|2||$39.00||Up to $3.12|
|3||$39.00||Up to $9.36|
|4||$39.00||Up to $18.72|
|5||$39.00||Up to $31.20|
at 24 hoursreleasing nominal 50 micrograms, 3.8 mg estradiol (equivalent to 3.9 mg of estradiol hemihydrate) containing 12.5 cm 2 patch.
Loss of ovarian function accompanied by decreased estrogen production leads to certain menopausal syndrome with vasomotor-vegetative and organic symptoms. Hormone replacement therapy aims to eliminate these complaints. Estradiol is the most potent in all physiological estrogens, showing the highest affinity to the estrogen receptor.
Like other steroid hormones, estrogen acts by regulating the transcription of a limited number of genes in estrogene-sensitive target organs, especially the uterus, hypothalamus, pituitary, vagina, urethra, breast, bones (osteoclasts). Following diffusion of the cell membrane, estradiol binds to the estrogen receptor with high affinity. Following activation of the estradiol ligand, the hormone receptor complex is translocated into the core. This complex binds to DNA sequences (hormone response elements) that accelerate transcription of neighboring genes. The number of proteins produced by Estrogen is not exactly known, but is estimated to be between 50-100.
Following menopause, the production of estradiol in women is reduced significantly. The remaining estradiol is mainly synthesized by the aromatization of androstenedione from precursors produced in the adrenal cortex and, less frequently, testosterone via the aromatase enzyme, respectively, as estrone and estradiol. Estron is converted to estradiol by means of 17-hydroxysteroid-dehydrogenase enzyme. Both enzymes are found in fat and muscle tissues and liver. The ratio of estradiol / estrone was greater than 1 in premenopausal women and about 0.2 in postmenopausal women.
Climacteric complaints can be improved by an estrogen replacement therapy with an average of 25-100 μg of estradiol per day via the transdermal route.
Estrogen doses required for the recovery of menopausal complaints show a dose-dependent stimulating effect on endometrium proliferation and mitosis regardless of the route of administration. Estrogen monotherapy increases the incidence of endometrial hyperplasia and thus increases the risk of endometrial cancer. For women who have not had hysterectomy, a 10-14 day cyclic progestagen treatment is recommended for the prevention of endometrial hyperplasia.
Following the dermal application of Climara, estradiol is well absorbed from the skin. An average absorption rate of 100 orpg per day was calculated for Climara.
During the weekly administration of Climara, regular estradiol and estrone serum level profiles are obtained in the desired range. As a result of repeated weekly applications, no accumulation of these substances was observed. After the application of 12.5 cm², approx. The mean serum levels of estradiol in the constant equilibrium, found at 35 pg / ml, indicate that the absolute height of the estradiol serum level profile is directly proportional to the patch area.
The metabolites of estradiol are mainly excreted in the form of sulphate and glucuronides.
Hormone replacement therapy (HRT) in the treatment of signs and symptoms of estrogen deficiency due to natural menopause or castration.
Prevention of postmenopausal osteoporosis.
Do not start HRT in the presence of the following conditions. If any of these conditions occur during HRT use, the treatment should be discontinued immediately:
• Pregnancy and lactation
• Unspecified abnormal genital bleeding
• Breast cancer or suspicion
• Pre-malignant conditions or suspicion of malignant disease or suspicion of sex hormones
• Liver tumor presence (benign or malignant)
• Acute arterial thromboembolism (eg. myocardial infarction, stroke)
• Active deep vein thrombosis, thromboembolic disorders, or a history documented for them.
• Hypersensitivity to any of the Climara patch components.
Warnings / precautions
An individual benefit / risk analysis should be performed before starting or continuing HRT if the following conditions / risk factors are present or deteriorating.
• Venous thromboembolism
Both randomized and epidemiological studies suggest that HRT may cause a relative risk increase for the development of venous thromboembolism (VTE; deep vein thrombosis or pulmonary embolism). While HRT treatment is recommended for women at risk for venous thromboembolism, the benefit / risk ratio should be carefully evaluated.
The risk factors generally defined for VTE are family history (VTE that occurs at a relatively early age, may indicate a genetic displacement) and obesity. The risk of VTE increases with age. There is no opinion about the possible role of varicose veins in VTE.
The risk of VTE may be increased temporarily by prolonged immobilization, major elective or posttraumatic surgical intervention or major trauma. Depending on the condition of the event and the duration of immobilization, HRT may be temporarily interrupted.
Treatment should be stopped immediately if there is any suspicion or suspicion of a thrombotic event.
Apr 3, 2022
Great shipping time, great product and great service! Thank you so much!
Recommended to buy: Yes