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Acute renal failure, hypoglycemia, the economic crisis and the crisis of pituitary cells, Brownstroke thyroid storm, in a coma. [3]

Parathyroid gland and loss of species was active in emergency situations created by medical emergency called Brown the patient's condition, the cells cannot control, surgical risk, particularly after mastectomy blood pressure stable (brutal ko Ka te ー en MI nn attenuation and calcium shall reimburse each gradually normalize), folded and the cardiovascular system. After emergency surgery the patient's symptoms, particularly considering the new efforts to stabilize and more effective drugs and choose the appropriate protocol instead of surgery or emergency situations, it remains controversial. Klinefelter Syndrome is usually random. Old mother has a slightly increased risk. The State will not be parents. [4] a total of 47 chromosomes related mechanisms within the chromosome x or y chromosome instead of the usual 46 alternatives, at least one will be added. [5 KS was diagnosed with a genetic test called chromosomes. [3]

Over time that can help treat. [6], physiotherapy, speech and language therapy, counseling, and education so that matches can be helpful. Use the low level of male hormone replacement may be caused by them. Breast augmentation can be removed. About half of the diseases of the male reproductive system, assistive technology, can be expensive to have a child carries risks. [7] the conditions close to normal. [6 of androgens (Greek prefix meaning male flowers) broad concept, also known as testoid hormones or any natural or synthetic compound, usually stimulate/development and maintenance of masculine characteristics in the skull of receptors hormones that control hormones. [1 of male secondary sexual characteristics, with the support of the development of sexual organs. For the first time in 1936, were discovered by male hormones. The precursor of all estrogens on steroids and anabolic hormones. Rogen, known as the main male sex hormone. -JI Hi do ro testosterone (DHT), the nn nn nn o te ro do Suu Kyi is unknown, but men are equally important. DHT-induced penile and testicular and prostate cancer later in life of the embryo differentiation, male pattern baldness, DHT prostate growth and helps in the sebaceous glands. Estrogen is menstruation, mating season a group of compounds called reproduction (you can see the difference in pronunciation). They are the female hormone. Natural estrogens, synthetic steroid hormones [Jn source]. Ἶ Ρ τ Ο ο σ ς Greek name (oistros) means 「about magic or inspiration 」 passion and desire [1] and refers to the generation of 「about maker 」.

All vertebrates [2], there are some insects, estrogen synthesis. [3] showed that the hormone estrogen is a species of vertebrates and insects is a long-term development.

Estrogen contraceptives, estrogen replacement therapy after menopause women andhormone replacement therapy for women.

All steroid hormones like estrogen can easily spread across the cell membrane. Cells are the manifestations of it there are a lot more genes control activates the estrogen receptor.[4] currently, the estrogen g protein coupled vessel GPR30. [5] breast cancer is mammary gland development and cancer. [1] breast cancer symptoms, breast, breasts, skin sagging,can contain articles about the liquid that comes from changes in the nipple or skin red,scaly. [2] at the remote transmission of the disease in patients with bone pain, lymph nodes, swelling, shortness of breath, or you can embed it in a yellow skin. [3]

Contains risk factors for breast cancer: women, obesity, lack of exercise, menopausal,ionizing radiation, first menstruation, hormone replacement therapy or play once in a whilethe alcoholic drink. 2 [4] case is about 5-10% have inherited the genes BRCA1 and BRCA2genes, they are parents, including among other things. Breast cancer infiltration of the milk ducts and bile ducts are typically designed with the back of the field. From developing countries from developing countries, known as pancreatic cancer pancreatic cancerpenetration. [2] in addition, 18 different species are more breast cancer. Some have developed cancer.

This choice is sufficient

Hormone antagonists and modulators :

Agents with antiestrogenic activity in professional sports often use to brake conversionof testosterone in female sex hormones (estrogens), as well as to increase muscle mass.

Very often the use of antièstrogenov combined with taking anabolic steroids. This is due to the metabolism of endogenous and exogenous anabolic steroid hormones in the body. The appearance of the body due to income from outside of exogenous steroids and (or) accumulation due to reduced functional ability of liver excessively high concentrations of endogenous anabolic steroid hormones, especially testosterone, causing an excess of testosterone does not have time to fully be metabolized through physiological pathways. In this case of the anabolic steroid hormones running through workaround metabolism — the aromatization of testosterone converts to estrogen via the aromatase enzyme. It is the conversion of testosterone to brake that increases the protein synthesis and thus contributes to hypertrophy of skeletal muscles, and also to reduce the content in the body of estrogen and shortening the duration of their validity, unscrupulous athletes in pursuit of a result can use agents with antiestrogenic activity.

Classification

Anti estrogens depending on mechanisms of influence can be divided into three classes:

selective (selective) estrogen receptor modulators (Tamoxifen and Clomiphene, toremifen) is applied after the course

aromatase inhibitors (Anastrozole, Letrozole)-apply for a course

other substances of antiestrogen.

There is another classification of antièstrogennyh drugs (Baum, 2001). According toher, they also can be divided into three main classes:

selective oestrogen receptors modifiers (SERM);

"clean" or steroid antiestrogens;

the aromatase inhibitors, non-steroidal derivatives: aminoglûtetimida (glutetimid,rogletimid) and derivatives of imidazole and triazole derivatives (letrozole, anastrozole);steroid-formestan, exemestane.

In our view, such a classification does not take into account reversibility andirreversibility of the effects of drugs on estrogenic receptors and do not sufficiently take into account the generation mechanism of action of drugs and at whatever steroidreceptors or nesteroidna structures of the drug product. Therefore, further describes the classes and groups of antièstrogennyh substances will be based on theclassification in the literature distributed much wider and much more justified.

All the classes are prohibited substances antièstrogennyh (list of prohibited substancesand methods, 2008). Taking these drugs is accompanied by near by side effects, the development of numerous pathological conditions and can even be fatal.

Selective (selective) estrogen receptor modulators 

The principal representatives of the election (selective) ekstrogenov-IMRÈ receptormodulators, or SERMS (Engl. Selective Estrogen-Receptor Modulators) are tamoxifen(synonyms-tamifen, Nolvadex, Nolvadex Forte, bilem, intam, jenoksifen, cemid,valodeks, cyto-zonium seu zitazonium), raloxifene (Evista and ®, "Eli Lilly", United Kingdom), toremifen (Fareston ®, "Orion Pharma", Finland), as well as the more recent,yet little explored analogues of tamoxifen (idoksifen, keoksifen, droloksifen). All thesepreparations of IMRÈ are structurally non-steroidal substances. K. IMRÈ class refers to a steroid's fulvestrant (fazlodeks).

Tamoxifen 

The first class of an anti estrogen, tamoxifen, IMRÈ was synthesized by SoIe in 1971, and started using it as a blocker of estrogen receptors. In the last decade createdvysokoselektivnyj a clean steroid estrogen-receptor blocker fulvestrant, which is currently undergoing phase III clinical trials.

The most commonly used in pharmacology medication class IMRÈ is tamoxifen, a competitive inhibitor of estrogen receptor of peripheral. Currently, point of view,demonstrating that tamoxifen does not have èstrogenopodobnym effects, rebutted,because it has been proven that the drug has estrogenic activity and is the ratio of antagonistic activity of 45/55.

Tamoxifen is a derivative of trifenilètilena; chemical structure of 1-[p-(2-dimethylamino)-ètoksi]-phenyl-TRANS-1, 2-di-phenyl-1-Boutin, in the form of citrate.Release form: tablets 10, 20, and 40 mg. Tamoxifen is well absorbed in the stomach;the first peak of its concentration in the blood plasma is registered through 1-6 h after the introduction, and the second is a 24-44 h Circulating drug levels in the blood for a long time — up to a maximum of 170 h.

Excretion of tamoxifen was protracted and two-phase nature. The initial half-life of the drug is 24-53 h and final

Side effects of tamoxifen 

The most widely known among the members of the class of drug has IMRÈ and a wide range of side effects. Although, it should be noted that a negative symptoms are observed after administration of all drugs of this class. Basic biological effects of tamoxifen are identified in endocrine organs. The drug has shown neither the androgen nor the anti androgen nogo, nor the gestagen nogo effect. In men when taken in high doses can reduce the weight of the testes, seminal vesicles and prostate, which further leads to infertility and impotence. After repeated administration of tamoxifen is the liver. The increase in body mass index end up lagging behind such athletes not taking such drugs. Tamoxifen may cause a decrease in blood glucose levels and blood in the blood, mainly through a number of lymphocyte cells, small but often dose-dependent decrease in the activity of alkaline phosphatase. The drug inhibits the antioxidant function of the liver. Using high doses causes stasis of bile (cholestasis) and education biliary stones. His repeated intake also leads to hyperplasia of the lymphoid tissue of the spleen and lymph nodes, distorting the natural response of the body's immune system. Tamoxifen and negatively affects bone system, significantly increasing the risk of osteoporosis and fractures.

Although tamoxifen reduces cholesterol in the blood, its positive effect on the rate of reduction of cardiac pathology is not shown. On the contrary, there are! observation of increasing the incidence of coronary heart disease, myocardial infarction and pulmonary artery thromboembolism. The women athletes taking tamoxifen in high doses may prevent implantation of the egg in the uterine wall. The use of anti èstrogena during early pregnancy frequently results in its termination by halting the growth of the uterus, called estradiol, and deformities in the fetus (teratogenic effects). With long-term use, tamoxifen has been the intensive growth of tumor cells. The 4 (!) times more likely than those not taking the drug, is the development of liver cancer and endometrium due to significant and prolonged increase in steroid hormones.

Therapeutic effect of tamoxifen and synthesized the drug later, second-generation selective estrogen receptor modulators: raloxifene is detected in high levels of estradiol against the Suppression of secreting prolactin. The primary effect of these medications sent directly to target the tumor cell, in which the antiestrogens block estrogen bindingto their specific receptors. In addition to the desired effect on tumor cells, antiestrogens class IMRÈ lead to inhibition of tumor growth through other mechanisms, acting onthe hypothalamus-gipofizarnuû system and the ovaries.

Raloxifene

Raloxifene, like tamoxifen, usually used to treat common and advanced breast cancer,as well as prevention of metastasis. Less frequently used in cancer chemotherapy the body of the uterus and breast cancer in men.

Compared with tamoxifen, raloxifene had fewer than a pronounced effect on the demineralization of the bones, to a lesser extent, affects the thickness of the endometrium. Raloxifene is manufactured in the form of tablets, coated tablets containing 60 mg of the active substance; It is recommended for use in a dose of 60 mg-d "1 before or during a meal. As the agonist effect on fabrics, and as the antagonist is reproductive. Increases globulin concentration between hormones (including sex, and thyroxin, corticosteroids), with simultaneous increase of their total content in the blood without increasing the level of free fraction. Approximately 60% of the drug is rapidly absorbed after administration inwards. Before entering the bloodstream raloxifene intensively metabolised education. Absolute bio availability of only 2%. Time until the average maximum concentration in plasma and bio availability depend on of raloxifene in systemic blood and transformation of glucuronid drug and its metabolites in the intestine and liver. Metabolism occurs mainly in the liver, so it is a direct violation of a contraindication for use of the drug. Raloxifene is widely distributed in the tissues of the body, with its distribution of the dose does not depend. A half-life of 27.7 hours most of the drug and its metabolites excreted within 5 days and is found mainly in the feces and urine (6 per cent).

Side effects of raloxifene

Tamoxifen and raloxifene helps to reduce the level of total cholesterol and LDL cholesterol without affecting HDL cholesterol. However, according to the results of a large-scale placebo-control

To reduce the side effects of tamoxifen and raloxifene in Finland has developed a new drugtoremifen (Fareston ®, "Orion Pharma"), which, according to experimental and clinical data,a number of advantages. First, as a result of the stabilization of the structural formula of tamoxifen by attaching chlorine atom is most stable molecular structure of drugs to metabolic changes, including hyper oxidation in the body. Secondly, the on cogenic andgepatotoksičeskij effects of toremifen are much rarer. At the same time, long-term use of toremifen documented cases of malignant tumors and their rapid progression. A number ofpeople who took the drug, there is a certain loss of sensitivity.

On the chemical structure of toremifen is a nonsteroidal derivative trifenilètilena-(Z) -4-chloro-1, 1-diphenyl-2-[4-[2-(di-methylamino) ètoksi]-phenyl)-1buten, available in the form of citrate. Like tamoxifen, toremifen binds to receptors of estrogen and antièstrogennyj (or èstrogen effect depending on the duration of treatment, the Nosological, sex of the patient, target organ and other features. Toremifen competitively binds to receptors to oestrogens and inhibits estrogen-mediated stimulation of DNA synthesis and replication of cells. The experimental models shows that the effect of the use of the drug in high doses, mainly mediated by anti èstrogennym action. However, it cannot be excluded that other mechanisms (changes in gene expression, induction of apoptosis factors secretion, impact on cell cycle kinetics) may also play a role in the therapeutic effects of the drug. Under the influence of Toremifene is moderately expressed reduced levels of cholesterol LDL cholesterol and total blood serum, although this fact has no effect on the incidence of complications from the circulatory system.

Release form: tablets of 20 and 60 mg. Toremifen rapidly absorbed after administration inwards. The maximum concentration in plasma achieved after an average of 3 hours (from2 up to 5 hours). Dynamics concentration in plasma is described curve.The half-life in the first phase (distribution) is 4 hours (from 2 to 12) of the hours in the second phase (elimination), the length of which is equal to an average of 5 days (from 2 up to 10 h), 99.5% of toremifen associated with blood plasma proteins, mainly albuminami. Pharmacokinetics of the drug when administered in doses of 680 mg-11-d "1 has a linearnature. Equilibrium concentration of toremifen when taken in the recommended dose (60mg/d-1), on average, 0.9 (0.6-1.3) g-d "1.

Toremifen actively metabolized in the body. The main metabolite is dimetiltoremifen with an average 11 half day (4-20) LPG. More than 99.9% metabolite associated with blood plasma proteins, which defines three other less significant metabolite, the predominant one  The body of the drug appears mostly in the form of metabolites through the DIGESTIVE TRACT, and 10% is excreted in the urine. Metabolism of Toremifeneis carried out with the participation of cytochrome p-450-dependent enzyme complex by N-demethylation.

Side effects of toremifen 

Side effects of toremifen than with tamoxifen are less pronounced and prolonged and primarily mediated by hormonal mechanism of action of the drug. In clinical studies the most common side effects are hot flashes (over 20 per cent), sweating (14), nausea (8), andlovokruženie (4), peripheral edema (3%), and vomiting. Occasionally there may be fatigue,headaches and back pain, weight gain, insomnia. the appearance of the symptoms, as well as the emergence of paresis, the tremor in the extremities, fatigue, anorexia is important forsports pharmacology.

The clinical use of toremifen in Oncology, as well as a similar action of tamoxifen athletesfocus shifts of hormones in the serum, but their variations are expressed less than a substantial (at 4 x) reduce the level of follicle stimulating hormone (FSH). When receiving Toremifene also increases estradiol, but this is about 70% of women who took the drug, is accompanied by the simultaneous increase of progesterone.

It should be noted that the absence of reliable changes of the investigated hormones due to large individual variation, although quite expressive dynamics on progesterone andprolactin, FSH evident (table 3.8).

Comparative analysis of effect of Toremifene and tamoxifen for hormone

Like other drugs of the class IMRÈ, toremifen invokes a breach of the liver, as evidenced bythe increase in the liver transaminaz in the serum. At the beginning of the reception of toremifen may develop hyper calcemia with the violation in a subsequent bone density