• Estriol Vaginal Cream

Overview Of Estradiol Vaginal Cream

Dosage Power Of Estradiol Vaginal Cream
0.2 mg/mL 30 mL Topi-Click PERL Dispenser
0.3 mg/mL 30 mL Topi-Click PERL Dispenser
0.4 mg/mL 30 mL Topi-Click PERL Dispenser
0.5 mg/mL 30 mL Topi-Click PERL Dispenser
0.625 mg/mL 30 mL Topi-Click PERL Dispenser
1 mg/mL 30 mL Topi-Click PERL Dispenser
1.25 mg/mL 30 mL Topi-Click PERL Dispenser
2.5 mg/mL 30 mL Topi-Click PERL Dispenser
5 mg/mL 30 mL Topi-Click PERL Dispenser
Generic Details
Estradiol is the principal intracellular human estrogen and is substantially more active than its metabolites, estrone and estriol, at the cellular level. Estradiol can be obtained from natural sources or prepared synthetically. There is no evidence that ‘natural’ estrogens are more or less efficacious or safe than ‘synthetic’ estrogens. Due to almost complete first-pass metabolism, estradiol must be given in a micronized oral dosage form to ensure therapeutic effect. Esterification of estradiol to estradiol cypionate or valerate increases the parenteral duration of action of estradiol to allow for parenteral intramuscular administration. Estradiol is primarily used to prevent osteoporosis and relieve vasomotor and genitourinary symptoms associated with menopause (natural or surgical), for postmenopausal osteoporosis prevention, and is also used to treat female hypogonadism and other abnormalities of female gonadotropin dysfunction. Various estrogen products have been marketed in the U.S. since 1938. Estradiol is available in many dosage forms, including oral tablets, transdermal systems, topical emulsions, topical gels, topical sprays, vaginal creams, vaginal rings, and parenteral depot injections. Vaginal therapies are preferred in postmenopausal women with exclusive genitourinary symptoms, due to lower systemic absorption/exposure with most of these dosage forms. Many estradiol products have been FDA-approved since the 1990’s, in accordance with the FDA’s guidance to provide efficacious low-dose estrogen therapies in alternate drug delivery systems.
The primary source of estrogens in premenopausal women is the ovary, which normally secretes 0.07 to 0.5 mg of estradiol daily, depending on the phase of the menstrual cycle. Once estrogens enter the cells of responsive tissues (e.g., female organs, breasts, hypothalamus, pituitary), they increase the rate of synthesis of DNA, RNA, and some proteins. The secretion of gonadotropin-releasing hormone by the hypothalamus is reduced during estrogen administration, causing reduction in follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary. Exogenous estrogens elicit all of the actions of endogenous estrogens. Estrogens are responsible for the growth and development of female sex organs and the maintenance of sex characteristics including growth of axillary and pubic hair and shaping of body contours and skeleton. At the cellular level, estrogens increase cervical secretions, cause proliferation of the endometrium, and increase uterine tone. Paradoxically, prolonged administration of estrogen can shrink the endometrium. During the preovulatory or nonovulatory phase of the menstrual cycle, withdrawal of estrogen can initiate menstruation; in the ovulatory phase, the decrease in progesterone secretion is the more significant factor causing menstruation. In post-menopausal use, amenorrhea occurs in most women within several months of oral estrogen use.
Estrogens have a weak anabolic effect and also can affect bone calcium deposition and accelerate epiphysial closure. Estrogens appear to prevent osteoporosis associated with the onset of menopause. Estrogens generally have a favorable effect on blood lipids, reducing LDL- and increasing HDL-cholesterol concentrations on average, by 15%. Serum triglycerides increase with estrogen administration. Estrogens increase the rate of synthesis of many proteins, including thyroid binding globulin and several clotting factors. Estrogens reduce levels of antithrombin III, and increase platelet aggregation. Estrogens also enhance sodium and fluid retention.
Unopposed estrogen has been associated with increased risk of endometrial cancer in menopausal women with an intact uterus; concomitant progestin therapy reduces, but does not eliminate, this risk. However, combination hormone replacement therapy (HRT) may add additional health risks for some women, as evidenced by the HERS trials the Women’s Health Initiative study and other investigations. In particular, the Women’s Health Initiative (WHI) study reported an increased risk of myocardial infarction, stroke, dementia, invasive breast cancer, and venous thromboembolism in patients taking combination HRT and an increased risk of stroke, dementia, and venous thromboembolism in patients taking estrogen only HRT; an increased risk of invasive breast cancer was not evident in women taking estrogen only. Because of these findings, patients should be prescribed estrogen HRT or estrogen-progestin HRT for the shortest duration consistent with the treatment goals. Estrogen HRT with or without a progestin is not indicated and should not be used to prevent coronary artery disease or other cardiovascular disease. The risks and benefits of HRT must be determined for a woman individually.
In men with advanced prostate cancer, estrogens exert their effect by inhibition of the hypothalamic-pituitary axis through negative feedback. This results in decreased secretion of luteinizing hormone (LH). Decreased testosterone production from the Leydig cells in the testes occurs, which may decrease tumor growth and lower prostate specific antigen (PSA) levels. Improvement in bone metastasis may also occur. In the past, high-dose estrogen therapy was also used in selected men and postmenopausal women with inoperable, progressive breast cancer. Since the development of selective estrogen receptor modifiers (SERMs), high-dose estrogen therapy for the palliative treatment of breast cancer is rarely used today.
Clinical Pharmacokinetics
Estradiol products are administered orally, intramuscularly, vaginally, transdermally, and topically. The pharmacokinetics of estradiol differ with the formulation used for delivery and the route of administration. Following systemic absorption, estradiol is rapidly transformed by the liver to estrone and estriol, the major circulating forms in the serum, by 17-beta-hydroxysteroid dehydrogenase. The estrogens are widely distributed and are strongly protein-bound, primarily to albumin and sex hormone-binding globulin (SHBG). Circulating estrogens exist in a dynamic equilibrium of metabolic interconversions. These transformations take place mainly in the liver. Estradiol is converted reversibly to estrone, and both can be converted to estriol, which is the major urinary metabolite. Estrogens are metabolized partially by CYP3A4 in the liver. Estrogens also undergo enterohepatic recirculation via sulfate and glucuronide conjugation in the liver, biliary secretion of conjugates into the intestine, and hydrolysis in the gut followed by reabsorption. In postmenopausal women, a significant proportion of the circulating estrogens exist as sulfate conjugates, especially estrone sulfate, which serves as a circulating reservoir for the formation of more active estrogens. Estradiol, estrone, and estriol undergo glucuronide and sulfate conjugation to a variety of minor metabolites which are excreted primarily in the urine. In vitro and in vivo studies indicate that estrogens are partially metabolized by CYP3A4. Interactions with drugs that are inhibitors or inducers of CYP3A4 are possible.

Route-Specific Pharmacokinetics:

Vaginal Route: In general, estradiol is well absorbed through the vaginal mucous membranes. The vaginal dosage applied determines systemic hormone exposure; as a result, systemic as well as local tissue effects may occur. However, the systemic effects differ with specific vaginal products and many products are not acceptable for treating systemic or vasomotor symptoms or preventing osteoporosis.

Special Populations

Hepatic Impairment: Specific pharmacokinetic data are not available. Estrogens are extensively metabolized in the liver and may be poorly metabolized in women with impaired liver function. Do not use estrogens in patients with severe hepatic disease of any type.

Renal Impairment: Specific pharmacokinetic data for patients with renal impairment are not available for most estradiol products. In postmenopausal women with end stage renal disease (ESRD) receiving maintenance hemodialysis, total estradiol serum levels are higher than in normal subjects at baseline and following oral doses of estradiol. Therefore, conventional transdermal estradiol doses used in individuals with normal renal function may be excessive for postmenopausal women with ESRD receiving maintenance hemodialysis. Dosages should be chosen in accordance with clinical response and tolerance.

Pediatrics: Specific pharmacokinetic studies are not available for most products in adolescents or children, though systemic and transdermal administration is common for selected patients. Recommended initial doses of estrogen therapy in this population are usually one-eighth to one-tenth the doses used for adult replacement, and vary depending on the formulation used.

Estrogens are contraindicated during pregnancy. There is no known approved indication for the use of estrogens during pregnancy. There appears to be little or no increased risk of birth defects in children born to women who have used estrogens and progestins from oral contraceptives inadvertently during early pregnancy. Estradiol and other estrogens freely cross the placenta to the fetus. Increased risk of a wide variety of fetal abnormalities, including modified development of sexual organs, cardiovascular anomalies and limb defects, have been reported following the continued use of estrogens in pregnant women. In any patient in whom pregnancy is suspected, pregnancy should be ruled out before continuing estrogen use. In select instances estradiol has been used off-label as an adjuvant to clomiphene treatment of infertility, or in donor oocyte program procedures in assisted reproduction technology (ART) under the direction of ART specialists; however, treatment is discontinued when pregnancy ensues.
Anastrozole is classified as FDA pregnancy risk category X. It is contraindicated for use in women who are pregnant or may become pregnant. Anastrozole may cause fetal harm when administered to pregnant women and offers no clinical benefit when administered to premenopausal women with breast cancer. Animal studies indicate that anastrozole increases pregnancy loss, both pre- and postimplantation. It crosses the placenta and causes fetal harm, including delayed fetal development, but there has been no evidence of teratogenicity. There have been no adequate studies in pregnant women, and anastrozole is only approved for the treatment of postmenopausal women, and should generally not be used in females of childbearing potential. If pregnancy occurs, however, while the patient is receiving anastrozole, she should be warned about the possible risk to the fetus and possible loss of pregnancy.
Caution should be used if a breast-feeding mother is receiving estradiol for hormone replacement. Estrogen administration to nursing women is generally avoided during lactation as estrogens have been shown to decrease the quantity and quality of the breast milk. Detectable amounts of estrogens have been identified in the milk of mothers receiving estradiol and other estrogens. Estrogens are not approved by the FDA for the treatment of postpartum breast engorgement.
Interactions: NOTE: In vitro and in vivo studies indicate that estrogens are partially metabolized by CYP3A4. Interactions with drugs that are inhibitors or inducers of CYP3A4 are possible.
Bromocriptine is used to restore ovulation and ovarian function in amenorrheic women. Estrogens can cause amenorrhea and, therefore, counteract the desired effects of bromocriptine. Concurrent use is not recommended.
Estrogens can increase calcium absorption. In general, the interaction between calcium salts and estrogen is beneficial and is used to therapeutic advantage in postmenopausal women who have osteoporosis. However, this interaction may not be advantageous in patients predisposed to hypercalcemia or nephrolithiasis.
There have been reports indicating the estrogens and/or progestins in oral contraceptives or non-oral combinatio contraceptives may inhibit the metabolism of cyclosporine. Delayed cyclosporine clearance and elevated cyclosporine concentrations can lead to seizures, nephrotoxicity and/or hepatotoxicity. Additionally, estrogens are metabolized by CYP3A4; cyclosporine may increase plasma concentrations of estrogens and cause estrogen-related side effects such as nausea and breast tenderness. If oral contraceptives, non-oral combination contraceptives, estrogens, or progestins are initiated or discontinued, the patient’s cyclosporine concentrations should be monitored closely. Additionally, patients should be monitored for estrogenic side effects if these drugs are used concomitantly.
Estrogens have been associated with elevated serum concentrations of corticosteroid binding globulin (CBG), leading to increased total circulating corticosteroids, although the free concentrations of these hormones may be lower; the clinical significance is not known.strogens have reportedly potentiated the anti-inflammatory effects of hydrocortisone. Patients should be monitored for increased corticosteroid effects if estrogens, oral contraceptives, or non-oral combination contraceptives are used with hydrocortisone.
Estrogens have been associated with elevated serum concentrations of corticosteroid binding globulin (CBG), leading to increased total circulating corticosteroids, although the free concentrations of these hormones may be lower; the clinical significance is not known. Ethinyl estradiol has reportedly delayed the clearance of prednisolone. Patients should be monitored for increased corticosteroid effects if estrogens, oral contraceptives, or non-oral combination contraceptives are used with prednisolone.
Concomitant use of dantrolene and estrogens may increase the risk of developing hepatotoxicity. While a definite drug interaction with dapsone and estrogen therapy has not yet been established, caution should be observed if the two drugs are to be given concomitantly. Hepatotoxicity has occurred more often, for example, in women over 35 years of age receiving concomitant estrogen therapy.
Estrogens interact with growth hormone (somatropin and somatrem) during pre-puberty by accelerating epiphysial maturation.
Estrogens increase the hepatic synthesis of prothrombin and factors VII, VIII, IX, and X and decrease antithrombin III; estrogens also increase norepinephrine-induced platelet aggregability. A positive relationship between hormone replacement therapy and the risk of thromboembolic disease has been demonstrated in the Women’s Health Initiative Trials (WHI trials). The US FDA has suggested class labeling of HRT products in accordance with this data. HRT products are generally contraindicated in patients with a current history of stroke, cerebrovascular disease, coronary artery disease, coronary thrombosis, thrombophlebitis (including pulmonary embolism and DVT), thromboembolic disease or valvular heart disease with complications. Concurrent use of HRT in female patients receiving anticoagulation therapy with warfarin is generally avoided. If concurrent use of an estrogen or estrogen-progestin containing HRT cannot be avoided in a pateint taking warfarin, carefully monitor for signs and symptoms of thromboembolic complications. If such occur, the estrogen or estrogen-progestin containing HRT regimen should be discontinued. HRT is not expected to significantly alter the INR or to affect the metabolism of warfarin. Dosage adjustment of warfarin should be based on the prothrombin time or INR value.
The use of estrogens, including oral contraceptives, with tamoxifen is controversial and is generally considered contraindicated in most, but not all, circumstances.
Raloxifene exerts its effects by blocking estrogen receptors. Since raloxifene and estrogens are pharmacological opposites, it would be illogical to coadminister them.
The oxidative metabolism of tricyclic antidepressants may be decreased by estrogens. Increased antidepressant serum concentrations may occur.
Cimetidine has been reported to reduce the hepatic clearance of estradiol; this interaction may partially explain the association between cimetidine therapy and gynecomastia.
There is a possibility of contraceptive failure when bosentan is coadministered with products containing estrogens and/or progestins. In addition, bosentan is teratogenic and is contraindicated during pregnancy. Effective contraception through additional forms of contraception must be practiced.
An alternative method or an additional method of contraception should be utilized during modafinil therapy and continued for one month after modafinil discontinuation. Similarly, a decrease in estrogen concentrations, and thus efficacy, may occur if modafinil is used in patients taking estrogens. Dosage adjustments may be necessary.
Phenytoin: pregnancy has been reported during therapy with estrogens, oral contraceptives, non-oral combination contraceptives, or progestins in patients receiving phenytoin concurrently.
An alternate or additional form of contraception should be considered in patients prescribed concomitant therapy with enzyme-inducing anticonvulsants, or higher-dose hormonal regimens may be indicated where acceptable or applicable. Epileptic women taking both anticonvulsants (AEDs) and Oral Contraceptives (OCs) may be at higher risk of folate deficiency secondary to additive effects on folate metabolism; if oral contraceptive failure occurs, the additive effects could potentially heighten the risk of neural tube defects in pregnancy. The alternative or additional contraceptive agent may need to be continued for one month after discontinuation of the interacting medication.
Estrogens and progestins are both susceptible to drug interactions with hepatic enzyme inducing drugs such as the carbamazepine family; barbiturates; rifampin, rifabutin, or rifapentine. Concurrent administration of said drugs with estrogens, oral contraceptives, non-oral combination contraceptives, or progestins may increase the hormone’s elimination.
Concomitant use of griseofulvin and oral contraceptives has been reported to reduce the efficacy of the oral contraceptive and cause breakthrough bleeding. An alternate or additional form of contraception should be used during concomitant treatment and should be continued for 1 month after griseofulvin discontinuation.
Topiramate can increase the clearance of ethinyl estradiol and compromise the efficacy of estrogens or progestins used for contraception or hormone replacement therapies. Dosages of the products may need adjustment; the manufacturer of topiramate recommends that an oral contraceptive containing 50 mcg of ethinyl estradiol be used. Different or additional forms of contraception may also be needed.
Based on very limited data, it appears felbamate can accelerate the clearance of the estrogen component of some oral contraceptives.Additionally, patients taking non-oral combination contraceptives or estrogens or progestins for hormone replacement therapy may also experience reduced clinical efficacy; dosage adjustments may be necessary.
Nevirapine may decrease plasma concentrations of oral contraceptives, non-oral combination contraceptives, and other hormones, including estrogens and progestins.
Grapefruit juice has been reported to decrease estrogen metabolism.
Patients receiving antidiabetic agents should be closely monitored for signs indicating loss of diabetic control or hypoglycemia when therapy with any of these agents is instituted or discontinued.
Dose adjustments may be needed in some hypothyroid patients receiving exogenous thyroid treatments who initiate estrogen therapy.
It appears that the simultaneous administration of estrogens and mineral oil, as a laxative, may decrease the absorption of the estrogens, resulting in lower estrogen plasma concentrations.
Estrogens could interfere competitively with the pharmacologic action of the aromatase inhibitors. Estrogen therapy is not recommended during aromatase inhibitor treatment, due to opposing pharmacologic actions.
Estrogens and combined hormonal and oral contraceptives may counteract the effectiveness of ursodeoxycholic acid, ursodiol.
Theoretically, the soy isoflavones may compete with or have additive effects with, drugs that have estrogenic activity or which selectively modulate estrogen receptors. Soy isoflavones should be used with caution in patients taking estrogens, since the effects of combining soy isoflavone dietary supplements with estrogens are not clear.
Bexarotene: it is recommended that two reliable forms of contraception be used simultaneously, unless abstinence is the chosen method, during oral bexarotene therapy (see Bexarotene Contraindications). Because of the potential interaction with hormonal contraceptives it is strongly recommended that one of the forms of contraception be non-hormonal.
Nefazodone: estrogenic-related side effects (e.g., nausea, breast tenderness) may potentially increase when nefazodone is coadministered with either estrogens or combined hormonal contraceptives, including oral contraceptives.
Application of sunscreen 10 minutes prior to the application of estradiol topical emulsion (i.e., Estrasorb) increases the exposure to estradiol by approximately 35%. Application of sunscreen 25 minutes after the application of estradiol topical emulsion (Estrasorb) increases the exposure to estradiol by approximately 15%.
Application of sunscreen 10 minutes prior to the application of estradiol topical emulsion (i.e., Estrasorb) increases the exposure to estradiol by approximately 35%. Application of sunscreen 25 minutes after the application of estradiol topical emulsion (Estrasorb) increases the exposure to estradiol by approximately 15%.
The efficacy of estrogens and/or progestins may be reduced when coadministered with aprepitant, fosaprepitant.
St. John’s wort, Hypericum perforatum appears to interact with estrogens and oral contraceptives. One report noted intermenstrual bleeding after the concurrent use of St. John’s wort in 8 premenstrual women who had been on oral contraceptives for long durations of time.
Erythromycin, amiodarone, systemic azole antifungals (fluconazole, itraconazole, ketoconazole, miconazole, posaconazole, and voriconazole), clarithromycin, conivaptan, danazol, dalfopristin,dasatinib, delavirdinine, diltiazem, duloxetine, fluvoxamine, imatinib, mifepristone, RU-486, propoxyphene, telithromycin, troleandomycin, verapamil, zafirlukast, zileuton: these compounds may increase plasma concentrations of estrogens and cause estrogen-related side effects.
Interactions between anti-retroviral protease inhibitors and estrogens or progestins are complex. It may be prudent to use caution and careful monitoring during coadministration of fosamprenavir or other retrovirals with estrogens or progestins.
Estradiol Vaginal Cream Side Effects & Reactions
Numbness; tingling; cold feeling; or weakness in your hand or wrist; problems with your fingers while gripping; hot flashes; joint pain or stiffness; depression; mood changes; sleep problems (insomnia); cough; sore throat; thinning hair; mild nausea; vomiting; back pain; bone pain
Hot flashes (11—36%) were the most commonly reported adverse reaction associated with anastrozole during clinical trials. Other commonly reported adverse reactions during controlled trials included vaginal irritation (i.e., dryness) (1—2%), vaginal bleeding (1—5%), vaginal discharge (4%), vaginitis (4%), and vulvovaginitis (6%). Vaginal bleeding occurs primarily during the first few weeks after changing from existing hormonal therapy to treatment with anastrozole. If bleeding persists, further evaluation should be considered.
Gastrointestinal/digestive adverse reactions occurred in up to one-third of patients receiving anastrozole during clinical trials. These reactions included abdominal pain (6—9%), anorexia (5—8%), constipation (7—9%), diarrhea (7—9%), dyspepsia (7%), nausea (11—20%), vomiting (8—13%), and xerostomia or dry mouth (4—6%). Weight gain was reported in 2—9% of patients taking anastrozole, but occurred less frequently than with megestrol (12%). Additionally, 2—5% of anastrozole recipients also experienced weight loss and elevated hepatic enzymes, with or without jaundice (< 0.01%). Elevations in hepatic enzymes, primarily serum gamma glutamyl transferase (GGT), were observed in patients with liver metastases receiving anastrozole or megestrol. These changes were likely due to the progression of liver disease in these patients, but other contributing factors cannot be ruled out. Hepatitis and hyperbilirubinemia have been reported during post-marketing use of anastrozole with an estimated incidence of >= 0.1% to < 1%. Due to the voluntary nature of post-market reports, neither a definitive incidence nor causal relationship can be established. Nervous system adverse reactions associated with the use of anastrozole during clinical trials include anxiety (2—6%), confusion (2—5%), depression (2—13%), dizziness (5—8%), drowsiness (2—5%), headache (7—18%), hypertonia (3%), insomnia (2—10%), lethargy (1%), malaise (2—5%), nervousness (2—5%), and paresthesias (5—7%). Administration of anastrozole has been associated with the development of thromboembolic events. Thromboembolism was reported in 2—4% of patients treated with anastrozole during clinical trials. The incidence of anastrozole-associated thrombosis was less than that reported with tamoxifen (2—6%) or megestrol (5%). Specific cases included angina (2.3—11.6%), cerebrovascular accident (stroke) specifically cerebral ischemia and cerebral infarct (2%), myocardial infarction (0.9—1.2%), myocardial ischemia (< 4%), pulmonary embolism (< 4%), retinal thrombosis (< 4%), and thrombo-phlebitis (2—5%). In the ATAC trial, women with pre-existing ischemic cardiac disease had a 17% incidence of ischemic cardiac events. In this patient population, angina occurred in 11.6% and myocardial infarction in 0.9%. Musculoskeletal reactions are some of the more common adverse events experienced by recipients of anastrozole therapy (36%). During clinical trials, patients receiving anastrozole reported symptoms including arthralgia (2—15%), arthritis (17%), arthrosis (7%), asthenia (13—19%), back pain (10—12%), bone pain (6—11%), breast pain (2—8%), carpal tunnel syndrome (2.5%), chest pain (unspecified) (5—7%), fatigue (19%), myalgia (2—6%), neck pain (2—5%), and pelvic pain (5%). Additionally, episodes of trigger finger have been reported during post-marketing use by 0.1—1% of anastrozole recipients. Due to the voluntary nature of post-market reports, neither a definitive incidence nor causal relationship with anastrozole can be established. Osteoporosis has been reported as an adverse event to anastrozole, but causality has not been determined. Data from clinical trials indicate that musculoskeletal events and bone fractures are significantly more common in patients receiving anastrozole (36% and 10%, respectively) versus tamoxifen (29% and 7%, respectively). The anatomical sites with the greatest increase in fracture incidence were wrist fractures (2%), spine fractures (1%), and hip fractures (1%). Of note, long-term data indicate that fracture rates were not different after anastrozole or tamoxifen discontinuation (median follow-up 100 months). Similarly, in the combined analysis of the ABCSG trial 8 and the ARNO 95 trials, after a median follow-up of 36 months, the odds of bone fractures in patients taking anastrozole were significantly increased (2% for anastrozole vs. 1% for tamoxifen, OR 2.14, 95% CI 1.14—4.17, P=0.015).11 Health care professionals are advised to consider bone mineral density testing prior to and during anastrozole therapy in those patients at risk of developing osteoporosis. During the ATAC trial, more patients receiving anastrozole were reported to have hypercholesterolemia compared to those receiving tamoxifen (9% vs. 3.5%, respectively). Other anastrozole-associated adverse events affecting the cardiovascular system included edema (7—11%), hypertension (2—13%), peripheral edema (5—10%), and peripheral vasodilation (25—36%). Dermatologic adverse events have been associated with anastrozole therapy. During clinical trials, patients treated with anastrozole experiences symptoms including alopecia (2—5%), diaphoresis (1—5%), pruritus (2—5%), and rash (unspecified) (6—11%). Additionally, rare cases (< 1 in 10,000 patients or < 0.01%) of serious anastrozole-induced skin reactions (e.g., skin lesion, skin ulcer, and skin blister) have also occurred. During post-market use, anaphylaxis, angioedema, erythema multiforme, Stevens-Johnson syndrome and urticaria were reported by anastrozole recipients. Due to the voluntary nature of post-market reports, neither a frequency nor a definitive causal relationship to anastrozole can be established. During clinical trials, the incidence of infections in patients receiving treatment with anastrozole was 2—9%. Reports identified the specific infection sites as bronchitis (2—5%), influenza (2—7%), pharyngitis (6—14%), sinusitis (2—6%), and urinary tract infections (2—8%). Symptoms reported by anastrozole recipients and potentially related to an infection included cough (7—11%), dyspnea (8—11%), fever (2—5%), leukorrhea (2—3%), and rhinitis (2—5%). Hematologic and lymphatic adverse events reported by recipients of anastrozole during clinical trials included anemia (2—5%), leukopenia (2—5%), and lymphedema (10%). There are currently no studies in pregnant humans; however, use of anastrozole in rats and rabbits has resulted in pregnancy failure, increased fetal abortion, and signs of delayed fetal development or teratogenesis. In both rats and rabbits, increased pregnancy loss was described as an increase in pre- and post-implantation loss, increased resorption, and decreased number of live fetuses. Additionally, adverse fetal effects associated with anastrozole included incomplete ossification and decreased fetal body weight. Use of anastrozole is contraindicated in pregnant women. Other adverse events associated with the use of anastrozole during clinical trials include accidental injury (2—10%), cataracts (6%), development of a cyst or neoplasm (5%), and tumor flare (3%). Hypercalcemia (with or without an increase in parathyroid hormone) has been reported in post-marketing use. Due to the voluntary nature of post-market reports, neither a definitive incidence nor causal relationship with anastrozole can be established. This list may not include all possible adverse reactions or side effects. Call your health care provider immediately if you are experiencing any signs of an allergic reaction: skin rash, itching or hives, swelling of the face, lips, or tongue, blue tint to skin, chest tightness, pain, difficulty breathing, wheezing, dizziness, red, a swollen painful area/areas on the leg.
How To Store
Store this medication in its original container at 68°F to 77°F (20°C to 25°C) and away from heat, moisture and light. Keep all medicine out of the reach of children. Throw away any unused medicine after the beyond use date. Do not flush unused medications or pour down a sink or drain.
Areas We Serve
You can order Estradiol Vaginal Cream from MediLab’s compounding pharmacy in the following Florida regions:

North Florida South Florida
Jacksonville Miami West Palm Beach Weston
Pensacola Hialeah Pompano Beach Delray Beach
Tallahassee Fort Lauderdale Davie Homestead
Ocala Port St. Lucie Miami Beach Tamarac
Gainesville Pembroke Pines Plantation Sarasota
Fort Walton Beach Hollywood Sunrise Wellington
Panama City Miramar Boca Raton Jupiter
Palm Coast Coral Springs Deerfield Beach Margate
Dunnellon Miami Gardens Boynton Beach Coconut Creek
Naples Lauderhill Broward
Spring hill Orlando
References [Click to open/close]
  • Axiron (testosterone) topical solution, package insert. Indianapolis, IN: Lilly USA, LLC; 2011 Dec.
  • Androderm (testosterone transdermal system) package insert. Corona, CA: Watson Phar.ma, Inc.; 2014 Jun.