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Anastrozole Capsule (Each)
0.1 mg0.15 mg0.4 mg0.75 mg Anastrozole Tablet (Each)0.125 mg0.25 mg0.5 mgAnastrozole Tablet (Each) †1 mg
† commercial product
Bupropion HCl
The aminoketone class of oral antidepressants includes bupropion. It has no relation to other recognized antidepressants and is not a tricyclic antidepressant. Bupropion has been well tolerated in individuals using tricyclic antidepressants for orthostatic hypotension; nonetheless, it has a higher risk of producing seizures than other antidepressants. Bupropion is also indicated for use as an aide to smoking cessation, and is used off-label for addiction to smokeless tobacco. The drug has been shown to help people with COPD quit smoking when combined with behavior modification. Bupropion is also used off-label for multiple neurological/psychological uses, including ADHD and neuropathic pain. Bupropion hydrochloride was originally approved by the FDA in December 1985 but was removed from marketing for several years due to concern over drug-induced seizures. It was reintroduced in July 1989 as an antidepressant (i.e., Wellbutrin), and later in a sustained-release formulation (i.e., Wellbutrin SR). Another sustained-release oral dosage form, Zyban, was approved for the management of smoking cessation in May 1997. Zyban received an additional indication for use in combination with nicotine transdermal systems (NTS) for treating the symptoms of smoking cessation in 1999. A controlled-release formulation (Wellbutrin XL) was approved in August 2003 as a once-daily formulation for major depression in adults. In June 2006, Wellbutrin XL was FDA-approved for prevention of major depressive episodes in patients with a history of seasonal affective disorder (SAD). Wellbutrin XL is the first prescription product approved for patients with a history of SAD. In April 2008, a once-daily formulation of bupropion hydrobromide (Aplenzin) was approved by the FDA for depression, and in August 2012 Aplenzin was approved for the prevention of seasonal major depressive episodes in patients with SAD. Aplenzin differs from all previously marketed formulations which are the hydrochloride salt of bupropion.
Phentermine HCl
Phentermine is an oral sympathomimetic amine used as an adjunct for short-term (e.g., 8—12 weeks) treatment of exogenous obesity. The pharmacologic effects of phentermine are similar to amphetamines. Phentermine resin complex was approved by the FDA in 1959, but is no longer marketed in the US. Phentermine hydrochloride was FDA approved in 1973. In the mid-90s, there was renewed interest in phentermine in combination with another anorectic, fenfluramine, for the treatment of obesity and substance abuse, however, little scientific data support this practice. On July 8, 1997, the FDA issued a ‘Dear Health Care Professional’ letter warning physicians about the development of valvular heart disease and pulmonary hypertension in women receiving the combination of fenfluramine and phentermine; fenfluramine was subsequently withdrawn from the US market in fall of 1997. Use of phentermine with other anorectic agents for obesity has not been evaluated and is not recommended. In May 2011, the FDA approved a phentermine hydrochloride orally disintegrating tablet (Suprenza) for the treatment of exogenous obesity.
Topiramate
Topiramate is an oral antiepileptic drug (AED) used for partial-onset, generalized primary tonic-clonic seizures, and as an adjunct therapy in Lennox-Gastaut syndrome. It is derived from the naturally occurring monosaccharide D-fructose and is structurally different from other AEDs. Unlike other AEDs, topiramate appears to block the spread of seizures rather than raise the seizure threshold. Topiramate possesses more than one mechanism of action, which may explain why it can be effective in patients with various seizures that are refractory to other agents. Topiramate continues to be studied as both add-on therapy and monotherapy in various refractory epilepsies in children and adults, including infantile spasms associated with West syndrome. It is also used for migraine prophylaxis in adult and pediatric patients. There is some evidence of a role for topiramate treatment ‘off-label’ for eating disorders such as binge-eating disorder, for tics due to Tourette’s syndrome or other chronic tic disorders, or for substance abuse disorders such as alcohol dependence.
Naltrexone HCl
Naltrexone is an oral opiate receptor antagonist. It is derived from thebaine and is very similar in structure to oxymorphone. Like parenteral naloxone, naltrexone is a pure antagonist (i.e., agonist actions are not apparent), but naltrexone has better oral bioavailability and a much longer duration of action than naloxone. Clinically, naltrexone is used to help maintain an opiate-free state in patients who are known opiate abusers. Naltrexone is of greatest benefit in patients who take the drug as part of a comprehensive occupational rehabilitative program or other compliance-enhancing program. Unlike methadone or LAAM, naltrexone does not reinforce medication compliance and will not prevent withdrawal. Naltrexone has been used as part of rapid and ultrarapid detoxification techniques. These techniques are designed to precipitate withdrawal by administering opiate antagonists. These approaches are thought to minimize the risk of relapse and allow quick initiation of naltrexone maintenance and psychosocial supports. Ultrarapid detoxification is performed under general anesthesia or heavy sedation. While numerous studies have been performed examining the role of these detoxification techniques, a standardized procedure including appropriate medications and dose, safety, and effectiveness have not been determined in relation to standard detoxification techniques. Naltrexone supports abstinence, prevents relapse, and decreases alcohol consumption in patients treated for alcoholism. Naltrexone is not beneficial in all alcoholic patients and may only provide a small improvement in outcome when added to conventional therapy. The FDA approved naltrexone in 1984 for the adjuvant treatment of patients dependent on opiate agonists. FDA approval of naltrexone for the treatment of alcoholism was granted January 1995. The FDA approved Vivitrol, a once-monthly intramuscular naltrexone formulation used to help control cravings for alcohol in April 2006, and then in October 2010, the FDA approved Vivitrol for the prevention of relapse to opioid dependence after opioid detoxification.
Methylcobalamin
Methylcobalamin, or vitamin B12, is a B-vitamin. It is found in a variety of foods such as fish, shellfish, meats, and dairy products. Although methylcobalamin and vitamin B12 are terms used interchangeably, vitamin B12 is also available as hydroxocobalamin, a less commonly prescribed drug product (see Hydroxocobalamin monograph), and methylcobalamin. Methylcobalamin is used to treat pernicious anemia and vitamin B12 deficiency, as well as to determine vitamin B12 absorption in the Schilling test. Vitamin B12 is an essential vitamin found in the foods such as meat, eggs, and dairy products. Deficiency in healthy individuals is rare; the elderly, strict vegetarians (i.e., vegan), and patients with malabsorption problems are more likely to become deficient. If vitamin B12 deficiency is not treated with a vitamin B12 supplement, then anemia, intestinal problems, and irreversible nerve damage may occur.
The most chemically complex of all the vitamins, methylcobalamin is a water-soluble, organometallic compound with a trivalent cobalt ion bound inside a corrin ring which, although similar to the porphyrin ring found in heme, chlorophyll, and cytochrome, has two of the pyrrole rings directly bonded. The central metal ion is Co (cobalt). Methylcobalamin cannot be made by plants or by animals; the only type of organisms that have the enzymes required for the synthesis of methylcobalamin are bacteria and archaea. Higher plants do not concentrate methylcobalamin from the soil, making them a poor source of the substance as compared with animal tissues.
Caffeine
Caffeine is a naturally occurring xanthine derivative used as a CNS and respiratory stimulant, or as a mild diuretic. Other xanthine derivatives include the bronchodilator theophylline and theobromine, a compound found in cocoa and chocolate. Caffeine is found in many beverages and soft drinks. Caffeine is often combined with analgesics or with ergot alkaloids for the treatment of migraine and other types of headache. Caffeine is also sold without a prescription in products marketed to treat drowsiness, or in products for mild water-weight gain. Caffeine was first approved by the FDA for use in a drug product in 1938. Clinically, it is used both orally and parenterally as a respiratory stimulant in neonates with apnea of prematurity. Caffeine reduces the frequency of apneic episodes by 30—50% within 24 hours of administration. Caffeine is preferred over theophylline in neonates due to the ease of once per day administration, reliable oral absorption, and a wide therapeutic window. A commercial preparation of parenteral caffeine, Cafcit®, was FDA approved for the treatment of apnea of prematurity in October 1999, after years of availability only under orphan drug status (e.g., Neocaf). The FDA has continued the orphan drug status of the approved prescription formulation.
Oxytocin
Endogenous oxytocin is a hormone secreted by the supraoptic and paraventricular nuclei of the hypothalamus and stored in the posterior pituitary. It stimulates contraction of uterine smooth muscle during gestation and causes milk ejection after milk has been produced in the breast. Oxytocin has been associated with mating, parental, and social behaviors. Oxytocin is released during intercourse in both men and women, which has led to the belief that it is involved in sexual bonding. There is speculation that in addition to facilitating lactation and the birthing process, the hormone facilitates the emotional bond between mother and child. Oxytocin has also been studied in autism and have some sort of relation to the social and developmental impairments associated with the disease. Clinically, oxytocin is used most often to induce and strengthen labor and control postpartum bleeding. Intranasal preparations of oxytocin, used to stimulate postpartum milk ejection, are no longer manufactured in the U.S. Oxytocin was approved by the FDA in 1962.
Metformin
Metformin is an oral biguanide antidiabetic agent similar to phenformin, a drug that was withdrawn from US marketing in 1977 due to the development of lactic acidosis. The risk for this adverse reaction is considerably lower with metformin, however. The actions of metformin differ from, yet complement, those of the sulfonylureas and other antidiabetic therapies. Compared to glyburide in type 2 diabetes, metformin was found to achieve similar glycemic control. although it lead to a higher incidence of digestive complaints. Metformin has been found useful in the treatment of polycystic ovary syndrome (PCOS); it lowers serum androgens and restores normal menstrual cycles and ovulation, and may improve pregnancy rates. Additionally, limited data indicate that it may delay puberty onset in females with precocious puberty and delay menarche onset in females with early-normal onset of puberty. The use of metformin versus intensive lifestyle modification in patients with impaired glucose tolerance has been investigated, and while both reduce the incidence of diabetes, lifestyle intervention has the greater effect. Although lifestyle intervention is highly effective, most patients fail lifestyle modifications when used alone within the first year of diagnosis. Therefore, a joint consensus algorithm for the treatment of type 2 diabetes mellitus, developed by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes, suggests that the combination of metformin with lifestyle interventions should be initiated at the time of diagnosis. Metformin was chosen as the initial drug therapy based on its efficacy, safety, and cost. Additionally, in a follow-up study to the UKPDS, researchers found that after 10-years of resuming typical care, patients originally randomized to metformin therapy had a 33% relative reduction (RR 0.67, 95% CI 0.51—0.89; p=0.005) in the risk of myocardial infarction and a 27% relative reduction (RR 0.73, 95% CI 0.59—0.89; p=0.002) in the risk of death from any cause as compared to patients originally randomized to conventional therapy; it should be noted that these reductions in cardiovascular risks persisted even though HbA1c concentrations were similar in the 2 groups after 1 year of follow-up. Metformin was introduced in Europe in the 1950’s but was not approved by the FDA until December 1994. It is approved for type 2 diabetes either as monotherapy or in combination with sulfonylureas, alpha-glucosidase inhibitors, or insulin. The regular-release tablets were approved for use in children >= 10 years in January 2001. An oral solution (Riomet) was approved in September 2003. Three extended-release formulations have been approved, Glucophage XR in October 2000, Fortamet in April 2004, and Glumetza in June 2005, each with a unique drug delivery system (see Pharmacokinetics section). The extended-release formulations provide similar glycemic control compared to regular-release metformin, but have the advantage of once-daily administration. Another advantage is a claim of decreased adverse events, specifically gastrointestinal-related adverse events (i.e., flatulence, diarrhea); however, larger trials comparing regular-release to extended-release metformin are needed to confirm these claims as current trial results are conflicting.
Anastrozole inhibits aromatase, the enzyme that catalyzes the final step in estrogen production. Anastrozole is an oral, competitive, non-steroidal inhibitor of aromatase and is less likely to exhibit agonist or antagonist steroidal properties.[6] The formation of adrenal corticosteroids or aldosterone is not affected by anastrozole; only serum estradiol concentrations are affected by anastrozole. In postmenopausal women, the principal source of circulating estrogens is from the conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by aromatase in peripheral tissues. Inhibition of aromatase may result in a more complete estrogen block than surgical ablation. Extraglandular sites are more amenable to aromatase inhibition by anastrozole than are premenopausal ovaries. Inhibiting the biosynthesis of estrogens is one way to deprive the tumor of estrogens and to restrict tumor growth. Estradiol plasma concentrations decrease about 80% from the baseline with continued dosing of anastrozole.[7] Aromatase inhibitors might also inhibit estrogen production at the tumor cell. However, tumor production of estradiol may be insignificant because aromatase activity appears to be low.[8] Anastrozole has little or no effect on CNS, autonomic, or neuromuscular function.
Contraindications & Precautions
Your health care provider needs to know if you have any of these conditions: heart disease, circulation problems, a history of stroke or blood clot, severe liver disease, high cholesterol, osteoporosis, or low bone mineral density. Anastrozole may not work as well if you take it together with tamoxifen or an estrogen medication (such as hormone replacement therapy, estrogen creams, or birth control pills, injections, implants, skin patches, and vaginal rings). You may need to keep taking anastrozole for up to 5 years.
In general, anastrozole should not be used in premenopausal females; anastrozole may not be able to inhibit the formation of estrogen from the ovaries and therefore is not expected to be effective, although it has been used successfully in the treatment of uterine leiomyomata in premenopausal women.[10] Hormone replacement therapy (i.e., exogenous estrogens) should not be administered concurrently with anastrozole.
Hepatic cirrhosis due to alcohol abuse reduces apparent oral clearance of anastrozole by about 30%. Anastrozole should be used with caution in patients with mild to moderate hepatic impairment, and patients should be closely monitored for adverse effects. However, no dosage adjustments are recommended for patients with hepatic disease because plasma anastrozole concentrations remain within the range of those seen in normal patients. No studies have been conducted in patients with severe hepatic impairment.
Consideration should be given to monitoring patients for signs and symptoms of osteoporosis, including decreased bone mineral density (BMD), during treatment with anastrozole, especially in patients with pre-existing osteoporosis, osteopenia, or risk factors for the development of osteoporosis. After a median follow-up of 68 months in the ATAC trial, the odds of bone fractures in patients taking anastrozole were significantly increased compared to patients taking tamoxifen (11% for anastrozole vs. 7.7% for tamoxifen, OR 1.49, 95% CI 1.25—1.77, P < 0.0001).[2] 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] Anastrozole should be used with caution in women with pre-existing ischemic cardiac disease. In the ATAC trial, women with pre-existing ischemic heart disease had an increased incidence of ischemic cardiovascular events (17% of patients receiving anastrozole versus 4% of patients in the overall study population). Safety and efficacy of anastrozole in children have not been established. Anastrozole is classified as FDA pregnancy risk category X.[12] 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. It is not known whether anastrozole is excreted into breast milk. Because many drugs are excreted in human milk and because of the tumorigenicity shown for anastrozole in animal studies, or the potential for serious adverse reactions in nursing infants, a decision should be made whether to discontinue breast-feeding or to discontinue the drug, taking into account the importance of the drug to the mother. Anastrozole is contraindicated in pre-menopausal females, so use during lactation would not be expected.[12] This list may not include all possible contraindications.
NOTE: High concentrations of anastrozole inhibited metabolic reactions catalyzed by cytochromes P450 (CYP) 1A2, 2C8/9, and 3A4. Anastrozole did not inhibit CYP2A6 or the polymorphic CYP2D6 in human liver microsomes. Per the manufacturer, it is unlikely that anastrozole administered at the recommended dose will inhibit the metabolism of cytochrome P450-mediated drugs given concomitantly.[13]
In a study in male volunteers (n=16), anastrozole did not alter the warfarin pharmacokinetics (Cmax or AUC), and did not alter warfarin anticoagulant activity as measured by prothrombin time, activated partial thromboplastin time, and thrombin time of both R- and S-warfarin.[13]
Anastrozole and tamoxifen should not be administered together. Clinical and pharmacokinetic results from the ATAC study demonstrate that concurrent administration of anastrozole and tamoxifen results in a reduction of anastrozole plasma levels by 27% compared to those achieved with anastrozole alone.[13][14] However, coadministration did not affect the pharmacokinetics of tamoxifen or N-desmethyltamoxifen.[13]
The goal of anastrozole therapy is to decrease circulating estrogen concentrations and inhibit the growth of hormonally-responsive cancers.[13] Anastrozole should not be given concurrently with any estrogens or estrogen-containing products, including combined oral contraceptives, as these could interfere with the pharmacologic action of anastrozole. In addition, in women receiving long-term aromatase inhibitor therapy, atrophic vaginitis due to estrogen suppression is common; atrophic vaginitis due to aromatase inhibitor therapy is sometimes treated with vaginal estrogen as the systemic exposure of estrogen from vaginal preparations is thought to be low. In a recent study of 7 women on aromatase inhibitor therapy, estrogen concentrations rose significantly after the addition of vaginally administered estrogen for atrophic vaginitis. Estrogen concentrations increased from a mean baseline level of < 5 pmol/l to 72 pmol/l at 2 weeks and to < 35 pmol/l at 4 weeks. Although the study was small, estrogen concentrations rose significantly in 6/7 patients. Clinicians should be aware that serum estrogen concentrations may increase with the use of vaginal estrogen preparations; alternative treatments for atrophic vaginitis in patients taking aromatase inhibitors should be considered.[15] Androstenedione is an important metabolic precursor for androgens and estrogens in both males and females. Androstenedione supplements should not be given concurrently with any aromatase inhibitors, as androstenedione could interfere with the pharmacologic action of the aromatase inhibitor. Conversely, aromatase inhibitors (e.g., aminoglutethimide, anastrozole, exemestane, letrozole, testolactone, vorozole) could interfere with biotransformation of androstenedione in both males and females; the enzyme aromatase converts androstenedione to estrone. Prasterone, dehydroepiandrosterone, DHEA is converted via hydrosteroid dehydrogenases and aromatase into androstenedione, testosterone, and estradiol by peripheral tissues.[16] Prasterone or DHEA supplements should not be given concurrently with any aromatase inhibitors, as DHEA could interfere with the pharmacologic action of the aromatase inhibitor and compromise aromatase inhibitor effectiveness. Conversely, aromatase inhibitors (e.g., aminoglutethimide, anastrozole, exemestane, letrozole,testolactone, vorozole could interfere with biotransformation of DHEA.[13][17][18][19]
Adverse Reactions / Side Effects
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.[12]
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.[12] 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%).12 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%.[12] 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.[12] 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).[3] 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.[12] During the ATAC trial, more patients receiving anastrozole were reported to have hypercholesterolemia compared to those receiving tamoxifen (9% vs. 3.5%, respectively).[14] 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%).[12] 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.[12] 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%).[12] Hematologic and lymphatic adverse events reported by recipients of anastrozole during clinical trials included anemia (2—5%), leukopenia (2—5%), and lymphedema (10%).[12] 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.[12] 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%).[12] 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.[9] 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.
Anastrozole is classified as FDA pregnancy risk category X.[12] 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.
It is not known whether anastrozole is excreted into breast milk. Because many drugs are excreted in human milk and because of the tumorigenicity shown for anastrozole in animal studies, or the potential for serious adverse reactions in nursing infants, a decision should be made whether to discontinue breast-feeding or to discontinue the drug, taking into account the importance of the drug to the mother. Anastrozole is contraindicated in pre-menopausal females, so use during lactation would not be expected.[12]
Store this medication 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.