Therapeutic indications
Physiological or postoperative menopause (hot flashes, sleep disorders, urogenital atrophy, mental instability, mood disorders); postmenopausal osteoporosis (prevention).
Composition:
Estradiol
Application:
Endocrine Therapy,Estrogenic,Replenishing Estrogen Deficiency,Sexual Hormones And Modulators Of The Genital System
It is used in the treatment of:
Atrophic Urethritis, Vaginal Atrophy, Hypogonadism, Hypoestrogenism, Menopause And Perimenopause, Osteoporosis, Primary Ovarian Insufficiency
Pharmacodynamics
The active substance of the drug Neofollin — synthetic 17ß-estradiol — is chemically and biologically identical to endogenous human estradiol produced in the body of women by the ovaries, starting from the first menstruation and up to menopause. Estrogens form a complex with specific receptors found in cells of various target organs – in the uterus, vagina, urethra, mammary gland, liver, hypothalamus, pituitary gland. The receptor-ligand complex interacts with estrogen-effector elements of the genome and specific intracellular proteins that induce the synthesis of mRNA, proteins and the release of cytokines and growth factors.
It has a feminizing effect on the body. It stimulates the development of the uterus, fallopian tubes, vagina, stroma and ducts of the mammary glands, pigmentation in the area of the nipples and genitals, the formation of secondary sexual characteristics of the female type, the growth and closure of the epiphyses of long tubular bones. Promotes timely rejection of the endometrium and regular bleeding, causes endometrial hyperplasia in high concentrations, suppresses lactation, inhibits bone resorption, stimulates the synthesis of a number of transport proteins (thyroxine-binding globulin; transcortin; transferrin; SHBG), fibrinogen. It has a procoagulant effect, increases the synthesis of vitamin-K-dependent blood clotting factors (II, VII, IX, X) in the liver, reduces the concentration of antithrombin III.
Increases blood concentrations of thyroxine, iron, copper. It has an anti-atherosclerotic effect, increases the content of HDL, reduces LDL and cholesterol, increases the concentration of triglycerides. Modulates the sensitivity of receptors to progesterone and sympathetic regulation of smooth muscle tone, stimulates the transfer of intravascular fluid into tissues and causes compensatory sodium and water retention. In large doses, it prevents the degradation of endogenous catecholamines by competing for active catechol-O-methyltransferase receptors.
After menopause, only a small amount of estradiol is formed in the body (from estrone found in the liver and in adipose tissue). A decrease in the content of estradiol produced in the ovaries is accompanied in many women by vasomotor and thermoregulatory instability (flushes of blood to the skin of the face), sleep disorders, as well as progressive atrophy of the mucous membrane of the genitourinary system.
Due to estrogen deficiency, osteoporosis develops (mainly of the spine). After ingestion, a larger amount of estradiol is metabolized in the lumen (microflora) and intestinal wall, as well as in the liver before entering the bloodstream (which leads to non-physiologically high concentrations of estrone in plasma, and with prolonged therapy — to the accumulation of estrone and estrone sulfate). The consequences of the accumulation of these metabolites in the body for a long time have not yet been clarified. It is known that the oral use of estrogens causes an increase in protein synthesis (including renin), which leads to an increase in blood pressure.
Causes moderate proliferation of the endometrium and improves the trophism of the genitourinary system. Estradiol plays an important role in bone metabolism and thus prevents the development of osteoporosis. Acting on the hypothalamic-pituitary system, eliminates vegetative-vascular and psychoemotional disorders.
Pharmacological group
- Estrogens, progestogens; their homologues and antagonists
- Antitumor hormonal agents and hormone antagonists
Interaction
Estradiol metabolism is accelerated when used simultaneously with barbiturates, tranquilizers (anxiolytics), narcotic analgesics, drugs for anesthesia, some antiepileptic drugs (carbamazepine, phenytoin), inducers of microsomal liver enzymes; herbal preparations containing St. John’s wort.
The concentration of estradiol in the blood also decreases with the simultaneous use of phenylbutazone, some antibiotics and antiviral drugs (ampicillin, rifampicin, rifabutin, nevirapine, efavirenz).
Ritonavir and nelfinavir, also known as strong HIV protease inhibitors, when combined with sex hormones, on the contrary, exhibit inducing properties.
The effect of estradiol is enhanced against the background of taking folic acid and thyroid hormone preparations.
With transdermal administration, it is possible to avoid the effect of primary passage through the liver, thus, the effect of HRT drugs with transdermal application of estrogens, perhaps to a lesser extent than with oral administration, depends on the action of inducers of microsomal liver enzymes.
In clinical practice, increased estrogen metabolism can lead to a weakening of the effect and changes in the nature of uterine bleeding.
Estradiol increases the effectiveness of hypolipidemic agents, weakens the effect of male sex hormone preparations, hypoglycemic, diuretic, hypotensive drugs and anticoagulants.
Barbiturates, tranquilizers, narcotic analgesics, anesthetic and some antiepileptic drugs (carbamazepine, phenytoin), inducers of microsomal liver enzymes accelerate the metabolism of estradiol, reduce the effect of the drug.
The plasma concentration decreases with the simultaneous use of phenylbutazone and some antibiotics (ampicillin, rifampicin), which is associated with a change in the microflora.
Folic acid and thyroid preparations enhance the effect of estradiol.
Estradiol increases the effectiveness of hypolipidemic agents.
It weakens the effects of male sex hormone preparations, hypoglycemic, diuretic, hypotensive drugs and anticoagulants.
Reduces glucose tolerance, so it may be necessary to adjust the dose of hypoglycemic agents.
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