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Photo :Valstar
obsessed on Valstar Generic Name: valrubicin Dosage Form: solution, concentrate Overview Side Effects Dosage Professional Interactions More Pregnancy Warnings User Reviews Support Group Q & A Pricing & Coupons INDICATIONS AND USAGE Valstar is an anthracycline topoisomerase inhibitor indicated for intravesical therapy of BCG-refractory carcinoma in situ (CIS) of the urinary bladder in patients for whom immediate cystectomy would be associated with unacceptable morbidity or mortality. Slideshow Looking Ahead: New Drug Approvals for 2017 DOSAGE AND ADMINISTRATION Recommended Dosing For Intravesical Use Only. Do NOT administer by intravenous or intramuscular routes. Valstar is recommended at a dose of 800 mg administered intravesically once a week for six weeks. Delay administration at least two weeks after transurethral resection and/or fulguration [ see Warnings and Precautions ( 5.2 , 5.3 )]. Preparation, Handling, and Administration Handle and dispose of Valstar in a manner consistent with other cytotoxic drugs. 1 The use of goggles, gloves, and protective gowns is recommended during preparation and administration of the drug. Valstar contains polyoxyl castor oil, which has been known to cause leaching of di(2-ethylhexyl) phthalate (DEHP) a hepatotoxic plasticizer, from polyvinyl chloride (PVC) bags and intravenous tubing. Valstar should be prepared and stored in glass, polypropylene, or polyolefin containers and tubing. It is recommended that non-DEHP containing administration sets, such as those that are polyethylene-lined, be used. Valstar is a sterile, clear red solution. Visually inspect for particulate matter and discoloration prior to administration. At temperatures below 4 C (39 F), polyoxyl castor oil may begin to form a waxy precipitate. If this happens, the vial should be warmed in the hand until the solution is clear. If particulate matter is still seen, do not administer Valstar. For each instillation, slowly allow four 5 mL vials (200 mg valrubicin/5 mL vial) to warm to room temperature, but do not heat. Withdraw 20 mL of Valstar from the four vials and dilute with 55 mL of 0.9% Sodium Chloride Injection, USP to provide 75 mL of a diluted Valstar solution. Valstar diluted in 0.9% Sodium Chloride Injection, USP for administration is stable for 12 hours at temperatures up to 25 C (77 F). Since compatibility data are not available, do not mix Valstar with other drugs. Insert a urethral catheter into the patient's bladder under aseptic conditions, drain the bladder, and instill the diluted 75 mL Valstar solution slowly via gravity flow over a period of several minutes. Withdraw the catheter and retain Valstar in the bladder for two hours before voiding. At the end of two hours, all patients should void. Some patients may be unable to retain the drug for the full two hours. Instruct patients to maintain adequate hydration following Valstar treatment [see Patient Counseling Information ( 17 )] . DOSAGE FORMS AND STRENGTHS 200 mg/5 mL sterile, clear red, solution in single-use vials for intravesical instillation upon dilution. CONTRAINDICATIONS Valstar is contraindicated in patients with: Perforated bladder [ see Warnings and Precautions ( 5.2 )] Known hypersensitivity to anthracyclines or polyoxyl castor oil Active urinary tract infection Small bladder capacity and unable to tolerate a 75 mL instillation WARNINGS AND PRECAUTIONS Risk of Metastatic Bladder Cancer with Delayed Cystectomy Inform patients that Valstar has been shown to induce complete response in only about 1 in 5 patients with BCG-refractory CIS, and that delaying cystectomy could lead to development of metastatic bladder cancer, which is lethal. The exact risk of developing metastatic bladder cancer from such a delay may be difficult to assess [see Clinical Studies ( 14 )] but increases the longer cystectomy is delayed in the presence of persisting CIS. If there is not a complete response of CIS to treatment after 3 months or if CIS recurs, reconsider cystectomy. Risks in Patients with Perforated Bladder Evaluate the bladder before the intravesical instillation of drug and do not administer Valstar to patients with a perforated bladder or to those in whom the integrity of the bladder mucosa has been compromised [see Contraindications ( 4 )] . In case of bladder perforation, delay the administration of Valstar until bladder integrity has been restored. One patient with a perforated bladder who received 800 mg of Valstar intravesically developed severe leukopenia and neutropenia approximately two weeks after drug administration [see Clinical Pharmacology ( 12.3 )] . Risk in Patients Undergoing Transurethral Resection of the Bladder (TURB) To avoid systemic exposure to Valstar for the patients undergoing TURB, evaluate the status of the bladder before the intravesical instillation of drug. Delay administration at least two weeks after transurethral resection and/or fulguration. Risk in Patients with Irritable Bladder Symptoms Use Valstar with caution in patients with severe irritable bladder symptoms. Bladder spasm and spontaneous discharge of the intravesical instillate may occur; clamping of the urinary catheter is not advised. Embryo-Fetal Toxicity Based on findings in animal studies and its mechanism of action, Valstar can cause fetal harm when administered to a pregnant woman [see Clinical Pharmacology ( 12.1 and 12.3 )] . In animal reproduction studies, intravenous administration of valrubicin to pregnant rats during the period of organogenesis at a dose about 0.2 times the recommended human intravesical dose caused embryo-fetal malformations and increased resorptions. Advise females who might become pregnant of the potential risk to a fetus. Advise females of reproductive potential to use effective contraception during treatment with Valstar and for 6 months following the final dose [see Use in Specific Populations ( 8.1 and 8.3 )] . ADVERSE REACTIONS Clinical Trial Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice. The safety of Valstar was assessed in 230 patients with transitional cell carcinoma of the bladder, including 205 patients who received multiple weekly doses. One hundred seventy-nine of the 205 patients received the approved dose and schedule of 800 mg weekly for multiple weeks. Approximately 84% of patients who received intravesical Valstar in clinical studies experienced local adverse reactions. The local adverse reactions associated with Valstar usually occur during or shortly after instillation and resolve within 1 to 7 days after the instillate is removed from the bladder. Seven out of 143 patients (5%) who were scheduled to receive six doses of Valstar failed to receive all of the planned doses because of the occurrence of local bladder symptoms. TABLE 1 displays the frequency of the local adverse reactions at baseline and during treatment among 179 patients who received 800 mg doses of Valstar in a multiple-cycle treatment regimen. TABLE 1 Local Adverse Reactions Before and During Treatment with Valstar (N=179) Adverse Reaction Before Treatment During 6-week Course of Treatment ANY LOCAL BLADDER SYMPTOM 45% 88% Urinary Frequency 30% 61% Dysuria 11% 56% Urinary Urgency 27% 57% Bladder Spasm 3% 31% Hematuria 11% 29% Bladder Pain 6% 28% Urinary Incontinence 7% 22% Cystitis 4% 15% Nocturia 2% 7% Local Burning Symptoms Procedure Related 0% 5% Urethral Pain 0% 3% Pelvic Pain 1% 1% Hematuria (Gross) 0% 1% TABLE 2 displays the adverse reactions other than local bladder symptoms that occurred in 1% or more of the 230 patients who received at least one dose of Valstar in a clinical trial. TABLE 2 Systemic Adverse Reactions (> 1%) Following Intravesical Administration of Valstar (N=230) Body System Preferred Term Body as a Whole Abdominal Pain 5% Asthenia 4% Headache 4% Malaise 4% Back Pain 3% Chest Pain 3% Fever 2% Cardiovascular Vasodilation 2% Digestive Nausea 5% Diarrhea 3% Vomiting 2% Flatulence 1% Hemic and Lymphatic Anemia 2% Metabolic and Nutritional Hyperglycemia 1% Peripheral Edema 1% Musculoskeletal Myalgia 1% Nervous Dizziness 3% Respiratory Pneumonia 1% Skin and Appendages Rash 3% Urogenital Urinary Tract Infection 15% Urinary Retention 4% Hematuria (miscroscopic) 3% Adverse reactions other than local reactions that occurred in less than 1% of the patients who received Valstar intravesically in clinical trials are listed below. Digestive System: Tenesmus Metabolic and Nutritional: Nonprotein nitrogen increased Skin and Appendages: Pruritus Special Senses: Taste loss Urogenital System: Local skin irritation, poor urine flow, and urethritis DRUG INTERACTIONS No drug interaction studies were conducted. USE IN SPECIFIC POPULATIONS Pregnancy Risk Summary Based on findings in animal studies and its mechanism of action, Valstar can cause fetal harm when administered to a pregnant females [see Clinical Pharmacology ( 12.1 and 12.3 )] . There are no available data in pregnant females to inform the drug-associated risk. In animal reproduction studies, intravenous administration of valrubicin to pregnant rats during the period of organogenesis at a dose about 0.2 times the recommended human intravesical dose caused embryo-fetal malformations and increased resorptions [see Data] . Advise females who are or might become pregnant of the potential risk to a fetus. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically-recognized pregnancies is 2% to 4% and 15% to 20%, respectively. Data Animal Data Daily intravenous administration of valrubicin to pregnant rats during the period of organogenesis at doses 12 mg/kg (about 0.2 times the recommended human intravesical dose on a mg/m 2 basis) was embryo-fetal toxic and teratogenic. Administration of 12 mg/kg resulted in fetal malformations. A dose of 24 mg/kg (about 0.3 times the recommended human intravesical dose on a mg/m 2 basis) caused numerous, severe alterations in the skull and skeleton of the developing fetuses. This dose also caused an increase in fetal resorptions and a decrease in viable fetuses. Lactation Risk Summary There are no data on the presence of valrubicin or its metabolites in human milk, the effects of valrubicin on the breast-fed infant, or its effects on milk production. Because of the potential for serious adverse reactions in breast-fed infants from valrubicin, advise a lactating female not to breastfeed during treatment with Valstar and for 2 weeks after the final dose. Females and Males of Reproduction Potential Contraception Females Valstar can cause fetal harm when administered to a pregnant female. Advise females of reproductive potential to use effective contraception during treatment with Valstar and for 6 months after the final dose [see Use in Specific Populations ( 8.1 )] . Males Based on genotoxicity findings, advise men with female partners of reproductive potential to use effective contraception during treatment with Valstar and for 3 months following the final dose [see Non Clinical Toxicology ( 13.1 )] Infertility Males Studies of the effects of Valstar on human male or female fertility have not been done. Based on findings in animal studies, Valstar may impair fertility in males of reproductive potential [see Nonclinical Toxicology ( 13.1 )] . Pediatric Use Safety and effectiveness in pediatric patients have not been established. Geriatric Use Because carcinoma in situ of the bladder generally occurs in older individuals, 85% of the patients enrolled in the clinical studies of Valstar were more than 60 years of age (49% of the patients were more than 70 years of age). In the primary efficacy studies, the mean age of the population was 69.5 years. There are no specific precautions regarding use of Valstar in geriatric patients who are otherwise in good health. OVERDOSAGE There is no known antidote for overdoses of Valstar. The primary anticipated complications of overdosage associated with intravesical administration would be consistent with irritable bladder symptoms. Myelosuppression is possible if Valstar is inadvertently administered systemically or if significant systemic exposure occurs following intravesical administration (e.g., in patients with bladder rupture/perforation). Under such inadvertent exposures in the peritoneal cavity, the expected toxicities include leukopenia and neutropenia, beginning within 1 week of dose administration, with nadirs by the second week, and recovery generally by the third week. If Valstar is administered when bladder rupture or perforation is suspected, weekly monitoring of complete blood counts should be performed for 3 weeks. DESCRIPTION Valstar contains valrubicin (N-trifluoroacetyladriamycin-14-valerate), which is a semisynthetic analog of the anthracycline doxorubicin as a cytotoxic agent. The chemical name of valrubicin is (2 S - cis )-2-[1,2,3,4,6,11-hexahydro-2,5,12-trihydroxy-7-methoxy-6,11-dioxo-4-[[2,3,6-trideoxy-3-[(trifluoroacetyl)amino]-α-L- lyxo -hexopyranosyl]oxyl]-2-naphthacenyl]-2-oxoethylpentanoate. Valrubicin is an orange or orange-red powder that is highly lipophilic, soluble in methylene chloride, ethanol, methanol and acetone, and relatively insoluble in water. Its chemical formula is C 34 H 36 F 3 NO 13 and its molecular weight is 723.65. The chemical structure is shown in FIGURE 1. FIGURE 1. Chemical Structure of Valrubicin Valstar is intended for intravesical administration in the urinary bladder. It is supplied as a nonaqueous solution that should be diluted before intravesical administration. Each vial of Valstar contains 200 mg valrubicin at a concentration of 40 mg/mL in 5 mL of 50% polyoxyl castor oil/50% dehydrated alcohol, USP without preservatives or other additives. The solution is sterile and nonpyrogenic. CLINICAL PHARMACOLOGY Mechanism of Action Valrubicin is an anthracycline that affects a variety of interrelated biological functions, most of which involve nucleic acid metabolism. In cells, it inhibits the incorporation of nucleosides into nucleic acids, causes chromosomal damage, and arrests the cell cycle in G 2 . Although valrubicin does not bind strongly to DNA, valrubicin metabolites interfere with the normal DNA breaking-resealing action of DNA topoisomerase II. Pharmacokinetics When 800 mg Valstar was administered intravesically to patients with carcinoma in situ , Valstar penetrated into the bladder wall. The mean total anthracycline concentration measured in bladder tissue exceeded the levels causing 90% cytotoxicity to human bladder cells cultured in vitro . During the two-hour dose-retention period, the metabolism of Valstar to its major metabolites N-trifluoroacetyladriamycin and N-trifluoroacetyladriamycinol in bladder tissue was negligible. After retention, the drug was almost completely excreted by voiding the instillate. Mean percent recovery of Valstar, N-trifluoroacetyladriamycin, and total anthracyclines in 14 urine samples from six patients was 98.6%, 0.4%, and 99.0% of the total administered drug, respectively. During the two-hour dose-retention period, only nanogram quantities of Valstar were absorbed into the plasma. N-trifluoroacetyladriamycin and N-trifluoroacetyladriamycinol were measured in blood. Total systemic exposure to anthracyclines during and after intravesical administration of Valstar is dependent upon the condition of the bladder wall. The mean AUC 0-6 hours (total anthracyclines exposure) for an intravesical dose of 900 mg of Valstar administered 2 weeks after transurethral resection of bladder tumors (n=6) was 78 nmol/L hr. In patients receiving 800 mg of Valstar 5 to 51 minutes after typical (n=8) and extensive (n=5) TURB tumors, the mean AUC 0-6 hours values for total anthracyclines were 409 and 788 nmol/L hr, respectively. The AUC 0-6 hours total exposure to anthracyclines was 18,382 nmol/L hr in one patient who experienced a perforated bladder following a transurethral resection that occurred 5 minutes before administration of an intravesical dose of 800 mg of Valstar. Administration of a comparable intravenous dose of Valstar (600 mg/m 2 ; n=2) as a 24-hour infusion resulted in an AUC 0-6 hours for total anthracyclines of 11,975 nmol/L hr. These results are shown in FIGURE 2. FIGURE 2. Comparison of Mean AUC0-6 hours in Valstar Clinical Studies (N=number of patients) NONCLINICAL TOXICOLOGY Carcinogenesis and Mutagenesis and Impairment of Fertility The carcinogenic potential of valrubicin has not been evaluated. In vitro, valrubicin was mutagenic in the bacterial reverse mutation (Ames) assayand clastogenic in the chromosomal aberration assay in Chinese Hamster Ovary (CHO) cells. Studies in animals evaluating the effects of valrubicin on male or female fertility have not been conducted. Based on effects on male reproductive organs in general toxicology studies in dogs with intravesical instillation, valrubicin may impair fertility in male patients. When instilled into the bladder of male dogs weekly for 6 weeks, valrubicin caused mild to moderate atrophy of the prostate with inflammation, diffuse decrease in acinar size, epithelial changes. It also caused testicular degeneration, marked germ cell depletion, spermatid giant cells and karyomegaly. CLINICAL STUDIES Valstar was administered intravesically to a total of 230 patients with transitional cell carcinoma of the bladder, including 205 patients who received multiple weekly doses ranging from 200 to 900 mg. One hundred seventy-nine of the 205 patients received the approved dose and schedule of 800 mg weekly for multiple weeks. Patients receiving Valstar for refractory carcinoma in situ were monitored for disease recurrence or progression with cystoscopy, biopsy, and urine cytology every 3 months. In the 90 study patients with BCG-refractory carcinoma in situ (CIS), 70% had received at least 2 courses of BCG and 30% had received one course of BCG and at least one additional course of treatment with another agent(s) - e.g., mitomycin, thiotepa, or interferon. Valstar was administered beginning at least two weeks after transurethral resection and/or fulguration. After intravesical administration of Valstar, 16 patients (18%) had a complete response documented by bladder biopsies and cytology at 6 months following initiation of therapy. Median duration of response from start of treatment varied according to the method of analysis (13.5 months if measured to last bladder biopsy without tumor and 21 months if measured until time of documented recurrence). A retrospective analysis in the 16 patients with complete response to Valstar demonstrated that time to recurrence of their disease after treatment with Valstar was longer than time to recurrence after previous courses of intravesical therapy. Of the 90 patients with BCG-refractory CIS, 11% (10 patients) developed metastatic or deeply-invasive bladder cancer during follow-up; four of these patients, none who underwent cystectomy, died with metastatic bladder cancer and six were found to have developed stage progression to deeply-invasive disease (T3), with lymph node involvement in one patient, at the time of cystectomy. It is uncertain to what extent the development of advanced bladder cancer in these patients was due to the delay in cystectomy required to receive treatment with Valstar (3 months was the time of follow-up to determine response), as cystectomy was often delayed or was never performed despite failure of treatment with Valstar. In the 10 patients documented to have invasive bladder cancer or metastatic disease, the delay between the time of treatment failure (when cystectomy should have been performed) and cystectomy or documentation of advanced bladder cancer was a median of 17.5 months. REFERENCES OSHA Hazardous Drugs. OSHA. http://www.osha.gov/SLTC/hazardousdrugs/index.html. HOW SUPPLIED Valstar is a sterile, clear red solution in polyoxyl castor oil/dehydrated alcohol, USP, containing 40 mg valrubicin per mL. Valstar is available in single-use, clear glass vials, individually packaged in the following sizes: NDC 67979-001-01 Carton of four 200 mg/5 mL single-use vials Store vials under refrigeration at 2 -8 C (36 -46 F) in the carton. DO NOT FREEZE. PATIENT COUNSELING INFORMATION Risk of Metastatic Bladder Cancer with Delayed Cystectomy Inform patients that Valstar has been shown to induce complete responses in only about 1 in 5 patients, and that delaying cystectomy could lead to development of metastatic bladder cancer, which is lethal. Discuss the relative risk of cystectomy versus the risk of metastatic bladder cancer [see Clinical Trials ( 14 )] and that the risk increases the longer cystectomy is delayed in the presence of persisting CIS. Local Adverse Reactions Before and During Treatment Inform patients that the major acute toxicities from Valstar are related to irritable bladder symptoms that may occur during instillation and retention of Valstar and for a limited period following voiding [see Adverse Reactions ( 6.1 )] . Inform patients that for the first 24 hours following administration, red-tinged urine is typical. Advise patients to report prolonged irritable bladder symptoms or prolonged passage of red-colored urine immediately to their physician. Instruct patients to maintain adequate hydration following Valstar treatment. Embryo-Fetal Toxicity Advise females of reproductive potential of the potential risk to a fetus and to use effective contraception during treatment with Valstar and for 6 months after the last dose. Advise females to inform their healthcare provider of a known or suspected pregnancy [see Warnings and Precautions ( 5.5 ), Use in Specific Populations ( 8.1 and 8.3 )] . Advise male patients with female partners of reproductive potential to use effective contraception during treatment with Valstar and for 3 months after the last dose [see Use in Specific Populations ( 8.3 )] . Lactation Advise females not to breastfeed during treatment with Valstar and for 2 weeks after the last dose [see Use in Specific Populations ( 8.2 )] . Healthcare professionals can telephone Endo Pharmaceuticals (1-800-462-3636) for information on this product. Distributed by: Endo Pharmaceuticals Solutions Inc. Malvern, PA 19355 Manufactured by: BSP Pharmaceuticals S.p.A Latina Scalo, Italy Valstar is a trademark of Endo International plc or one of its affiliates. 2017 Endo Pharmaceuticals Solutions Inc. All rights reserved. 01USF104 Package Label Principle Display Panel Vial Label Package Label Principle Display Panel Carton 4 Vials Package Label Principle Display Panel Carton 24 Vials Valstar valrubicin solution, concentrate Product Information Product Type HUMAN PRESCRIPTION DRUG LABEL Item Code (Source) NDC:67979-001 Route of Administration INTRAVESICAL DEA Schedule Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength VALRUBICIN (VALRUBICIN) VALRUBICIN 40 mg in 1 mL Inactive Ingredients Ingredient Name Strength ALCOHOL POLYOXYL 35 CASTOR OIL NITROGEN Packaging # Item Code Package Description 1 NDC:67979-001-01 4 VIAL in 1 CARTON 1 5 mL in 1 VIAL Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date NDA NDA020892 10/01/1998 Labeler - Endo Pharmaceuticals Solutions Inc. (178074951) Establishment Name Address ID/FEI Operations BSP Pharmaceuticals SPA 857007830 MANUFACTURE(67979-001) Revised: 05/2017 Endo Pharmaceuticals Solutions Inc. Next Interactions Print this page Add to My Med List More about Valstar (valrubicin) Side Effects During Pregnancy Dosage Information Drug Interactions Support Group Pricing & Coupons En Español 0 Reviews Add your own review/rating Drug class: antibiotics/antineoplastics Consumer resources Valstar Valstar (Advanced Reading) Related treatment guides Urinary Tract Tumors} FEATURED: CAR-T Cell Therapy Overview Mechanism of Action KTE-C19 Studies KTE-C19 Cancer Targets Adverse Events Manufacturing Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Manufacturer Endo Pharmaceuticals Inc. Drug Class Antibiotics / antineoplastics Related Drugs antibiotics / antineoplastics Adriamycin , doxorubicin , mitomycin , Doxil , epirubicin , bleomycin Urinary Tract Tumors bcg , TheraCys , Tice BCG , valrubicin , More... Valstar Rating No Reviews - Be the first! No Reviews - Be the first! Not Rated - Be the first!} } growing old


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Photo :Corphedra (Intravenous)
residences Corphedra (Intravenous) Generic Name: ephedrine (Intravenous route) e-FED-rin Overview Side Effects Dosage Professional Interactions More Pregnancy Warnings User Reviews Support Group Q & A Commonly used brand name(s) In the U.S. Akovaz Corphedra Available Dosage Forms: Solution Therapeutic Class: Vasopressor Pharmacologic Class: Adrenergic Chemical Class: Alkylarylamine Slideshow Men's Health Month And Movember: Raising The Profile Of Men's Health One Stache At A Time Uses For Corphedra Ephedrine injection is used to treat hypotension (low blood pressure) caused by anesthesia (numbing medicines). This medicine is to be given only by or under the direct supervision of your doctor. Before Using Corphedra In deciding to use a medicine, the risks of taking the medicine must be weighed against the good it will do. This is a decision you and your doctor will make. For this medicine, the following should be considered: Allergies Tell your doctor if you have ever had any unusual or allergic reaction to this medicine or any other medicines. Also tell your health care professional if you have any other types of allergies, such as to foods, dyes, preservatives, or animals. For non-prescription products, read the label or package ingredients carefully. Pediatric Appropriate studies have not been performed on the relationship of age to the effects of ephedrine injection in the pediatric population. Safety and efficacy have not been established. Geriatric Appropriate studies performed to date have not demonstrated geriatric-specific problems that would limit the usefulness of ephedrine injection in the elderly. However, elderly patients are more likely to have kidney, liver, or heart problems, which may require caution and an adjustment in the dose for patients receiving this medicine. Breast Feeding There are no adequate studies in women for determining infant risk when using this medication during breastfeeding. Weigh the potential benefits against the potential risks before taking this medication while breastfeeding. Interactions with Medicines Although certain medicines should not be used together at all, in other cases two different medicines may be used together even if an interaction might occur. In these cases, your doctor may want to change the dose, or other precautions may be necessary. When you are receiving this medicine, it is especially important that your healthcare professional know if you are taking any of the medicines listed below. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive. Using this medicine with any of the following medicines is not recommended. Your doctor may decide not to treat you with this medication or change some of the other medicines you take. Cyclopropane Halothane Isocarboxazid Rasagiline Selegiline Using this medicine with any of the following medicines is usually not recommended, but may be required in some cases. If both medicines are prescribed together, your doctor may change the dose or how often you use one or both of the medicines. Acetyldigoxin Clorgyline Deslanoside Digitalis Digitoxin Digoxin Ergonovine Furazolidone Iobenguane I 123 Iproniazid Methylergonovine Metildigoxin Midodrine Nialamide Oxytocin Pargyline Phenelzine Procarbazine Tranylcypromine Interactions with Food/Tobacco/Alcohol Certain medicines should not be used at or around the time of eating food or eating certain types of food since interactions may occur. Using alcohol or tobacco with certain medicines may also cause interactions to occur. The following interactions have been selected on the basis of their potential significance and are not necessarily all-inclusive. Other Medical Problems The presence of other medical problems may affect the use of this medicine. Make sure you tell your doctor if you have any other medical problems, especially: Heart disease or Hypertension (high blood pressure) or Stroke, or history of Use with caution. May make these conditions worse. Kidney disease Use with caution. The effects may be increased because of slower removal of the medicine from the body. Proper Use of ephedrine This section provides information on the proper use of a number of products that contain ephedrine. It may not be specific to Corphedra. Please read with care. A doctor or other trained health professional will give you this medicine. This medicine is given through a needle placed in your veins. Precautions While Using Corphedra Your doctor will check your progress closely while you are receiving this medicine . This will allow your doctor to see if the medicine is working properly and to check for unwanted effects. Hypertension (high blood pressure) may occur after receiving this medicine. It is very important that your doctor check your blood pressure after receiving this medicine. If you notice any changes to your normal blood pressure, call your doctor right away. Using this medicine repeatedly may cause a rapid decrease of response to the drug. Do not take other medicines unless they have been discussed with your doctor. This includes prescription or nonprescription (over-the-counter [OTC]) medicines and herbal or vitamin supplements. Corphedra Side Effects Along with its needed effects, a medicine may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention. Check with your doctor or nurse immediately if any of the following side effects occur: Incidence not known Blurred vision dizziness fast, pounding, or irregular heartbeat or pulse headache nervousness pounding in the ears slow or fast heartbeat Some side effects may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them: Incidence not known Nausea or vomiting restlessness Other side effects not listed may also occur in some patients. If you notice any other effects, check with your healthcare professional. Call your doctor for medical advice about side effects. You may report side effects to the FDA at 1-800-FDA-1088. Side Effects (complete list) The information contained in the Truven Health Micromedex products as delivered by Drugs.com is intended as an educational aid only. It is not intended as medical advice for individual conditions or treatment. It is not a substitute for a medical exam, nor does it replace the need for services provided by medical professionals. Talk to your doctor, nurse or pharmacist before taking any prescription or over the counter drugs (including any herbal medicines or supplements) or following any treatment or regimen. Only your doctor, nurse, or pharmacist can provide you with advice on what is safe and effective for you. The use of the Truven Health products is at your sole risk. These products are provided "AS IS" and "as available" for use, without warranties of any kind, either express or implied. Truven Health and Drugs.com make no representation or warranty as to the accuracy, reliability, timeliness, usefulness or completeness of any of the information contained in the products. Additionally, TRUVEN HEALTH MAKES NO REPRESENTATION OR WARRANTIES AS TO THE OPINIONS OR OTHER SERVICE OR DATA YOU MAY ACCESS, DOWNLOAD OR USE AS A RESULT OF USE OF THE THOMSON REUTERS HEALTHCARE PRODUCTS. ALL IMPLIED WARRANTIES OF MERCHANTABILITY AND FITNESS FOR A PARTICULAR PURPOSE OR USE ARE HEREBY EXCLUDED. Truven Health does not assume any responsibility or risk for your use of the Truven Health products. Copyright 2017 Truven Health Analytics, Inc. All Rights Reserved. Next Side Effects Print this page Add to My Med List More about Corphedra (ephedrine) Side Effects During Pregnancy Dosage Information Drug Interactions Support Group 0 Reviews Add your own review/rating Drug class: vasopressors Consumer resources Other brands: Akovaz Professional resources Corphedra (FDA) Ephedrine Sulfate (AHFS Monograph) Related treatment guides Hypotension} Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Approval History Drug history at FDA WADA Class Anti-Doping Classification Manufacturer Par Pharmaceutical, Inc. Drug Class Vasopressors Related Drugs Hypotension midodrine , phenylephrine , Levophed , ephedrine , norepinephrine , ProAmatine , Northera , droxidopa , Orvaten , Akovaz , More... Corphedra Rating No Reviews - Be the first! No Reviews - Be the first! Not Rated - Be the first! Help and Support Looking for answers? Ask a question or go join the Corphedra support group to connect with others who have similar interests.} } a quirky


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Photo :Atgam
seems Atgam Generic Name: Antithymocyte Globulin (Equine) (an te THY moe site GLOB yu lin, E kwine) Brand Name: Atgam Overview Side Effects Dosage Professional Interactions More Pregnancy Warnings User Reviews Support Group Q & A Warning Unsafe allergic effects may happen. You will be closely watched by your doctor. Uses of Atgam: It is used to keep the body from turning down the kidney after a kidney transplant. It is used to treat aplastic anemia. It may be given to you for other reasons. Talk with the doctor. Slideshow Donate Life: What You Need To Know About Organ Donorship What do I need to tell my doctor BEFORE I take Atgam? If you have an allergy to lymphocytic immune globulin, horse proteins, or any other part of Atgam (antithymocyte globulin (equine)). If you are allergic to any drugs like this one, any other drugs, foods, or other substances. Tell your doctor about the allergy and what signs you had, like rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other signs. This medicine may interact with other drugs or health problems. Tell your doctor and pharmacist about all of your drugs (prescription or OTC, natural products, vitamins) and health problems. You must check to make sure that it is safe for you to take this medicine with all of your drugs and health problems. Do not start, stop, or change the dose of any drug without checking with your doctor. What are some things I need to know or do while I take Atgam? Tell all of your health care providers that you take Atgam. This includes your doctors, nurses, pharmacists, and dentists. Avoid driving and doing other tasks or actions that call for you to be alert until you see how this medicine affects you. You may have more chance of getting an infection. Wash hands often. Stay away from people with infections, colds, or flu. You may bleed more easily. Be careful and avoid injury. Use a soft toothbrush and an electric razor. This medicine is made from human plasma (part of the blood) and may have viruses that may cause disease. This medicine is screened, tested, and treated to lower the chance that it carries an infection. Talk with the doctor. Talk with your doctor before getting any vaccines while you take Atgam and after you stop taking it. Vaccine use with this medicine may either raise the chance of an infection or make the vaccine not work as well. Talk with your doctor. Have blood work checked as you have been told by the doctor. Talk with the doctor. Tell your doctor if you are pregnant or plan on getting pregnant. You will need to talk about the benefits and risks of using Atgam while you are pregnant. Tell your doctor if you are breast-feeding. You will need to talk about any risks to your baby. How is this medicine (Atgam) best taken? Use this medicine as ordered by your doctor. Read all information given to you. Follow all instructions closely. It is given as a shot into a vein over a period of time. You will be given a test dose before your first dose. What do I do if I miss a dose? Call your doctor to find out what to do. Dosage Information (comprehensive) What are some side effects that I need to call my doctor about right away? WARNING/CAUTION: Even though it may be rare, some people may have very bad and sometimes deadly side effects when taking a drug. Tell your doctor or get medical help right away if you have any of the following signs or symptoms that may be related to a very bad side effect: Signs of an allergic reaction, like rash; hives; itching; red, swollen, blistered, or peeling skin with or without fever; wheezing; tightness in the chest or throat; trouble breathing or talking; unusual hoarseness; or swelling of the mouth, face, lips, tongue, or throat. Signs of infection like fever, chills, very bad sore throat, ear or sinus pain, cough, more sputum or change in color of sputum, pain with passing urine, mouth sores, or wound that will not heal. Chest pain or pressure or a fast heartbeat. Shortness of breath. Very bad dizziness or passing out. Any unexplained bruising or bleeding. Back pain. Feeling very tired or weak. Feeling confused. Very bad skin irritation. Irritation where the shot is given. Seizures. What are some other side effects of Atgam? All drugs may cause side effects. However, many people have no side effects or only have minor side effects. Call your doctor or get medical help if any of these side effects or any other side effects bother you or do not go away: Headache. Muscle or joint pain. Upset stomach. These are not all of the side effects that may occur. If you have questions about side effects, call your doctor. Call your doctor for medical advice about side effects. You may report side effects to the FDA at 1-800-FDA-1088. You may also report side effects at http://www.fda.gov/medwatch. Side Effects (complete list) If OVERDOSE is suspected: If you think there has been an overdose, call your poison control center or get medical care right away. Be ready to tell or show what was taken, how much, and when it happened. How do I store and/or throw out Atgam? If you need to store Atgam at home, talk with your doctor, nurse, or pharmacist about how to store it. Consumer Information Use and Disclaimer If your symptoms or health problems do not get better or if they become worse, call your doctor. Do not share your drugs with others and do not take anyone else's drugs. Keep a list of all your drugs (prescription, natural products, vitamins, OTC) with you. Give this list to your doctor. Talk with the doctor before starting any new drug, including prescription or OTC, natural products, or vitamins. Keep all drugs in a safe place. Keep all drugs out of the reach of children and pets. Check with your pharmacist about how to throw out unused drugs. Some drugs may have another patient information leaflet. Check with your pharmacist. If you have any questions about this medicine, please talk with your doctor, nurse, pharmacist, or other health care provider. If you think there has been an overdose, call your poison control center or get medical care right away. Be ready to tell or show what was taken, how much, and when it happened. This information should not be used to decide whether or not to take Atgam or any other medicine. Only the healthcare provider has the knowledge and training to decide which medicines are right for a specific patient. This information does not endorse any medicine as safe, effective, or approved for treating any patient or health condition. This is only a brief summary of general information about this medicine. It does NOT include all information about the possible uses, directions, warnings, precautions, interactions, adverse effects, or risks that may apply to Atgam. This information is not specific medical advice and does not replace information you receive from the healthcare provider. You must talk with the healthcare provider for complete information about the risks and benefits of using this medicine. Review Date: November 1, 2017 Next Side Effects Print this page Add to My Med List More about Atgam (lymphocyte immune globulin, anti-thy (equine)) Side Effects During Pregnancy Dosage Information Drug Interactions Support Group En Español 0 Reviews Add your own review/rating Drug class: selective immunosuppressants Consumer resources Atgam equine Professional resources Atgam (AHFS Monograph) Atgam (FDA) Related treatment guides Aplastic Anemia Renal Transplant Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Atgam Rating No Reviews - Be the first! No Reviews - Be the first! Not Rated - Be the first! Manufacturer Pfizer Inc. Drug Class Selective immunosuppressants Related Drugs Aplastic Anemia Promacta , eltrombopag , Leukine , sargramostim , lymphocyte immune globulin, anti-thy (equine) , More... Renal Transplant furosemide , Lasix , azathioprine , Imuran , Thymoglobulin , Azasan , lymphocyte immune globulin, anti-thy (equine) , More... Related: Aplastic Anemia is quite


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day after day Understandably, if an investigational drug helps you, you may wish to continue to take it after the trial has been completed. In some instances, a medication that is being investigated for use in treating your illness may have been approved by the Food and Drug Administration (FDA) for other uses. If you find that you benefit from such a medication, your own doctor can prescribe it for you. Often, the company developing a new drug may try to see that you can continue to get it, even before the FDA has approved it for sale. You may be able to do this under what is termed a compassionate plea basis. This means that because the new drug has been so helpful, the manufacturer can give it to a physician, who may then prescribe it for you. While companies often make such a new drug available, there may also be good reasons why a company cannot. Perhaps only a very small amount of a drug was prepared for the research project, and no more is available for use afterwards. Then again, a manufacturer may want to further test the drug under certain conditions, or to examine the results of a research study more fully before releasing it for compassionate plea use. A company would be especially careful if a new medication required that the doctor who prescribed it have some special knowledge or skill to monitor its safe use. You and any family members interested in your well-being should discuss with the director of the research your questions about compassionate plea use. Each case is different, so the agreement has to be between the drug manufacturer and your own doctor. If you decide to take part in a research study and, especially one that takes place in a hospital you may find that you will have to stop, or interrupt, the care you now are getting for a mental disorder. Doing that, even temporarily, may result in your losing access to a program of personal care that had been expensive and hard to come by. The director of research on your study often will help you to get back into a program of care when the study is finished. The investigator s institution may assist in arranging for follow-up care. Related Articles Related Content from Our Sponsors Read more articles by this author Hot Topics Today 1 5 Types of People Who Are Naturally Attracted to Each Other 2 PTSD Patients Show Heightened Sensitivity to Deviant Sounds 3 Developing the Evidence Base for Mindfulness Therapies 4 Dominant Hand May Begin in Womb 5 Why Empaths and Sensitives Must Take Special Care of Their Energies Most Popular News Dominant Hand May Begin in Womb PTSD Patients Show Heightened Sensitivity to Deviant Sounds Developing the Evidence Base for Mindfulness Therapies Bipolar or Depression? Heart Test May Help Tell the Difference Avatar Therapy May Ease Schizophrenia Symptoms Join Over 195,000 Subscribers to Our Weekly Newsletter Find a Therapist Enter ZIP or postal code you can get


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different EEMT Tablets Generic Name: estrogens, esterified and methyltestosterone Dosage Form: tablet, coated Overview Side Effects Dosage Professional Interactions More Pregnancy Warnings User Reviews Drug Images Support Group Q & A Pricing & Coupons Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. For further information about unapproved drugs, click here. Physician Labeling ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE Tablets WARNINGS 1. ESTROGENS HAVE BEEN REPORTED TO INCREASE THE RISK OF ENDOMETRIAL CARCINOMA Three independent case control studies have reported an increased risk of endometrial cancer in postmenopausal women exposed to exogenous estrogens for prolonged periods. 1-3 This risk was independent of the other known risk factors for endometrial cancer. These studies are further supported by the finding that incidence rates of endometrial cancer have increased sharply since 1969 in eight different areas of the United States with population-based cancer reporting systems, an increase which may be related to the rapidly expanding use of estrogens during the last decade. 4 The three case control studies reported that the risk of endometrial cancer in estrogen users was about 4.5 to 13.9 times greater than in nonusers. The risk appears to depend on both duration of treatment 1 and on estrogen dose. 3 In view of these findings, when estrogens are used for the treatment of menopausal symptoms, the lowest dose that will control symptoms should be utilized and medication should be discontinued as soon as possible. When prolonged treatment is medically indicated, the patient should be reassessed on at least a semiannual basis to determine the need for continued therapy. Although the evidence must be considered preliminary, one study suggests that cyclic administration of low doses of estrogen may carry less risk than continuous administration, 3 it therefore appears prudent to utilize such a regimen. Close clinical surveillance of all women taking estrogens is important. In all cases of undiagnosed persistent or recurring abnormal vaginal bleeding, adequate diagnostic measures should be undertaken to rule out malignancy. There is no evidence at present that "natural" estrogens are more or less hazardous than "synthetic" estrogens at equiestrogenic doses. 2. ESTROGENS SHOULD NOT BE USED DURING PREGNANCY The use of female sex hormones, both estrogens and progestogens, during early pregnancy may seriously damage the offspring. It has been shown that females exposed in utero to diethylstilbestrol, a non-steroidal estrogen, have an increased risk of developing in later life a form of vaginal or cervical cancer that is ordinarily extremely rare. 5,6 This risk has been estimated as not greater than 4 per 1000 exposures. 7 Furthermore, a high percentage of such exposed women (from 30 to 90 percent) have been found to have vaginal adenosis, 8-12 epithelial changes of the vagina and cervix. Although these changes are histologically benign, it is not known whether they are precursors of malignancy. Although similar data are not available with the use of other estrogens, it cannot be presumed they would not induce similar changes. Several reports suggest an association between intrauterine exposure to female sex hormones and congenital anomalies, including congenital heart defects and limb reduction defects. 13-16 One case control study 16 estimated a 4.7 fold increased risk of limb reduction defects in infants exposed in utero to sex hormones (oral contraceptives, hormone withdrawal tests for pregnancy, or attempted treatment for threatened abortion). Some of these exposures were very short and involved only a few days of treatment. The data suggest that the risk of limb reduction defects in exposed fetuses is somewhat less than 1 per 1000. In the past, female sex hormones have been used during pregnancy in an attempt to treat threatened or habitual abortion. There is considerable evidence that estrogens are ineffective for these indications, and there is no evidence from well controlled studies that progesterones are effective for these uses. IF ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH or ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH is used during pregnancy, or if the patient becomes pregnant while taking this drug, she should be apprised of the potential risks to the fetus, and the advisability of pregnancy continuation. Slideshow Osteoporosis: A Battle For Your Bones EEMT Tablets Description ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH: Each light green, capsule-shaped, film-coated oral tablet contains: 1.25 mg of Esterified Estrogens, USP and 2.5 mg of Methyltestosterone, USP. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH: Each light blue, capsule-shaped, film-coated oral tablet contains: 0.625 mg of Esterified Estrogens, USP and 1.25 mg of Methyltestosterone, USP. Esterified Estrogens Esterified Estrogens, USP is a mixture of the sodium salts of the sulfate esters of the estrogenic substances, principally estrone, that are of the type excreted by pregnant mares. Esterified Estrogens contain not less than 75.0 percent and not more than 85.0 percent of sodium estrone sulfate, and not less than 6.0 percent and not more than 15.0 percent of sodium equilin sulfate, in such proportion that the total of these two components is not less than 90.0 percent. Category: Estrogens Methyltestosterone Methyltestosterone is an androgen. Androgens are derivatives of cyclopentano-perhydrophenanthrene. Endogenous androgens are C-19 steroids with a side chain at C-17, and with two angular methyl groups. Testosterone is the primary endogenous androgen. Fluoxymesterone and methyltestosterone are synthetic derivatives of testosterone. Methyltestosterone is a white to light yellow crystalline substance that is virtually insoluble in water but soluble in organic solvents. It is stable in air but decomposes in light. Methyltestosterone structural formula: C 20 H 30 O 2 . 302.46 Androst-4-en-3-one, 17-hydroxy-17-methyl-, (17B)-. Category: Androgen. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH TABLETS and ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH TABLETS contain the following inactive ingredients: lactose, magnesium stearate, microcrystalline cellulose, titanium dioxide, and other minor ingredients. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH TABLETS also contain: FD&C Blue No. 1 and D&C Yellow No. 10 and PEG. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH TABLETS also contain: D&C Yellow No. 10, FD&C Blue No. 1. EEMT Tablets - Clinical Pharmacology Estrogens Estrogens are important in the development and maintenance of the female reproductive system and secondary sex characteristics. They promote growth and development of the vagina, uterus, and fallopian tubes, and enlargement of the breasts. Indirectly, they contribute to the shaping of the skeleton, maintenance of tone and elasticity of urogenital structures, changes in the epiphyses of the long bones that allow for the pubertal growth spurt and its termination, growth of axillary and pubic hair, and pigmentation of the nipples and genitals. Decline of estrogenic activity at the end of the menstrual cycle can bring on menstruation, although the cessation of progesterone secretion is the most important factor in the mature ovulatory cycle. However, in the preovulatory or nonovulatory cycle, estrogen is the primary determinant in the onset of menstruation. Estrogens also affect the release of pituitary gonadotropins. The pharmacologic effects of esterified estrogens are similar to those of endogeneous estrogens. They are soluble in water and are well absorbed from the gastrointestinal tract. In responsive tissues (female genital organs, breasts, hypothalamus, pituitary) estrogens enter the cell and are transported into the nucleus. As a result of estrogen action, specific RNA and protein synthesis occurs. Estrogen Pharmacokinetics Metabolism and inactivation occur primarily in the liver. Some estrogens are excreted into the bile; however they are reabsorbed from the intestine and returned to the liver through the portal venous system. Water soluble esterified estrogens are strongly acidic and are ionized in body fluids, which favor excretion through the kidneys since tubular reabsorption is minimal. Androgens Endogenous androgens are responsible for the normal growth and development of the male sex organs and for maintenance of secondary sex characteristics. These effects include the growth and maturation of prostate, seminal vesicles, penis, and scrotum; the development of male hair distribution, such as beard, pubic, chest and axillary hair, laryngeal enlargement, vocal cord thickening, alterations in body musculature, and fat distribution. Drugs in this class also cause retention of nitrogen, sodium, potassium, phosphorus, and decreased urinary excretion of calcium. Androgens have been reported to increase protein anabolism and decrease protein catabolism. Nitrogen balance is improved only when there is sufficient intake of calories and protein. Androgens are responsible for the growth spurt of adolescence and for the eventual termination of linear growth centers. In children, exogenous androgens accelerate linear growth rates, but may cause a disproportionate advancement in bone maturation. Use over long periods may result in fusion of the epiphyseal growth centers and termination of growth process. Androgens have been reported to stimulate the production of red blood cells by enhancing the production of erythropoietic stimulating factor. Androgen Pharmacokinetics Testosterone given orally is metabolized by the gut and 44 percent is cleared by the liver in the first pass. Oral doses as high as 400 mg per day are needed to achieve clinically effective blood levels for full replacement therapy. The synthetic androgens (methyltestosterone and fluoxymesterone) are less extensively metabolized by the liver and have longer half-lives. They are more suitable than testosterone for oral administration. Testosterone in plasma is 98 percent bound to a specific testosteroneestradiol binding globulin, and about 2 percent is free. Generally, the amount of this sex-hormone binding globulin in the plasma will determine the distribution of testosterone between free and bound forms, and the free testosterone concentration will determine its halflife. About 90 percent of a dose of testosterone is excreted in the urine as glucuronic and sulfuric acid conjugates of testosterone and its metabolites; about 6 percent of a dose is excreted in the feces, mostly in the unconjugated form. Inactivation of testosterone occurs primarily in the liver. Testosterone is metabolized to various 17-keto steroids through two different pathways. There are considerable variations of the half-life of testosterone as reported in the literature, ranging from 10 to 100 minutes. In many tissues the activity of testosterone appears to depend on reduction to dihydrotestosterone, which binds to cytosol receptor proteins. The steroid-receptor complex is transported to the nucleus where it initiates transcription events and cellular changes related to androgen action. Indications and Usage for EEMT Tablets ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH and ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH are indicated in the treatment of: Moderate to severe vasomotor symptoms associated with the menopause in those patients not improved by estrogens alone. (There is no evidence that estrogens are effective for nervous symptoms or depression without associated vasomotor symptoms, and they should not be used to treat such conditions.) ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH and ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH HAVE NOT BEEN SHOWN TO BE EFFECTIVE FOR ANY PURPOSE DURING PREGNANCY AND ITS USE MAY CAUSE SEVERE HARM TO THE FETUS (SEE BOXED WARNING ). Contraindications Estrogens should not be used in women with any of the following conditions: Known or suspected cancer of the breast except in appropriately selected patients being treated for metastatic disease. Known or suspected estrogen-dependent neoplasia. Known or suspected pregnancy (See Boxed Warning ). Undiagnosed abnormal genital bleeding. Active thrombophlebitis or thromboembolic disorders. A past history of thrombophlebitis, thrombosis, or thromboembolic disorders associated with previous estrogen use (except when in treatment of breast malignancy). Methyltestosterone should not be used in: The presence of severe liver damage. Pregnancy and in breast-feeding mothers because of the possibility of masculinization of the female fetus or breast-fed infant. Warnings Associated with Estrogens Induction of malignant neoplasms. Long term continuous administration of natural and synthetic estrogens in certain animal species increases this frequency of carcinomas of the breast, cervix, vagina, and liver. There is now evidence that estrogens increase the risk of carcinoma of the endometrium in humans (See Boxed Warning ). At the present time there is no satisfactory evidence that estrogens given to postmenopausal women increase the risk of cancer of the breast, 18 although a recent long-term follow-up of a single physician's practice has raised this possibility. 18a Because of the animal data, there is a need for caution in prescribing estrogens for women with a strong family history of breast cancer or who have breast nodules, fibrocystic disease, or abnormal mammograms. Gallbladder disease. A recent study has reported a 2 to 3-fold increase in the risk of surgically confirmed gallbladder disease in women receiving postmenopausal estrogens, 18 similar to the 2-fold increase previously noted in users of oral contraceptives. 19-24a In the case of oral contraceptives the increased risk appeared after two years of use. 24 Effects similar to those caused by estrogen-progesterone oral contraceptives. There are several serious adverse effects of oral contraceptives, most of which have not, up to now, been documented as consequences of postmenopausal estrogen therapy. This may reflect the comparatively low doses of estrogen used in postmenopausal women. It would be expected that the larger doses of estrogen used to treat prostatic or breast cancer or postpartum breast engorgement are more likely to result in these adverse effects, and, in fact, it has been shown that there is an increased risk of thrombosis in men receiving estrogens for prostatic cancer and women for postpartum breast engorgement. 20-23 Thromboembolic disease. It is now well established that users of oral contraceptives have an increased risk of various thromboembolic and thrombotic vascular diseases, such as thrombophlebitis, pulmonary embolism, stroke, and myocardial infarction. 24-31 Cases of retinal thrombosis, mesenteric thrombosis, and optic neuritis have been reported in oral contraceptive users. There is evidence that the risk of several of these adverse reactions is related to the dose of the drug. 32-33 An increased risk of postsurgery thromboembolic complications has also been reported in users of oral contraceptives. 34-35 If feasible, estrogen should be discontinued at least 4 weeks before surgery of the type associated with an increased risk of thromboembolism, or during periods of prolonged immobilization. While an increased rate of thromboembolic and thrombotic disease in postmenopausal users of estrogens has not been found, 18-36 this does not rule out the possibility that such an increase may be present or that subgroups of women who have underlying risk factors or who are receiving relatively large doses of estrogens may have increased risk. Therefore estrogens should not be used in persons with active thrombophlebitis or thromboembolic disorders, and they should not be used (except in treatment of malignancy) in persons with a history of such disorders in association with estrogen use. They should be used with caution in patients with cerebral vascular or coronary artery disease and only for those in whom estrogens are clearly needed. Large doses of estrogen (5 mg esterified estrogens per day), comparable to those used to treat cancer of the prostate and breast, have been shown in a large prospective clinical trial in men 37 to increase the risk of nonfatal myocardial infarction, pulmonary embolism and thrombophlebitis. When estrogen doses of this size are used, any of the thromboembolic and thrombotic adverse effects associated with oral contraceptive use should be considered a clear risk. Hepatic adenoma. Benign hepatic adenomas appear to be associated with the use of oral contraceptives. 38-40 Although benign and rare, these may rupture and may cause death through intra-abdominal hemorrhage. Such lesions have not yet been reported in association with other estrogen or progestogen preparations but should be considered in estrogen users having abdominal pain and tenderness, abdominal mass, or hypovolemic shock. Hepatocellular carcinoma has also been reported in women taking estrogen-containing oral contraceptives. 39 The relationship of this malignancy to these drugs is not known at this time. Elevated blood pressure. Increased blood pressure is not uncommon in women using oral contraceptives. There is now a report that this may occur with use of estrogens in the menopause 41 and blood pressure should be monitored with estrogen use, especially if high doses are used. Glucose tolerance. A worsening of glucose tolerance has been observed in a significant percentage of patients of estrogen-containing oral contraceptives. For this reason, diabetic patients should be carefully observed while receiving estrogens. Hypercalcemia. Administration of estrogens may lead to severe hypercalcemia in patients with breast cancer and bone metastases. If this occurs, the drug should be stopped and appropriate measures taken to reduce the serum calcium level. Associated with Methyltestosterone In patients with breast cancer, androgen therapy may cause hypercalcemia by stimulating osteolysis. In this case the drug should be discontinued. Prolonged use of high doses of androgens has been associated with the development of peliosis hepatis and hepatic neoplasms including hepatocellular carcinoma. (See PRECAUTIONS Carcinogenesis ). Peliosis hepatis can be a life-threatening or fatal complication. Cholestatic hepatitis and jaundice occur with 17-alpha-alkylandrogens at a relatively low dose. If cholestatic hepatitis with jaundice appears or if liver function tests become abnormal, the androgen should be discontinued and the etiology should be determined. Drug-induced jaundice is reversible when the medication is discontinued. Edema with or without heart failure may be a serious complication in patients with preexisting cardiac, renal, or hepatic disease. In addition to discontinuation of the drug, diuretic therapy may be required. Precautions Associated with Estrogens A. General Precautions A complete medical and family history should be taken prior to the initiation of any estrogen therapy. The pretreatment and periodic physical examinations should include special reference to blood pressure, breasts, abdomen, and pelvic organs, and should include a Papanicolaou smear. As a general rule, estrogen should not be prescribed for longer than one year without another physical examination being performed. Fluid retention Because estrogens may cause some degree of fluid retention, conditions which might be influenced by this factor such as asthma, epilepsy, migraine, and cardiac or renal dysfunction, require careful observation. Certain patients may develop undesirable manifestations of excessive estrogenic stimulation, such as abnormal or excessive uterine bleeding, mastodynia, etc. Oral contraceptives appear to be associated with an increased incidence of mental depression. 24 Although it is not clear whether this is due to the estrogenic or progestogenic component of the contraceptive, patients with a history of depression should be carefully observed. Preexisting uterine leiomyomata may increase in size during estrogen use. The pathologist should be advised of estrogen therapy when relevant specimens are submitted. Patients with a past history of jaundice during pregnancy have an increased risk of recurrence of jaundice while receiving estrogen-containing oral contraceptive therapy. If jaundice develops in any patient receiving estrogen, the medication should be discontinued while the cause is investigated. Estrogens may be poorly metabolized in patients with impaired liver function and they should be administered with caution in such patients. Because estrogens influence the metabolism of calcium and phosphorus, they should be used with caution in patients with metabolic bone diseases that are associated with hypercalcemia or in patients with renal insufficiency. Because of the effects of estrogens on epiphyseal closure, they should be used judiciously in young patients in whom bone growth is not complete. Certain endocrine and liver function tests may be affected by estrogen-containing oral contraceptives. The following similar changes may be expected with larger doses of estrogen: Increased sulfobromophthalein retention. Increased prothrombin and factors VII, VIII, IX and X; decreased antithrombin 3: increased norepinephrineinduced platelet aggregability. Increased thyroid binding globulin (TBG) leading to increased circulating total thyroid hormone, as measured by PBI, T4 by column, or T4 by radioimmunassay. Free T3 resin uptakes is decreased, reflecting the elevated TBG; free T4 concentration is unaltered. Impaired glucose tolerance. Decreased pregnanediol excretion. Reduced response to metyrapone test. Reduced serum folate concentration. Increased serum triglyceride and phospholipid concentration. B. Information for the Patient See text of Patient Package Insert which appears after the REFERENCES. C. Pregnancy Category X See CONTRAINDICATIONS and Boxed WARNING . D. Nursing Mothers As a general principle, the administration of any drug to nursing mothers should be done only when clearly necessary since many drugs are excreted in human milk. Associated with Methyltestosterone A. General Precautions Women should be observed for signs of virilization (deepening of the voice, hirsutism, acne, clitoromegaly, and menstrual irregularities). Discontinuation of drug therapy at the time of evidence of mild virilism is necessary to prevent irreversible virilization. Such virilization is usual following androgen use at high doses. Prolonged dosage of androgen may result in sodium and fluid retention. This may present a problem, especially in patients with compromised cardiac reserve or renal disease. Hypersensitivity may occur rarely. PBI may be decreased in patients taking androgens. Hypercalcemia may occur. If this does occur, the drug should be discontinued. B. Information for the Patient The physician should instruct patients to report any of the following side effects of androgens: Women: Hoarseness, acne, changes in menstrual periods, or more hair on the face. All Patients: Any nausea, vomiting, changes in skin color of ankle swelling. C. Laboratory Tests Women with disseminated breast carcinoma should have frequent determination of urine and serum calcium levels during the course of androgen therapy (see WARNINGS ). Because of the hepatotoxicity associated with the use of 17-alpha-alkylated androgens, liver function tests should be obtained periodically. Hemoglobin and hematocrit should be checked periodically for polycythemia in patients who are receiving high doses of androgens. D. Drug Interactions Anticoagulants C-17 substituted derivatives of testosterone, such as methandrostenolone, have been reported to decrease the anticoagulant requirements of patients receiving oral anticoagulants. Patients receiving oral anticoagulant therapy require close monitoring, especially when androgens are started or stopped. Oxyphenbutazone. Concurrent administration of oxyphenbutazone and androgens may result in elevated serum levels of oxyphenbutazone. Insulin. In diabetic patients the metabolic effects of androgens may decrease blood glucose and insulin requirements. E. Drug/Laboratory Test Interferences Androgens may decrease levels of thyroxine-binding globulin, resulting in decreased T 4 serum levels and increased resin uptake of T 3 and T 4 . Free thyroid hormone levels remain unchanged, however, and there is no clinical evidence of thyroid dysfunction. F. Carcinogenesis Animal Data. Testosterone has been tested by subcutaneous injection and implantation in mice and rats. The implant induced cervical-uterine tumors in mice, which metastasized in some cases. There is suggestive evidence that injection of testosterone into some strains of female mice increases their susceptibility to hepatoma. Testosterone is also known to increase the number of tumors and decrease the degree of differentiation of chemically induced carcinomas of the liver in rats. Human Data. There are rare reports of hepatocellular carcinoma in patients receiving long-term therapy with androgens in high doses. Withdrawal of the drugs did not lead to regression of the tumors in all cases. Geriatric Patients treated with androgens may be at an increased risk for the development of prostatic hypertrophy and prostatic carcinoma. G. Pregnancy Teratogenic Effects. Pregnancy Category X (see CONTRAINDICATIONS ). H. Nursing Mothers It is not known whether androgens are excreted in human milk. Because many drugs are excreted in human milk and because of the potential for serious adverse reactions in nursing infants from androgens, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Adverse Reactions Associated with Estrogens (See Warnings regarding induction of neoplasia, adverse effects on the fetus, increased incidence of gallbladder disease, and adverse effects similar to those of oral contraceptives, including thromboembolism). The following additional adverse reactions have been reported with estrogenic therapy, including oral contraceptives: Genitourinary system. Breakthrough bleeding, spotting, change in menstrual flow. Dysmenorrhea. Premenstrual-like syndrome. Amenorrhea during and after treatment. Increase in size of uterine fibromyomata. Vaginal candidiasis. Change in cervical erosion and in degree of cervical secretion. Cystitis-like syndrome. Breasts. Tenderness, enlargement, secretion. Gastrointestinal. Nausea, vomiting. Abdominal cramps, bloating. Cholestatic jaundice. Skin. Chloasma or melasma which may persist when drug is discontinued. Erythema multiforme. Erythema nodosum. Hemorrhagic eruption. Loss of scalp hair. Hirsutism. Eyes. Steepening of corneal curvature. Intolerance to contact lenses. CNS. Headache, migraine, dizziness. Mental depression. Chorea. Miscellaneous. Increase or decrease in weight. Reduced carbohydrate tolerance. Aggravation of porphyria. Edema. Changes in libido. Associated with Methyltestosterone A. Endocrine and Urogenital. Female: The most common side effects of androgen therapy are amenorrhea and other menstrual irregularities, inhibition of gonadotropin secretion, and virilization, including deepening of the voice and clitoral enlargement. The latter usually is not reversible after androgens are discontinued. When administered to a pregnant woman androgens cause virilization of external genitalia of the female fetus. Skin and Appendages: Hirsutism, male pattern of baldness, and acne. Fluid and Electrolyte Disturbances: Retention of sodium, chloride, water, potassium, calcium, and inorganic phosphates. Gastrointestinal: Nausea, cholestatic jaundice, alterations in liver function test, rarely hepatocellular neoplasms, and peliosis hepatis (see WARNINGS ). Hematologic: Suppression of clotting factors, II, V, VII, and X, bleeding in patients on concomitant anticoagulant therapy, and polycythemia. Nervous System: Increased or decreased libido, headache, anxiety, depression, and generalized paresthesia. Metabolic: Increased serum cholesterol. Miscellaneous: Inflammation and pain at site of intramuscular injection or subcutaneous implantation of testosterone containing pellets, stomatitis with buccal preparations, and rarely anaphylactoid reactions. Overdosage Numerous reports of ingestion of large doses of estrogen-containing oral contraceptives by young children indicate that serious ill effects do not occur. Overdosage of estrogen may cause nausea, and withdrawal bleeding may occur in females. There have been no reports of acute overdosage with the androgens. EEMT Tablets Dosage and Administration 1. Given cyclically for short-term use only: For treatment of moderate to severe vasomotor symptoms associated with the menopause in patients not improved by estrogen alone. The lowest dose that will control symptoms should be chosen and medication should be discontinued as promptly as possible. Administration should be cyclic (e.g., three weeks on and one week off). Attempts to discontinue or taper medication should be made at three to six month intervals. Usual Dosage Range 1 tablet of ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE FULL STRENGTH or 1 to 2 tablets of ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE HALF STRENGTH daily as recommended by the physician. Treated patients with an intact uterus should be monitored closely for signs of endometrial cancer and appropriate diagnostic measures should be taken to rule out malignancy in the event of persistent or recurring abnormal vaginal bleeding. How is EEMT Tablets Supplied ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE TABLETS Full Strength in bottles of 100. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE TABLETS Full Strength light green, capsule-shaped, film-coated, oral tablets, debossed "SYNTHO" on one side and "231" on other. Contains: 1.25 mg of Esterified Estrogens, USP and 2.5 mg of Methyltestosterone, USP. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE TABLETS Half Strength in bottles of 100. ESTERIFIED ESTROGENS AND METHYLTESTOSTERONE TABLETS Half Strength light blue, capsule-shaped, film-coated, oral tablets, debossed "SYNTHO" on one side and "230" on other. Contains: 0.625 mg of Esterified Estrogens, USP and 1.25 mg of Methyltestosterone, USP. Store at 20 -25 C (68 -77 F); excursions permitted to 15 -30 C (59 -86 F). [See USP Controlled Room Temperature.] Rx only REFERENCES 1. Ziel, H.K. et al.: N. Engl. J. Med. 293: 1167-1170, 1975. 2. Smith, D.C., et al.: N. Engl. J. Med. 293: 1164-1167, 1975. 3. Mack, T.M., et al.: N. Engl. J. Med. 294: 1262-1267, 1976. 4. Weiss, N.S. et al.: N. Engl. J. Med. 294: 1259-1262, 1976. 5. Herbst, A.L. et al.: N. Engl. J. Med. 284: 878-881, 1971. 6. Greenwald, P., et al.: N. Engl. J. Med. 285: 390-392, 1971. 7. Lanier, A., et al.: Mayo Clin. Proc. 48: 793-799, 1973. 8. Herbst, A., et al.: Obstet. Gynecol. 40: 287-298, 1972. 9. Herbst, A., et al.: Am. J. Obstet. Gynecol. 118: 607-615, 1974. 10. Herbst, A., et al.: N. Engl. J. Med. 292: 334-339, 1975. 11. Stafl, A., et al.: Obstet. Gynecol. 43: 118-128, 1974. 12. Sherman, A.I., et al.: Obstet. Gynecol. 44: 531-545, 1974. 13. Gal, I., et al.: Nature 216 : 83, 1967. 14. Levy, E.P., et al.: Lancet 1: 611, 1973. 15. Nora, J., et al.: Lancet 1: 941-942, 1973. 16. Janerich, D.T., et al.: N. Engl. J. Med. 291: 697-700, 1974. 17. Estrogens for Oral or Parenteral Use: Federal Register 40: 8212, 1975. 18. Boston Collaborative Drug Surveillance Program: N. Engl. J. Med. 290: 15-19. 1974. 18a. Hoover, R. et al.: N. Engl. J. Med. 295: 401-405, 1976. 19. Boston Collaborative Drug Surveillance Program: Lancet 1: 1399-1404, 1973. 20. Daniel, D.G., et al.: Lancet 2: 287-289, 1967. 21. The Veterans Administration Cooperative Urological Research Group: J. Urol, 98: 516-522, 1967. 22. Bailar, J.C.: Lancet 2: 560, 1967. 23. Blackard, C., et al.: Cancer 26: 249-256, 1970. 24. Royal College of General Practitioners: J.R. Coll, Gen. Pract. 13: 267-279, 1967. 25. Inman, W.H.W., et al.: Br. Med. J. 2: 193-199, 1968. 26. Vessey, M.P., et al.: Br. Med. J. 2: 651-657, 1969. 27. Sartwell, P.E., et al.: Am. J. Epidemiol, 90: 365-380, 1969. 28. Collaborative Group for the Study of Stroke in Young Women: N. Engl. J. Med. 288: 871-878, 1973. 29. Collaborative Group for the Study of Stroke in Young Women: J.A.M.A 231: 718-722, 1975. 30. Mann, J.I., et al.: Br. Med. J. 2: 245-248, 1 a number of


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solutions [grade:<4 C, warm vial in the hand until solution is clear (do not use vial if particulate still present). Dilute 800 mg (20 mL) with 55 mL NS (total volume of 75 mL). Use non-PVC containers (glass, polyolefin, or polypropylene) and administration sets to avoid leaching of DEHP plasticizers. Stable for 12 hours at room temperature when diluted in 0.9% sodium chloride. Do not mix with other drugs. Administration For intravesical use only; not for IV or IM use. Intravesicular bladder instillation: Insert urinary catheter, empty bladder prior to instillation, slowly by gravity flow, instill 800 mg/75 mL (in 0.9% sodium chloride injection), remove catheter. Retain in the bladder for 2 hours, then void. Administer through non-PVC tubing due to the polyoxyl castor oil component. Maintain adequate hydration following treatment. Storage Store intact vials at 2 C to 8 C (36 F to 48 F). Do not freeze. Solutions diluted in 0.9% sodium chloride are stable for 12 hours at room temperature. Drug Interactions There are no known significant interactions. Adverse Reactions In general, local adverse reactions occur during or shortly after instillation and resolve within 1 to 7 days.> 10%: Genitourinary: Irritable bladder (88%), urinary frequency (61%), urinary urgency (57%), dysuria (56%), bladder spasm (31%), hematuria (29%; microscopic: 3%; gross hematuria: 1%), bladder pain (28%), urinary incontinence (22%), cystitis (15%), urinary tract infection (15%), red urine discoloration 1% to 10%: Cardiovascular: Chest pain (3%), vasodilatation (2%), peripheral edema (1%) Central nervous system: Localized burning (5%), headache (4%), malaise (4%), dizziness (3%) Dermatologic: Skin rash (3%) Endocrine & metabolic: Hyperglycemia (1%) Gastrointestinal: Abdominal pain (5%), nausea (5%), diarrhea (3%), vomiting (2%), flatulence (1%) Genitourinary: Nocturia (7%), urinary retention (4%), urethral pain (3%), pelvic pain (1%) Hematologic & oncologic: Anemia (2%) Neuromuscular & skeletal: Weakness (4%), back pain (3%), myalgia (1%) Respiratory: Pneumonia (1%) Miscellaneous: Fever (2%) <1% (Limited to important or life-threatening): Ageusia, increased nonprotein nitrogen, pruritus, reduced urine flow, skin irritation (local), tenesmus, urethritis Warnings/Precautions Concerns related to adverse effects: Bladder irritation: Irritable bladder symptoms may occur during instillation and retention, and for a brief time after voiding. Use with caution in patients with severe irritable bladder symptoms;. Prolonged symptoms should prompt contact with the physician. Red-tinged urine: May occur in first 24 hours after instillation. Prolonged discoloration should prompt contact with the physician. Disease-related concerns: Bladder perforation: Evaluate bladder status prior to instillation. Do not administer if mucosal integrity of bladder has been compromised or bladder perforation is present; delay treatment until restoration of bladder integrity. Bladder procedures: Delay valrubicin therapy for at least 2 weeks after transurethral resection and/or fulguration. Other warnings/issues: Administration: Use aseptic technique to prevent urinary tract infection or traumatizing urinary mucosa. Although clamping of the urinary catheter after administration is not recommended, use caution and appropriate medical supervision if performed. Appropriate use: Delaying cystectomy for intravesical treatment may lead to metastatic bladder cancer; the risk for metastatic disease increases with delay duration; reconsider cystectomy for recurrence or if complete response to treatment does not occur within 3 months. Polyoxyl castor oil: Contains polyoxyl castor oil which may be associated with hypersensitivity reactions. Use is contraindicated in patients with hypersensitivity to polyoxyl castor oil. Monitoring Parameters Cystoscopy, biopsy, and urine cytology every 3 months for recurrence or progression Pregnancy Risk Factor C Pregnancy Considerations Adverse effects were observed in animal reproduction studies. Systemic exposure (eg, with bladder perforation) during human pregnancy may result in fetal harm. Women of childbearing potential should avoid becoming pregnant during treatment. All patients of reproductive age should use an effective method of contraception during the treatment period. Patient Education Discuss specific use of drug and side effects with patient as it relates to treatment. (HCAHPS: During this hospital stay, were you given any medicine that you had not taken before? Before giving you any new medicine, how often did hospital staff tell you what the medicine was for? How often did hospital staff describe possible side effects in a way you could understand?) Patient may experience bladder irritation, polyuria, urinary incontinence, abdominal pain, nausea, or urine discoloration. Have patient report immediately to prescriber painful urination, hematuria, change in amount of urine passed, or urinary retention (HCAHPS). Educate patient about signs of a significant reaction (eg, wheezing; chest tightness; fever; itching; bad cough; blue skin color; seizures; or swelling of face, lips, tongue, or throat). Note: This is not a comprehensive list of all side effects. Patient should consult prescriber for additional questions. Intended Use and Disclaimer: Should not be printed and given to patients. This information is intended to serve as a concise initial reference for health care professionals to use when discussing medications with a patient. You must ultimately rely on your own discretion, experience, and judgment in diagnosing, treating, and advising patients. Next Interactions Print this page Add to My Med List More about valrubicin Side Effects During Pregnancy Dosage Information Drug Interactions Support Group En Español 0 Reviews Add your own review/rating Drug class: antibiotics/antineoplastics Consumer resources Valrubicin Valrubicin Intravesical (Advanced Reading) Professional resources Other brands: Valstar Related treatment guides Urinary Tract Tumors> ] Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Approval History Drug history at FDA Valrubicin Rating No Reviews - Be the first! No Reviews - Be the first! Not Rated - Be the first! Drug Class Antibiotics / antineoplastics Related Drugs antibiotics / antineoplastics Adriamycin , doxorubicin , mitomycin , Doxil , Valstar , epirubicin Urinary Tract Tumors Valstar , bcg , TheraCys , Tice BCG , More... everybody


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of ethical Corona Multi-Purpose Ointment Generic Name: lanolin ointment Dosage Form: FOR ANIMAL USE ONLY Print this page Disclaimer: This drug has not been found by FDA to be safe and effective, and this labeling has not been approved by FDA. For further information about unapproved drugs, click here. Corona Multi-Purpose Ointment Drug Facts Active Ingredient Purpose Lanolin 30% Skin protectant Purpose - Skin protectant Uses For Body and Legs, Head and Face Temporarily protects and helps relieve minor cuts, lacerations, scrapes, burns and sores. Keeps affected areas soft and supple Soothes dry skin, chapping, sunburns, and skin irritations. Warnings If conditions persist or become worse, or in case of deep wounds, or serious burns, consult y our veterinarian For external use only for veterinary use only Keep out of reach of children Directions: For minor wounds: Clean the area and apply a thick coat at least once daily. Repeat as needed Other Information Sore at 20 - 25 degrees C (68-77 degrees F) Inactive Ingredients Beeswax (yellow wax), Disodium EDTA, Fragrance, Lanolin Alcohol, Mineral Oil, Oxyquinoline, Petralatum, Purified Water, Sodium Borate, Sorbitan Sesquioleate. For questions or comments call 1-800-241-6996 or visit www.coronastable.com FOR CUTS SORES CHAPPING SCRAPES DRY SKIN SINCE 1096 CORONA MULTI-PURPOSE OINTMENT Helps promote healing Ensures moisture balance Lanolin-based protection Prevents drying and cracking Soothes chapping and sunburns CORONA MULTIPURPOSE OINTMENT Used since 1906 for: Horses, Cattle, Small Animals, and Pets SUMMIT INDUSTRIES, INC. P.O. BOX 7329 Marietta, GA 30065 CORONA MULTI-PURPOSE lanolin ointment Product Information Product Type OTC ANIMAL DRUG Item Code (Source) NDC:12090-0029 Route of Administration TOPICAL DEA Schedule Active Ingredient/Active Moiety Ingredient Name Basis of Strength Strength LANOLIN (LANOLIN) LANOLIN 30 g in 100 g Inactive Ingredients Ingredient Name Strength YELLOW WAX EDETATE DISODIUM LANOLIN ALCOHOLS MINERAL OIL OXYQUINOLINE PETROLATUM WATER SODIUM BORATE SORBITAN SESQUIOLEATE Packaging # Item Code Package Description 1 NDC:12090-0029-0 5 g in 1 POUCH 2 NDC:12090-0029-6 56.7 g in 1 TUBE 3 NDC:12090-0029-8 396.9 g in 1 JAR 4 NDC:12090-0029-9 1020.6 g in 1 JAR Marketing Information Marketing Category Application Number or Monograph Citation Marketing Start Date Marketing End Date unapproved drug other 09/17/2010 Labeler - SUMMIT INDUSTRIES (003279189) Registrant - SUMMIT INDUSTRIES (003279189) Establishment Name Address ID/FEI Operations SUMMIT INDUSTRIES 003279189 manufacture Revised: 09/2010 SUMMIT INDUSTRIES FEATURED: CAR-T Cell Therapy Overview Mechanism of Action KTE-C19 Studies KTE-C19 Cancer Targets Adverse Events Manufacturing Recently Approved Lonhala Magnair Lonhala Magnair (glycopyrrolate) is a long-acting muscarinic antagonist (LAMA) bronchodilator for... Ozempic Ozempic (semaglutide) is a glucagon-like peptide-1 (GLP-1) analog administered once-weekly for the... Ogivri Ogivri (trastuzumab-dkst) is a HER2 / neu receptor antagonist biosimilar to Herceptin indicated for... Sublocade Sublocade (buprenorphine) is a once-monthly injectable partial opioid agonist formulation for the... More good move


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no need [1%:<4 mg/mL prepared using 0.9% sodium chloride injection, 5% dextrose and 0.225% sodium chloride injection, or 5% dextrose and 0.45% sodium chloride injection are stable for up to 24 hours. b Dextrose injection should not be used as a diluent for antithymocyte globulin (equine) solution. b Highly acid infusion solutions should not be used as a diluent for antithymocyte globulin (equine) solution. b Although reconstituted solutions are physically and chemically stable at room temperature for up to 24 hours, room temperature storage is not recommended by the manufacturer since the preparation contains no preservatives; use immediately. b Use diluted solutions immediately. b Actions Equine-derived polyclonal antibody immunosuppressive agent. 7 10 17 18 19 20 21 22 23 24 25 26 27 28 30 31 32 33 34 35 51 52 53 54 55 83 a b c Exact mechanism of immunosuppressive action not fully elucidated; appears to involve clearance of peripheral antigen-reactive T lymphocytes (T cells) and/or alteration of T-cell function. 2 3 4 5 6 8 9 14 a b Exact mechanism of hematologic effects variable, complex, and not fully elucidated. 48 49 89 90 a In vitro studies indicate ATG (equine) essentially binds to all circulating lymphocytes (both T and B cells), 58 87 a granulocytes, 87 a and platelets. 87 a May produce leukopenia, 2 7 19 32 35 a b thrombocytopenia, 2 7 17 19 23 33 35 a b and/or hemolysis. 2 a b Also produces a hematopoietic response in some patients with aplastic anemia. 36 37 38 39 40 41 42 91 107 108 a Appears to have some antineoplastic activity against malignant lymphomas. 57 58 59 60 a Advice to Patients Importance of informing patients about the potential benefits of ATG (equine) and attendant risks of immunosuppressive therapy. b Risk of decreased number of WBCs (including lymphocytes), which could increase risk of infection; less commonly, anemia and hemolysis also may occur. a b Necessity of administration under supervision of a clinician with careful monitoring for signs of reduced WBC and platelet counts. a b Importance of informing clinicians promptly if any signs or symptoms of infection occur. a b Advise patient of risk of possible fever, chills, allergic reactions, malaise, arthralgia, nausea and vomiting, lymphadenopathy, and/or rash during or following ATG (equine) infusion and that medication will be given to help control these reactions. a b Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and herbal or nutritional supplements, as well as any concomitant illnesses. b Importance of women informing their clinicians if they are or plan to become pregnant or plan to breast-feed. b Importance of informing patients of other important precautionary information. b (See Cautions.) Preparations Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details. Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations. Antithymocyte Globulin (Equine) Routes Dosage Forms Strengths Brand Names Manufacturer Parenteral For injection, concentrate, for IV use only 50 mg of equine IgG per mL Atgam (with glycine) Pfizer AHFS DI Essentials. Copyright 2017, Selected Revisions June 1, 2012. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814. Use is not currently included in the labeling approved by the US Food and Drug Administration. References 1. Pharmacia. Atgam prescribing information. Kalamazoo, MI; 2000 Jun. 2. The Upjohn Company. Drug reference: Atgam . Kalamazoo, MI; 1981 Nov. 3. Lance EM. Mode of action of antilymphocyte serum. Fed Proc . 1970; 29:209-11. [PubMed 4904625] 4. Martin WJ, Miller JFAP. Site of action of antilymphocyte globulin. Lancet . 1967; 2:1285-7. [PubMed 4168616] 5. Levey RH, Medawar PB. Nature and mode of action of antilymphocytic antiserum. Proc Natl Acad Sci USA . 1966; 56:1130-7. [PubMed 5339289] 6. Wohlman MH, Toledo-Pereyra LH, Zeichner WD. The immunosuppressive properties of antilymphocyte serum preparations: a current review. Dial Transplant . 1981; 10:19-28. 7. Wechter WJ, Brodie JA, Morrell RM et al. Antithymocyte globulin (Atgam) in renal allograft recipients. Transplantation . 1979; 28:294-302. [PubMed 388762] 8. Zimmerman B, Tsui F. Immunosuppressive antilymphocyte serum: different subpopulations of T lymphocytes are influenced at different doses of antilymphocyte serum. Transplantation . 1979; 28:323-8. [PubMed 315628] 9. Bach JF. Mechanism and significance of rosette inhibition by antilymphocyte serum. In: Bach JF, Dormont J, Eyquem A et al., eds. International symposium on antilymphocyte serum; symposium series on immunobiology standardization, vol 16; New York: S Karger; 1970:189-98. 10. Wechter WJ, Nelson JW, Perper RJ et al. Manufacture of antithymocyte globulin (Atgam) for clinical trials. Transplantation . 1979; 28:303-7. [PubMed 116400] 11. Harris NS, Merino GE, Najarian JS. Mode of action of antilymphocyte sera (ALS). Transplant Proc . 1971; 3:797-9. [PubMed 4398511] 12. Sheagren JN, Barth RF, Edelin JB et al. Reticuloendothelial blockade produced by antilymphocyte serum. Lancet . 1969; 2:297-8. [PubMed 4184214] 13. Starzl TE, Marchioro TL, Porter KA et al. The use of heterologous antilymphoid agents in canine renal and liver homotransplantation and in human renal homotransplantation. Surg Gynecol Obstet . 1967; 124:301-18. [PubMed 4163340] 14. Pirofsky B, Beaulieu R, Bardana EJ et al. Antithymocyte antiserum effects in man. Am J Med . 1974; 56:290-6. [PubMed 4130597] 15. Vaughan VC III. Developmental pediatrics the newborn infant. In: Behrman RE, Vaughan VC III, eds. Nelson textbook of pediatrics. 12th ed. Philadelphia: WB Saunders Company; 1983:13-4. 16. Hong R. Immunity, allergy, and related diseases the immunologic system. In: Behrman RE, Vaughan VC III, eds. Nelson textbook of pediatrics. 12th ed. Philadelphia: WB Saunders Company; 1983:498. 17. Cosimi AB. The clinical value of antilymphocyte antibodies. Transplant Proc . 1981; 13:462-8. [PubMed 7022874] 18. Cosimi AB. The clinical usefulness of antilymphocyte antibodies. Transplant Proc . 1983; 15:583-9. 19. Wechter WJ, Morrell RM, Bergan J et al. Extended treatment with antithymocyte globulin (Atgam) in renal allograft recipients. Transplantation . 1979; 28:365-7. [PubMed 392832] 20. Kountz SL, Butt KHM, Rao TKS et al. Antithymocyte globulin (ATG) dosage and graft survival in renal transplantation. Transplant Proc . 1977; 9:1023-5. [PubMed 325728] 21. Cho SI, Bradley JW, Carpenter CB et al. Antithymocyte globulin, pretransplant blood transfusion, and tissue typing in cadaver kidney transplantation. Am J Surg . 1983; 145:464-71. [PubMed 6340551] 22. Kreis H, Mansouri R, Descamps JM et al. Antithymocyte globulin in cadaver kidney transplantation: a randomized trial based on T-cell monitoring. Kidney Int . 1981; 19:438-44. [PubMed 7017244] 23. Cosimi AB, Wortis HH, Delmonico FL et al. Randomized clinical trial of antithymocyte globulin in cadaver renal allograft recipients: importance of T cell monitoring. Surgery . 1976; 80:155-63. [PubMed 781887] 24. Kerman RH, Floyd M, Van Buren CT et al. Improved allograft survival of strong immune responder-high risk recipients with adjuvant antithymocyte globulin therapy. Transplantation . 1980; 30:450-4. [PubMed 7008294] 25. Turcotte JG, Feduska NJ, Haines RF et al. Antithymocyte globulin in renal transplant recipients: a clinical trial. Arch Surg . 1973; 106:484-8. [PubMed 4572345] 26. Diethelm AG, Aldrete JS, Shaw JF et al. Clinical evaluation of equine antithymocyte globulin in recipients of renal allografts: analysis of survival, renal function, rejection, histocompatibility, and complications. Ann Surg . 1974; 180:20-8. [PubMed 4599406] 27. Butt KMH, Zielinski CM, Parsa I et al. Trends in immunosuppression for kidney transplantation. Kidney Int . 1978; 13(Suppl 8):S95-8. 28. Cho SI, Cosimi AB, Monaco AP. Low-dose rabbit ATG versus high-dose equine ATG in clinical kidney transplantation. Surg Forum . 1981; 32:370-2. 29. Cho SI, Bradley JW, Monaco AP et al. Comparison of kidney transplant survival between patients treated with cyclosporine and those treated with azathioprine and antithymocyte globulin. Am J Surg . 1984; 147:518-23. [PubMed 6370008] 30. Filo RS, Smith EJ, Leapman SB. Reversal of acute renal allograft rejection with adjunctive ATG therapy. Transplant Proc . 1981; 13:482-90. [PubMed 7022879] 31. Hardy MA, Nowygrod R, Elberg A et al. Use of ATG in treatment of steroid-resistant rejection. Transplantation . 1980; 29:162-4. [PubMed 6986690] 32. Shield CF III, Cosimi AB, Tolkoff-Rubin N et al. Use of antithymocyte globulin for reversal of acute allograft rejection. Transplantation . 1979; 28:461-4. [PubMed 390784] 33. Nelson PW, Cosimi AB, Delmonico FL et al. Antithymocyte globulin as the primary treatment for renal allograft rejection. Transplantation . 1983; 36:587-9. [PubMed 6356523] 34. Nowygrod R, Appel G, Hardy MA. Use of ATG for reversal of acute allograft rejection. Transplant Proc . 1981; 13:469-72. [PubMed 7022875] 35. Simonian SJ, Lyons P, Chvala R et al. Reversal of acute cadaveric renal allograft rejection with added ATG treatment. Transplant Proc . 1983; 15:604-7. 36. Champlin RE. Treatment of aplastic anemia, pp. 480-3. In: Gale RP, moderator. Aplastic anemia: biology and treatment. Ann Intern Med . 1981; 95:477-94. [PubMed 6116472] 37. Champlin R, Ho W, Gale RP. Antithymocyte globulin treatment in patients with aplastic anemia. N Engl J Med . 1983; 308:113-8. [PubMed 6336819] 38. Rothmann SA, Streeter RR, Bukowski RM et al. Treatment of severe aplastic anemia with antithymocyte globulin. Exp Hematol . 1982; 10:809-16. [PubMed 6983454] 39. Doney KC, Weiden PL, Buckner CD et al. Treatment of severe aplastic anemia using antithymocyte globulin with or without an infusion of HLA haploidentical marrow. Exp Hematol . 1981; 9:829-34. [PubMed 7035206] 40. Cairo MS, Baehner RL. The use of antithymocyte globulin in the treatment of severe aplastic anemia in children. J Pediatr . 1982; 100:307-11. [PubMed 6120221] 41. Cosimi AB, Peters C, Harmon D et al. Treatment of severe aplastic anemia with a prolonged course of anti-thymocyte globulin. Transplant Proc . 1982; 14:761-4. [PubMed 6984802] 42. Amare M, Abdou NL, Robinson MG et al. Aplastic anemia associated with bone marrow suppressor T-cell hyperactivity: successful treatment with antithymocyte globulin. Am J Hematol . 1978; 5:25-32. [PubMed 311583] 43. Doney K, Dahlberg SJ, Monroe D et al. Therapy of aplastic anemia with anti-human thymocyte globulin and androgens: the effect of HLA-haploidentical marrow infusion. Blood . 1984; 63:342-8. [PubMed 6362750] 44. Thomas ED, Storb R. Acquired severe aplastic anemia: progress and perplexity. Blood . 1984; 64:325-8. [PubMed 6378271] 45. Weiden PL, Doney K, Storb R et al. Anti-human thymocyte globulin (ATG) for prophylaxis and treatment of graft-versus-host disease in recipients of allogeneic marrow grafts. Transplant Proc . 1978; 10:213-6. [PubMed 345561] 46. Weiden PL, Doney K, Storb R et al. Antihuman thymocyte globulin for prophylaxis of graft-versus-host disease: a randomized trial in patients with leukemia treated with HLA-identical sibling marrow grafts. Transplantation . 1979; 27:227-30. [PubMed 35869] 47. Doney KC, Weiden PL, Storb R et al. Failure of early administration of antithymocyte globulin to lessen graft-versus-host disease in human allogeneic marrow transplant recipients. Transplantation . 1981; 31:141-3. [PubMed 7020176] 48. Harada M, Gale RP. Evaluation of antithymocyte globulin for human bone marrow transplantation. III. Effect of antithymocyte globulin treatment on T cell precursors. Transplantation . 1981; 31:233-7. [PubMed 7013171] 49. Harada M, Gale RP. Evaluation of antithymocyte globulin for human bone marrow transplantation: antihematopoietic and immunosuppressive activity. Transplantation . 1982; 33:625-30. [PubMed 7048664] 50. Doney KC, Weiden PL, Storb R et al. Treatment of graft-versus-host disease in human allogeneic marrow graft recipients: a randomized trial comparing antithymocyte globulin and corticosteroids. Am J Hematol . 1981; 11:1-8. [PubMed 7023233] 51. Burke JF, Quinby WC, Bondoc CC et al. Immunosuppression and temporary skin transplantation in the treatment of massive third degree burns. Ann Surg . 1975; 182:183-97. [PubMed 809014] 52. Cosimi AB, Burke JF, Russell PS. Transplantation of skin. Surg Clin North Am . 1978; 58:435-51. [PubMed 349742] 53. Russell PS, Cosimi AB. Transplantation. N Engl J Med . 1979; 301:470-9. [PubMed 111125] 54. Griepp RB, Stinson EB, Dong E Jr et al. Use of antithymocyte globulin in human heart transplantation. Circulation . 1972; 45(Suppl 1):I147-53. 55. English TAH, Cooper DKC, Cory-Pearce R. Recent experience with heart transplantation. Br Med J . 1980; 281:699-702. [PubMed 7000272] 56. Griepp R, Stinson EB, Bieber CP et al. Human heart transplantation: current status. Ann Thorac Surg . 1976; 22:171-5. [PubMed 788661] 57. Fisher RI, Kubota TT, Mandell GL et al. Regression of a T-cell lymphoma after administration of antithymocyte globulin. Ann Intern Med . 1978; 88:799-800. [PubMed 149512] 58. Fisher RI, Silver BA, Vanhaelen CP et al. Objective regressions of T- and B-cell lymphomas in patients following treatment with anti-thymocyte globulin. Cancer Res . 1982; 42:2465-9 (IDIS 152225) [PubMed 7042086] 59. Wong KK, Sweet DL, Variakojis D. The treatment of lymphoblastic lymphoma with antithymocyte globulin. Cancer . 1982; 50:57-61. [PubMed 6979380] 60. Edelson RI, Raafat J, Berger CL et al. Antithymocyte globulin in the management of cutaneous T-cell lymphoma. Cancer Treat Rep . 1979; 63:675-80. [PubMed 312698] 61. Edelson RL, Brown JA, Grossman ME et al. Anti-thymocyte globulin in treatment of T-cell lymphoma. Lancet . 1977; 2:249-50. [PubMed 69857] 62. Chudwin DS, Cowan MJ, Greenberg PL et al. Response of agranulocytosis to prolonged antithymocyte globulin therapy. J Pediatr . 1983; 103:223-7. [PubMed 6875713] 63. Ring J, Seifert J, Lob G et al. Intensive immunosuppression in the treatment of multiple sclerosis. Lancet . 1974; 2:1093-6. [PubMed 4139403] 64. Mertin J, Rudge P, Kremer M et al. Double-blind controlled trial of immunosuppression in the treatment of multiple sclerosis: final report. Lancet . 1982; 2:351-4. [PubMed 6124759] 65. Tatum AH, Bollinger RR, Sanfilippo F. Rapid serologic diagnosis of serum sickness from antithymocyte globulin therapy using enzyme immunoassay. Transplantation . 1984; 38:582-6. [PubMed 6334386] 66. Harkiss GD, Brown DL, Cory-Pearce R et al Serial analysis of circulating immune complexes, complement, and antithymocyte globulin antibodies in heart transplant recipients. J Clin Immunol . 1983; 3:117-26. 67. Cheeseman SH, Rubin RH, Stewart JA et al. Controlled clinical trial of prophylactic human-leukocyte interferon in renal transplantation: effects on cytomegalovirus and herpes simplex virus infections. N Engl J Med . 1979; 300:1345-9. [PubMed 220536] 68. Pass RF, Whitley RJ, Diethelm AG et al. Cytomegalovirus infection in patients with renal transplants: potentiation by antithymocyte globulin and an incompatible graft. J Infect Dis . 1980; 142:9-17. [PubMed 6249875] 69. Rubin RH, Cosimi AB, Hirsch MS et al. Effects of antithymocyte globulin on cytomegalovirus infection in renal transplant recipients. Transplantation . 1981; 31:143-5. [PubMed 6266084] 70. Cheeseman SH, Henle W, Rubin RH et al. Epstein-Barr virus infection in renal transplant recipients: effects of antithymocyte globulin and interferon. Ann Intern Med . 1980; 93(Part 1):39-42. [PubMed 6156614] 71. Uittenbogaart CH, Robinson BJ, Malekzadeh MH et al. Use of antithymocyte globulin (dose by rosette protocol) in pediatric renal allograft recipients. Transplantation . 1979; 28:291-3. [PubMed 388761] 72. Moel DI, Butt KMH. Renal transplantation in children less than 2 years of age. J Pediatr . 1981; 99:535-9 (IDIS 140339) [PubMed 7024498] 73. Kwun YA, Butt KMH, Kim KH et al. Successful renal transplantation in a 3-month-old infant. J Pediatr . 1978; 92:426-9. [PubMed 344847] 74. Iwatsuki S, Geis WP, Molnar Z et al. Systemic lymphoblastic response to antithymocyte globulin in renal allograft recipients: an initial report. J Surg Res . 1978; 24:428-34. [PubMed 349267] 75. Geis WP, Iwatsuki S, Molnar Z et al. Pseudolymphoma in renal allograft recipients. Arch Surg . 1978; 113:461-6. [PubMed 205191] 76. Kheirbek AO, Molnar ZV, Choudhury A et al Malignant lymphoma in a renal transplant recipient treated with antithymocyte globulin. Transplantation . 1983; 35:267-8. 77. Cosimi AB, Delmonico FL, Burdick JF et al Individualized management of immunosuppression according to serial monitoring of immunocompetence. Transplant Proc . 1978; 10:647-50. 78. Geis WP, Giacchino JL, Buckingham JM et al. Does suppression of T-RFC determine in vivo immunosuppressive effect of ATG? Transplant Proc . 1979; 11:1433-4. 79. Cosimi AB, Colvin RB, Burton RC et al. Use of monoclonal antibodies to T-cell subsets for immunologic monitoring and treatment in recipients of renal allografts. N Engl J Med . 1981; 305:308-14. [PubMed 6454075] 80. Delmonico FL, Nelson PW, Colvin RB et al. Immunologic monitoring of antithymocyte globulin treatment for acute allograft rejection. Transplant Proc . 1984; 16:1492-3. [PubMed 6390852] 81. Camitta BM, Storb R, Thomas ED. Aplastic anemia (first of two parts): pathogenesis, diagnosis, treatment, and prognosis. N Engl J Med . 1982; 306:645-52. [PubMed 7035946] 82. Zoumbos NC, Gascon P, Djeu JY et al. Circulating activated suppressor T lymphocytes in aplastic anemia. N Engl J Med . 1985; 312:257-65. [PubMed 2981406] 83. Cosimi AB, Skamene E, Bonney WW et al. Experience with large-dose intravenous antithymocyte globulin in primates and man. Surgery . 1970; 68:54-61. [PubMed 4193070] 84. Burke JF. Current burn therapy. Adv Surg . 1979; 13:69-91. [PubMed 391004] 85. Reviewers comments (personal observations); 1985 Mar. 86. Cohon MS (The Upjohn Company, Kalamazoo, MI): Personal communications; 1985 Mar. 87. Greco B, Bielory L, Stephany D et al. Antithymocyte globulin reacts with many normal human cell types. Blood . 1983; 62:1047-54. [PubMed 6354303] 88. Chatenoud L, Kreis H, Jungers P et al. The effect of immunosuppressive agents on T-cell subsets, as evaluated by use of monoclonal anti-T-cell antibodies. Transplant Proc . 1981; 13:1651-6. [PubMed 7029828] 89. Zoumbos N, Gascon P, Young N. The function of lymphocytes in normal and suppressed hematopoiesis. Blut . 1984; 48:1-9. [PubMed 6197116] 90. Gascon P, Zoumbos NC, Scala G et al. Lymphokine abnormalities in aplastic anemia: implications for the mechanism of action of antithymocyte globulin. Blood . 1985; 65:407-13. [PubMed 2981588] 91. Young N, Speck B. Antithymocyte and antilymphocyte globulins: clinical trials and mechanism of action. In: Young N, Levine A, Humphries RK, eds. Aplastic anemia: stem cell biology and advances in treatment. New York: Alan R. Liss, Inc.; 1984:221-6. 92. Zoumbos NC, Gascon P, Djeu JY et al. Interferon is a mediator of hematopoietic suppression in aplastic anemia in vitro and possibly in vivo . Proc Natl Acad Sci USA . 1985; 82:188-92. [PubMed 3918301] 93. Shadduck RK, Winkelstein A, Zeigler Z et al. Response to antithymocyte globulin (ATG) in severe aplastic anemia. Clin Res . 1982; 30:508A. 94. Champlin RE, Ho WG, Feig SA et al. Do androgens enhance the response to antithymocyte globulin in patients with aplastic anemia? A prospective randomized trial. Blood . 1985; 66:184-8. [PubMed 4005428] 95. Yee GC, McGuire TR. Allogeneic bone marrow transplantation in the treatment of hematologic diseases. Clin Pharm . 1985; 4:149-60. [PubMed 3886273] 96. Ramsay NKC, Kersey JH, Robison LL et al. A randomized study of the prevention of acute graft-versus-host disease. N Engl J Med . 1982; 306:392-7. [PubMed 7035950] 97. Neudorf S, Filipovich A, Ramsay N et al. Prevention and treatment of acute graft-versus-host disease. Semin Hematol . 1984; 21:91-100. [PubMed 6377502] 98. Sullivan KM, Shulman HM, Storb R et al. Chronic graft-versus-host disease in 52 patients: adverse natural course and successful treatment with combination immunosuppression. Blood . 1981; 57:267-76. [PubMed 7004534] 99. Wallwork J, Cory-Pearce R, English TAH. Cyclosporine for cardiac transplantation: U.K. Trial. Transplant Proc . 1983; 15(Suppl 1):2559-66. 100. Oyer PE, Stinson EB, Jamieson SW et al. Cyclosporine in cardiac transplantation: a 2 year follow-up. Transplant Proc . 1983; 15(Suppl 1):2546-52. [PubMed 6420962] 101. Jamieson SW, Baldwin J, Stinson EB et al. Clinical heart-lung transplantation. Transplantation . 1984; 37:81-4. [PubMed 6420957] 102. Jacobs AD, Champlin RE, Golde DW. Pure red cell aplasia characterized by erythropoietic maturation arrest: response to anti-thymocyte globulin. Am J Med . 1985; 78:515-7. [PubMed 3919580] 103. Lawley TJ, Bielory L, Gascon P et al. A prospective clinical and immunologic analysis of patients with serum sickness. N Engl J Med . 1984; 311:1407-13. [PubMed 6387492] 104. Bielory L, Gascon P, Lawley TJ et al. Serum sickness and hematopoietic recovery with antithymocyte globulin in bone marrow failure patients. (unpublished observations) 105. Hanto DW, Gajl-Peczalska KJ, Frizzera G et al. Epstein-Barr virus (EBV) induced polyclonal and monoclonal B-cell lymphoproliferative diseases occurring after renal transplantation: clinical, pathologic, and virologic findings and implications for therapy. Ann Surg . 1983; 198:356-69. [PubMed 6311121] 106. Starzl TE, Nalesnik MA, Porter KA et al Reversibility of lymphomas and lymphoproliferative lesions developing under cyclosporin-steroid therapy. Lancet . 1984; 1:583-7. 107. Champlin R, Ho W, Bayever E et al. Treatment of aplastic anemia: results with bone marrow transplantation, antithymocyte globulin, and a monoclonal anti-T cell antibody. In: Young N, Levine A, Humphries RK, eds. Aplastic anemia: stem cell biology and advances in treatment. New York: Alan R. Liss, Inc; 1984:227-38. 108. Doney KC, Torok-Storb B, Dahlberg S et al. Immunosuppressive therapy of severe aplastic anemia. In: Young N, Levine A, Humphries RK, eds. Aplastic anemia: stem cell biology and advances in treatment. New York: Alan R. Liss, Inc; 1984:259-70. 109. Cho SI, Bradley JW, Carpenter CB et al. Antithymocyte globulin, pretransplant blood transfusion, and tissue typing in cadaver kidney transplantation. Am J Surg . 1983; 145:464-71. [PubMed 6340551] 110. Halloran PF, Lien J, Aprile M et al. Preliminary results of a randomized comparison of cyclosporine and Minnesota antilymphoblast globulin. Transplant Proc . 1982; 14:627-30. [PubMed 6301117] 111. Najarian JS, Fryd DS, Strand M et al. A single institution, randomized, prospective trial of cyclosporine versus azathioprine-antilymphocyte globulin for immunosuppression in renal allograft recipients. Ann Surg . 1985; 201:142-57. [PubMed 3882063] 112. Hall BM, Tiller DJ, Horvath JS et al. Treatment of renal transplantation rejection: cyclosporin A versus conventional treatment with azathioprine, prednisone and antithymocyte immunoglobulin in primary cadaveric renal transplantation. Med J Aust . 1985; 142:179-85. [PubMed 3881654] 114. Hunter RF, Roth PA, Huang AT. Predictive factors for response to anti-thymocyte globulin in acquired aplastic anemia. Am J Med . 1985; 79:73-8. [PubMed 3874546] 115. Bielory L, Yancey KB, Young NS et al. Cutaneous manifestations of serum sickness in patients receiving antithymocyte globulin. J Am Acad Dermatol . 1985; 13:411-7. [PubMed 3877081] a. Antithymocyte globulin (equine). Accessed January 2008. b. Pharmacia & Upjohn Company, Division of Pfizer Inc. Atgam (lymphocyte immune globulin [equine] sterile solution) prescribing information. New York, NY; 2005 Nov. c. Hong JC, Kahan BD. Immunosuppressive agents in organ transplantation: past, present, and future. Semin Nephrol. 2000; 20:108-25. [PubMed 10746855] d. Hsu B, May R, Carrum G et al. Use of antithymocyte globulin for treatment of steroid-refractory acute graft-versus-host disease: an international practice survey. Bone Marrow Transplant. 2001; 28:945-50. [PubMed 11753549] e. Kim SS. Treatment options in steroid-refractory acute graft-versus-host disease following hematopoietic stem cell transplantation. Ann Pharmacother. 2007; 41:1436-44. [PubMed 17684033] f. MacMillan ML, Weisdorf DJ, Davies SM et al. Early antithymocyte globulin therapy improves survival in patients with steroid-resistant acute graft-versus-host disease. Biol Blood Marrow Transplant. 2002; 8:40-6. [PubMed 11858189] g. Deeg HJ. How I treat refractory acute GVHD. Blood . 2007; 109:4119-26. [PubMed 17234737] h. Khoury HK, Kashyap A, Adkins DR et al. Treatment of steroid-resistant acute graft-versus-host disease with anti-thymocyte globulin. Bone Marrow Transplant. 2001; 27:1059-64. [PubMed 11438821] i. MacMillan ML, Couriel D, Weisdorf DJ et al. A phase 2/3 multicenter randomized clinical trial of ABX-CBL versus ATG as secondary therapy for steroid-resistant acute graft-versus-host disease. Blood. 2007; 109:2657-62. [PubMed 17110457] j. Lindenfeld J, Miller GG, Shaker SF et al. Drug therapy in the heart transplant recipient. Part I: Cardiac rejection and immunosuppressive drugs. Circulation. 2004; 110:3734-40. [PubMed 15596559] k. Eisen HJ, Jessup M. Acute cardiac allograft rejection: treatment. From UpToDate web site.Updated 2008 Feb 13. Accessed 2008 Mar 28. l. Doyle RL, Nador RG. Heart-lung transplantation. From UpToDate web site. Updated 2007 Sep 21. Accessed 2008 Apr 22. m. Reilly JJ Jr. Evaluation and treatment of acute lung transplant rejection. From UpToDate web site. Updated 2008 Jan 3. Accessed 2008 Apr 22. n. Mullen JC, Oreopoulos A, Lien DC et al. A randomized, controlled trial of daclizumab vs. anti-thymocyte globulin induction for lung transplantation. J Heart Lung Transplant. 2007; 26:504-10. [PubMed 17449421] o. Young NS, Abkowitz JL, Luzzatto L. New insights into the pathophysiology of acquired cytopenias. Hematology. 2000; 2000:18-38. p. Charles RJ, Sabo KM, Kidd PG et al. The pathophysiology of pure red cell aplasia: implications for therapy. Blood. 1996; 87:4831-8. [PubMed 8639856] q. Schrier SL. Acquired pure red cell aplasia. From UpToDate web site. Updated 2007 Jul 20. Accessed 2008 Mar 28. r. Cragg L, Blazar BR, Defor T et al. A randomized trial comparing prednisone with antithymocyte globulin/prednisone as an initial systemic therapy for moderately severe acute graft-versus-host disease. Biol Blood Marrow Transplant. 2000; 6:441-7. [PubMed 10975513] s. Couriel D, Caldera H, Champlin et al. Acute graft versus host disease: pathophysiology, clinical manifestations, and management. Cancer. 2004; 101:1936-46. [PubMed 15372473] t. Novartis Pharmaceuticals Corporation. Simulect (basiliximab) for injection prescribing information. East Hanover, NJ; 2005 Sep. u. Hoffmann-La Roche Inc. Zenapax (daclizumab) sterile concentrate for injection prescribing information. Nutley, NJ; 2005 Sep. v. Durrant S, Mollee P, Morton AJ et al. Combination therapy with tacrolimus and anti-thymocyte globulin for the treatment of steroid-resistant acute graft-versus-host disease developing during cyclosporine prophylaxis. Br J Haematol. 2001; 113:217-23. [PubMed 11328304] w. Trulock EP, Christie JD, Edwards LB et al. Registry of the international society for heart and lung transplantation: twenty-fourth official adult lung and heart-lung transplantation report-2007. J Heart Lung Transplant. 2007; 26:782-95. [PubMed 17692782] x. Burton CM, Andersen CB, Jensen AS et al. The incidence of acute cellular rejection after lung transplantation: a comparative study of anti-thymocyte globulin and daclizumab. J Heart Lung Transplant. 2006; 25:638-47. [PubMed 16730569] y. Hachem RR, Chakinala MM, Yusen RD et al. A comparison of basiliximab and anti-thymocyte globulin as induction agents after lung transplantation. J Heart Lung Transplant. 2005; 24:1320-26. [PubMed 16143251] z. Brock MV, Borja MC, Ferber L et al. Induction therapy in lung transplantation: a prospective, controlled clinical trial comparing OKT3, anti-thymocyte globulin, and daclizumab. J Heart Lung Transplant. 2001; 20:1282-90. [PubMed 11744411] aa. Snell GI, Westall GP. Immunosuppression for lung transplantation: evidence to date. Drugs. 2007; 67:1531-9. [PubMed 17661526] bb. Abkowitz JL, Powell JS, Nakamura JM et al. Pure red cell aplasia: response to therapy with anti-thymocyte globulin. Am J Hematol. 1986; 23:363-71. [PubMed 3098093] cc. Raghavachar A. Pure red cell aplasia: review of treatment and proposal for a treatment strategy. Blut. 1990; 61:47-51. [PubMed 1698487] dd. National Transplantation Pregnancy Registry. Available from website. Accessed 2008 Jun 10. ee. Gaber AO, First MR, Tesi RJ et al. Results of the double-blind, randomized, multicenter, phase III clinical trial of Thymoglobulin versus Atgam in the treatment of acute graft rejection episodes after renal transplantation. Transplantation . 1998; 66:29-37. [PubMed 9679818] ff. Gorrie M, Thomson G, Lewis DM et al. Dose titration during anti-thymocyte globulin therapy: monitoring by CD3 count or total lymphocyte count?. Clin Lab Haematol . 1997; 19:53-6. [PubMed 9146948] gg. Abouna GM, al-Abdullah IH, Kelly-Sullivan D et al. Randomized clinical trial of antithymocyte globulin induction in renal transplantation comparing a fixed daily dose with dose adjustment according to T cell monitoring. Transplantation. 1995; 59:1564-8. [PubMed 7778170] hh. Macdonald PS, Keogh AM, Marshman D et al. A double-blind placebo-controlled trial of low-dose ganciclovir to prevent cytomegalovirus disease after heart transplantation. J Heart Lung Transplant. 1995; 14:32-38. [PubMed 7727473] ii. Fishman JA, Doran MT, Volpicelli SA et al. Dosing of intravenous ganciclovir for the prophylaxis and treatment of cytomegalovirus infection in solid organ transplant recipients. Transplantation. 2000; 15:389-94. jj. Brennan DC, Garlock KA, Singer GG et al. Prophylactic oral ganciclovir compared with deferred therapy for control of cytomegalovirus in renal transplant recipients. Transplantation. 1997; 64:1843-46. [PubMed 9422429] kk. Brennan DC, Garlock KA, Lippmann BA et al. Control of cytomegalovirus-associated morbidity in renal transplant patients using intensive monitoring and either preemptive or deferred therapy. J Am Soc Nephrol. 1997; 8:118-25. ll. Kalil AC, Levitsky J, Lyden E et al. Meta-Analysis: The efficacy of strategies to prevent organ disease by cytomegalovirus in solid organ transplant recipients. Ann Int Med. 2005; 143:870-80. [PubMed 16365468] Next Interactions Print this page Add to My Med List More about Atgam (lymphocyte immune globulin, anti-thy (equine)) Side Effects During Pregnancy Dosage Information Drug Interactions Support Group En Español 0 Reviews Add your own review/rating Drug class: selective immunosuppressants Consumer resources Atgam equine Atgam Professional resources Atgam (FDA) Antithymocyte Globulin (Equine) (AHFS Monograph) Related treatment guides Aplastic Anemia Renal Transplant> ]} FEATURED: CAR-T Cell Therapy Overview Mechanism of Action KTE-C19 Studies KTE-C19 Cancer Targets Adverse Events Manufacturing Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Manufacturer Pfizer Inc. Drug Class Selective immunosuppressants Related Drugs Aplastic Anemia Promacta , eltrombopag , Leukine , sargramostim , lymphocyte immune globulin, anti-thy (equine) , More... 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