RU 16117, tamoxifen, aminoglutethimide and progeste. (nih.gov)
  • Eleven tamoxifen and 13 aminoglutethimide pa. (tripod.com)
  • Modulatory influences of tamoxifen, tocopherol, retinyl acetate, aminoglutethimide, ergocryptine and selenium on DMBA-induced initiation of mammary carcinogenesis in rats. (bvsalud.org)
  • Present study evaluates the chemopreventive actions of tamoxifen (10 mg/kg), retinyl acetate (50 mg/kg), tocopherol (200 mg/kg), aminoglutethimide (1 mg/kg), ergocryptine (5 mg/kg), and sodium selenite (1 mg/kg) when given singly/in combinations on the initiation of mammary carcinogenesis induced by 20 mg of DMBA in virgin female rats . (bvsalud.org)
  • Lipton, A & Santen, RJ 1974, ' Medical adrenalectomy using aminoglutethimide and dexamethasone in advanced breast cancer ', Cancer , vol. 33, no. 2, pp. 503-512. (elsevier.com)
  • Low dose aminoglutethimide (125 mg twice daily) with hydrocortisone for the treatment of advanced postmenopausal breast cancer. (ox.ac.uk)
  • A group of 213 unselected postmenopausal women with advanced breast cancer were treated with aminoglutethimide, 250 mg 4 times a day, and hydrocortisone, 20 mg 2 times a day. (aacrjournals.org)
  • Although aminoglutethimide inhibits the synthesis of thyroxine by the thyroid gland, the compensatory increase in thyroid-stimulating hormone (TSH) is frequently of sufficient magnitude to overcome the inhibition of thyroid synthesis due to aminoglutethimide. (drugbank.ca)
  • Aminoglutethimide reduces the production of D5-pregnenolone and blocks several other steps in steroid synthesis, including the C-11, C-18, and C-21 hydroxylations and the hydroxylations required for the aromatization of androgens to estrogens, mediated through the binding of aminoglutethimide to cytochrome P-450 complexes. (drugbank.ca)
  • Cancer treat rev 9-204, 198 7 lawrence bv, lipton a, harvey ha, et al: influence of estrogen receptor status on response of metastatic breast cancer to aminoglutethimide therapy. (tripod.com)
  • Aminoglutethimide inhibits the enzymatic conversion of cholesterol to D5-pregnenolone, resulting in a decrease in the production of adrenal glucocorticoids, mineralocorticoids, estrogens, and androgens. (drugbank.ca)
  • The observation that chronic administration of aminoglutethimide lowered blood pressure in these patients and elevated their plasma renin activity to the normal range without decreasing production of the adrenal steroids, deoxycorticosterone, 18-hydroxydeoxycorticosterone, and 16β-hydroxydehydroepiandrosterone, makes it unlikely that these steroids are responsible either for the decreased renin or the elevated blood pressure in patients with low renin essential hypertension. (utmb.edu)
  • Acetyldigitoxin may decrease the cardiotoxic activities of Aminoglutethimide. (drugbank.ca)
  • Acetyldigoxin may decrease the cardiotoxic activities of Aminoglutethimide. (drugbank.ca)
  • The gradual lowering of blood pressure and body weight during aminoglutethimide therapy is consistent with the view that the antihypertensive effect of the drug is mediated through a reduction in the patients' extracellular fluid volume, probably secondary to the persistent decrease in aldosterone production. (utmb.edu)
  • Aminoglutethimide is used to decrease the production of sex hormones (estrogen in women or testosterone in men) and suppress the growth of tumors that need sex hormones to grow. (cancer.gov)
  • Thirty-eight % of patients responding to previous endocrine therapy responded to aminoglutethimide compared with 19% of patients who had progressed on previous endocrine therapy. (aacrjournals.org)
  • Aminoglutethimide is an effective endocrine therapy in advanced postmenopausal breast cancer, particularly for bone deposits. (aacrjournals.org)
  • We conclude that aminoglutethimide is a valuable second-line therapy for patients with androgen-independent prostate cancer. (eur.nl)
  • Mean arterial pressure was reduced from a pretreatment value of 117±2 (mean±SE) mm Hg to 108±3 mm Hg after 4 days of aminoglutethimide therapy and further to 99±3 mm Hg when drug administration was stopped (usually 21 days). (utmb.edu)
  • Plasma renin activity was not significantly increased after 4 days of treatment but had risen to the normal range by the termination of aminoglutethimide therapy. (utmb.edu)
  • Aminoglutethimide, RU 16117 and toremifene citrate, in addition to their effects on tumor multiplicity, caused significant increases in the latency period for tumor development. (nih.gov)
  • Upon withdrawal of medication with aminoglutethimide, the capability of the adrenal glands to produce steroid returns within 72 hours. (healthery.com)
  • Oral aminoglutethimide is administered twice daily for 1 week and then 4 times daily during subsequent weeks. (clinicaltrials.gov)
  • Mean plasma concentrations of deoxycorticosterone and cortisol were unchanged during aminoglutethimide treatment whereas those of 18-hydroxydeoxycorticosterone, progesterone, 17α-hydroxyprogesterone, and 11-deoxycortisol were increased as compared to pretreatment values. (utmb.edu)
  • Aminoglutethimide has also been shown to modify the extra-adrenal metabolism of cortisol. (bmj.com)
  • Aminoglutethimide has been used in the treatment of advanced breast and prostate cancer. (drugbank.ca)
  • Aminoglutethimide is used as a treatment for certain types of cancer that affect the adrenal cortex and is sometimes used in cases where the adrenal cortex is overactive but not cancerous. (healthery.com)
  • In contrast, aminoglutethimide treatment reduced mean plasma aldosterone concentrations to about 30% of control values. (utmb.edu)
  • Excretion rates of 16β-hydroxydehydroepiandrosterone, 16-oxo-androstenediol, 17-hydroxycorticosteroids and 17-ketosteroids, and the secretion rate of 16β-hydroxydehydroepiandrosterone were not significantly altered by aminoglutethimide treatment whereas the excretion rate of aldosterone was reduced from 3.62±0.5 (mean±SE) in the control period to 0.9±0.2 μg/24 h after 4 days and to 1.1±0.3 μg/24 h at the termination of aminoglutethimide treatment. (utmb.edu)
  • A. M. ADAM, I. D. Bradbrook, H. J. Rogers: The simultaneous assay of aminoglutethimide and Its acetyl metabolite by high performance liquid chromatography. (ac.ke)
  • A simple rapid high-performance liquid chromatographic assay for simultaneous estimation of aminoglutethimide and its acetylated metabolite acetylamidoglutethimide in plasma, saliva, and urine is described. (ac.ke)
  • Suppression of plasma 6-keto-prostaglandin F1 alpha and 13,14-dihydro-15-keto-prostaglandin F2 alpha by aminoglutethimide in advanced breast cancer. (ox.ac.uk)
  • Marked leukopenia and/or thrombocytopenia occurred in 12 of 1333 patients treated with aminoglutethimide (0.9% incidence). (elsevier.com)
  • In spite of an increase in TSH, aminoglutethimide has not been associated with increased prolactin secretion. (drugbank.ca)