Ciprofloxacina Fabra may be available in the countries listed below.
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Alfacalcidol is reported as an ingredient of Alsiodol in the following countries:
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Medobeta may be available in the countries listed below.
Betamethasone is reported as an ingredient of Medobeta in the following countries:
Betamethasone 17α-valerate (a derivative of Betamethasone) is reported as an ingredient of Medobeta in the following countries:
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Citrum C may be available in the countries listed below.
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Class: Estrogen Agonists-Antagonists
ATC Class: G03XC01
VA Class: HS900
Chemical Name: 6-Hydroxy-2-(p-hydroxyphenyl)benzo[b]thien-3-yl-p-(2-piperidinoethoxy)phenyl ketone hydrochloride
Molecular Formula: C28H27NO4S•ClH
CAS Number: 82640-04-8
Brands: Evista
Increased risk for DVT and pulmonary embolism.1 Contraindicated in women with active or past episodes of venous thrombosis.1 (See Contraindications and Cardiovascular Effects under Cautions.)
Increased risk of fatal stroke reported in women with CHD or increased risk for CHD.1 Weigh risks versus benefits in women at risk for stroke.1 (See Cardiovascular Effects under Cautions.)
Estrogen agonist-antagonist; a nonsteroidal benzothiophene derivative.1 2 3 13 14 15 16 17 55 69 70
Prevention of osteoporosis in postmenopausal women.1 2 3 4 5 6 7 16 17 23 55 69 108
Treatment of osteoporosis in postmenopausal women.1 53 69 98 99 108
Use supplemental calcium and/or vitamin D concomitantly if daily dietary intake is considered inadequate.1 2 3 4 5 6 7 16 17 23 55 69 108
May prevent or treat corticosteroid-induced bone loss†.107 American College of Rheumatology states that raloxifene can be offered to selected postmenopausal corticosteroid-treated women who refuse hormone replacement therapy or other antiresorptive agents (e.g., bisphosphonates, calcitonin) or in whom such therapies are contraindicated.107
Reduction in the incidence of invasive breast cancer in postmenopausal women with osteoporosis.1 93 100
Reduction in the incidence of invasive breast cancer in postmenopausal women at high risk for developing the disease.1 109 113 Effect comparable to that of tamoxifen in reducing the risk of invasive breast cancer (STAR trial).1 109 113 No effect on the risk of lobular carcinoma in situ or ductal carcinoma in situ (STAR trial).113 Effect on breast cancer incidence in women with BRCA1 or BRCA2 genetic mutations not established.1
Not indicated for the treatment of breast cancer or to reduce the risk of recurrence of breast cancer.1 Not indicated for reduction in the risk of noninvasive breast cancer.1
Administer orally once daily without regard to meals or time of day.1 2 55
Available as raloxifene hydrochloride; dosage expressed in terms of the salt.1
60 mg daily.1 2 55
60 mg daily.1 98
60 mg daily.1 Optimum duration of therapy unknown.1
Active or past episodes of venous thrombosis, including DVT, pulmonary embolism, or retinal vein thrombosis.1 52
Women who are or may become pregnant.1
Lactating women.1
Increased risk of venous thromboembolic events (e.g., DVT, pulmonary embolism).1 55 69 72
Discontinue raloxifene ≥72 hours before and during prolonged immobilization (e.g., postsurgery recovery, prolonged bed rest); resume therapy once patient is fully ambulatory.1 52
Assess potential benefit versus risk in women at risk of thromboembolic disease secondary to CHF, superficial thrombophlebitis, or active malignancy.1 2
Increased risk for fatal stroke reported in women with CHD or increased risk for CHD (RUTH study).1 115 Assess potential benefit versus risk in women at risk of stroke secondary to history of stroke or TIA, atrial fibrillation, hypertension, or cigarette smoking.1
Not indicated for the primary or secondary prevention of cardiovascular disease.1
May cause fetal harm.1 58 59 60 61 62 63 Embryotoxic and teratogenic effects demonstrated in animals.1 60 61 If inadvertently used during pregnancy or if patient becomes pregnant, apprise of potential fetal hazard.1 (See Contraindications.)
Not indicated.1 Safety not established.1
Potential for increased serum triglyceride concentrations in women with a history of substantial hypertriglyceridemia during oral estrogen therapy; monitor serum triglycerides in these women.1
Not studied in women with a history of breast cancer.1
Investigate unexplained breast abnormality.1 Does not eliminate risk of breast cancer.1
Safety and efficacy not evaluated.1
Not associated with endometrial proliferation.1 Investigate unexplained uterine bleeding.1
Category X.1 (See Fetal/Neonatal Morbidity and Mortality and also Contraindications under Cautions.)
Contraindicated.1
Not known whether raloxifene is distributed into milk.1
Not indicated.1
No substantial differences in safety, efficacy, or pharmacokinetic profile relative to younger adults.1
Use with caution; safety and efficacy not established in patients with hepatic impairment.1 (See Special Populations under Pharmacokinetics.)
Use with caution in patients with moderate to severe renal impairment; safety and efficacy not established in these patients.1 (See Special Populations under Pharmacokinetics.)
Hot flushes (flashes), leg cramps, peripheral edema, flu-like syndrome, arthralgia, sweating.1 2 23 69 72 88 93 96 98
Metabolism apparently not mediated by CYP isoenzymes.1
Concomitant administration with other highly protein-bound drugs not expected to affect plasma raloxifene concentrations.1 Caution advised if used concomitantly with other highly protein-bound drugs.1
Drug | Interaction | Comments |
|---|---|---|
Amoxicillin and ampicillin | Ampicillin: Decreased peak plasma raloxifene concentrations; no change in systemic exposure to raloxifene1 Amoxicillin: No change in raloxifene concentrations1 | Can be administered concomitantly1 |
Anion-exchange resins (cholestyramine) | Decreased absorption and enterohepatic cycling of raloxifene with concomitant cholestyramine administration; similar interaction expected with other anion-exchange resins1 | Concomitant administration with cholestyramine not recommended1 52 |
Antacids (aluminum- and magnesium-containing, calcium carbonate) | No change in systemic exposure of raloxifene1 | Can be administered concomitantly1 |
Anticoagulants, oral | Decreased warfarin effects; no effect on warfarin pharmacokinetics observed1 | Monitor PT carefully1 |
Antilipemic agents | Concomitant use not specifically studied1 | |
Diazepam | Potential for altered protein binding of diazepam1 | Caution advised1 |
Diazoxide | Potential for altered protein binding of diazoxide1 | Caution advised1 |
Digoxin | No change in digoxin pharmacokinetics1 | Can be administered concomitantly1 |
Estrogens | Not studied1 | Concomitant use not recommended1 |
Gemfibrozil | No substantial change in plasma raloxifene concentrations1 | |
Lidocaine | Potential for altered protein binding of lidocaine1 | Caution advised1 |
Methylprednisolone | No change in methylprednisolone pharmacokinetics1 | Can be administered concomitantly with corticosteroids1 |
Phenytoin | No change in protein binding of phenytoin1 |
Rapidly absorbed from GI tract; 60% of an oral dose is absorbed, but absolute bioavailability as unchanged drug is only 2% because of extensive first-pass glucuronidation.1 27 33 34 35 45 69
Following oral administration, peak plasma concentrations achieved at 6 hours (raloxifene) and 1 hour (glucuronide conjugates).33 35
High-fat meal increases peak plasma concentration and extent of absorption of raloxifene, but does not substantially affect systemic exposure.1
Plasma raloxifene concentrations are 150% higher in patients with cirrhosis (Child-Pugh class A) and total serum bilirubin concentrations of 0.6–2 mg/dL than in individuals with normal hepatic function.1 Pharmacokinetics not studied in individuals with moderate or severe hepatic impairment.1
Plasma raloxifene concentrations in those with mild renal impairment are similar to values in women with normal renal function.1 96 AUC of raloxifene is 122% higher in individuals with moderate renal impairment (Clcr 31–50 mL/minute) or severe renal impairment (Clcr ≤30 mL/minute) than in individuals with normal renal function.1
Raloxifene and its monoglucuronide conjugates: >95%.1 69 96 Raloxifene binds to albumin and α1-acid glycoprotein but not to testosterone-estradiol binding globulin (sex hormone binding globulin).1
Undergoes extensive first-pass metabolism to glucuronide conjugates.1 27 33 34 35 36 55 Does not appear to be metabolized by CYP isoenzymes.1 Conjugates converted back to the parent drug in various tissues.1 27
Excreted principally in feces as unabsorbed drug and via biliary elimination as glucuronide conjugates (subsequently metabolized by bacteria in GI tract to the parent drug).1 45 55 69 96
32.5 hours.1 55
20–25°C.1
Selective estrogen receptor modulator (SERM); exhibits estrogen agonist activity on bone, but estrogen antagonist activity on breast and uterine tissue.1 2 3 4 5 6 7 8 9 13 14 15 16 17 18 21 28 69 70 88 89 101
Differs chemically and pharmacologically from naturally occurring estrogens, synthetic steroidal and nonsteroidal compounds with estrogenic activity, and agents described as antiestrogens (e.g., clomiphene, tamoxifen, toremifene).4 13 14 15 16 17
In postmenopausal women or women who have undergone oophorectomy, principal action in bone is to decrease the rate of bone resorption, thus slowing the rate of bone loss.1 2 3 4 5 6 7 16 17 19 20 23 37
Inhibits estradiol-dependent proliferation of MCF-7 human mammary tumor cells in vitro.7 16 17 43 69
Importance of providing patient a copy of manufacturer’s patient information.1
Risk of venous thromboembolic events.1 Notify clinician if signs or symptoms of thromboembolic disorder occur.52 Avoid prolonged restrictions in movement while traveling.1 52 Discontinue raloxifene ≥72 hours before and during prolonged immobilization (e.g., postsurgery recovery, prolonged bed rest).1
Potential for increased incidence of hot flushes (flashes); drug is not effective in reducing hot flushes associated with estrogen deficiency.1
When used for osteoporosis, importance of taking supplemental calcium and/or vitamin D if daily dietary intake is inadequate.1 Importance of weight-bearing exercise and modification of other risk factors for osteoporosis (e.g., smoking, alcohol intake) if needed.1
When used to reduce the incidence of invasive breast cancer, advise patient regarding benefits and risks of therapy as well as appropriate indications.1 Need for regular breast examinations and mammograms.1
Importance for women who are or may become pregnant or who are lactating to avoid taking the drug.1
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.1
Importance of informing patients of other important precautionary information.1 (See Cautions.)
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 60 mg | Evista | Lilly |
This pricing information is subject to change at the sole discretion of DS Pharmacy. This pricing information was updated 03/2011. Actual costs to patients will vary depending on the use of specific retail or mail-order locations and health insurance copays.
Evista 60MG Tablets (LILLY): 30/$139.99 or 90/$369.95
This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.
The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.
AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions April 2008. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.
† Use is not currently included in the labeling approved by the US Food and Drug Administration.
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3. Boss SM, Huster WJ, Neild JA et al. Effects of raloxifene hydrochloride on the endometrium of postmenopausal women. Am J Obstet Gynecol. 1997; 177:1458-64. [IDIS 399175] [PubMed 9423751]
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86. Maricic M. Early prevention vs late treatment for osteoporosis. Arch Intern Med. 1997; 157:2545-6. [IDIS 397757] [PubMed 9531221]
87. Heaney RP. Bone mass, bone loss, and osteoporosis prophylaxis. Ann Intern Med. 1998; 128:313-4. [IDIS 401677] [PubMed 9471936]
88. Walsh BW, Kuller LH, Wild RA et al. Effects of raloxifene on serum lipids and coagulation factors in healthy postmenopausal women. JAMA. 1998; 279:1445-51. [IDIS 405187] [PubMed 9600478]
89. Rifkind BM, Rossouw JE. Of designer drugs, magic bullets, and gold standards. JAMA. 1998; 279:1483-5. [IDIS 405190] [PubMed 9600485]
90. Powles TJ, Hickish T, Kanis JA et al. Effect of tamoxifen on bone mineral density measured by dual-energy x-ray absorptiometry in healthy premenopausal and postmenopausal women. J Clin Oncol. 1996; 14:78-84. [IDIS 358669] [PubMed 8558225]
91. Reviewers’ comments (personal observations).
92. Jordan VC, Glusman JE, Eckert S et al. Incident primary breast cancers are reduced by raloxifene: integrated data from multicenter, double-blind, randomized trials in 12,000 postmenopausal women. Proc Am Soc Clin Oncol. 1998; 17:122A.
93. Cummings SR, Eckert S, Krueger KA et al. The effect of raloxifene on risk of breast cancer in postmenopausal women: results from the MORE randomized trial. JAMA. 1999; 281:2189-97. [IDIS 426871] [PubMed 10376571]
94. Gradishar WJ, Glusman JE, Vogel CL et al. Raloxifene HCl, a new endocrine agent, is active in estrogen receptor positive (ER+) metastatic breast cancer. Breast Cancer Research and Treatment; 20th Annual San Antonio Breast Cancer Symposium; 1997 Dec 3-6; San Antonio. Dordrecht/Boston/London: Kluwer Academic Publishers. Changes and additions to program. Abstract 209.
95. Gluer CC, Cummings SR, Bauer DC et al. Osteoporosis: assocation of recent fractures with quatititative US findings. Radiology. 1996; 199:725-32. [PubMed 8637996]
96. Eli Lilly and Company, Indianapolis, IN: Personal communication.
97. Vilches AR, Pérez V, Suchecki DE. Raloxifene-associated hepatitis. Lancet. 1998; 352:1524-5. [IDIS 415661] [PubMed 9820309]
98. Ettinger B, Black DM, Mitlak BH et al. Reduction of vertebral fracture risk in postmenopausal women with osteoporosis treated with raloxifene: results from a 3-year randomized clinical trial. JAMA. 1999; 282:637-45. [IDIS 430444] [PubMed 10517716]
99. McClung MR. Therapy for fracture prevention. JAMA. 1999; 282:687-9. [IDIS 430446] [PubMed 10517723]
100. Cauley JA, Norton L, Lippman ME et al. Continued breast cancer reduction in postmenopausal women treated with raloxifene: 4-year results from the MORE trial. Breast Ca Res Treat. 2001; 65:125-34.
101. Khovidhunkit W, Shoback DM. Clinical effects of raloxifene hydrochloride in women. Ann Intern Med. 1999; 130:431-9. [IDIS 421483] [PubMed 10068418]
102. Chlebowski RT, Col N, Winer EP at al. American Society of Clinical Oncology technology assessment of pharmacologic interventions for breast cancer risk reduction including tamoxifen, raloxifene, and aromatase inhibition. J Clin Oncol. 2002; 20:3328-43. [IDIS 486567] [PubMed 12149307]
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105. National Osteoporosis Foundation. Physician’s guide to prevention and treatment of osteoporosis. Washington, DC; 1998.
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In the US, Timolide (hydrochlorothiazide/timolol systemic) is a member of the drug class antihypertensive combinations and is used to treat High Blood Pressure.
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Hydrochlorothiazide is reported as an ingredient of Timolide in the following countries:
Timolol maleate (a derivative of Timolol) is reported as an ingredient of Timolide in the following countries:
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Dermorizin may be available in the countries listed below.
Pantethine is reported as an ingredient of Dermorizin in the following countries:
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Amiada may be available in the countries listed below.
Terbinafine hydrochloride (a derivative of Terbinafine) is reported as an ingredient of Amiada in the following countries:
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Rec.INN
A02BX07
0000051-77-4
C27-H44-O2
400
Antispasmodic agent
Treatment of peptic ulcer
4,8,12-Tetradecatrienoic acid, 5,9,13-trimethyl-, 3,7-dimethyl-2,6-octadienyl ester, (E,E,E)-
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Glossary
| BAN | British Approved Name |
| IS | Inofficial Synonym |
| JAN | Japanese Accepted Name |
| OS | Official Synonym |
| Rec.INN | Recommended International Nonproprietary Name (World Health Organization) |
Glimeryl may be available in the countries listed below.
Glimepiride is reported as an ingredient of Glimeryl in the following countries:
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D-Sigyent may be available in the countries listed below.
Levonorgestrel is reported as an ingredient of D-Sigyent in the following countries:
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NasenTropfen-ratiopharm may be available in the countries listed below.
Xylometazoline hydrochloride (a derivative of Xylometazoline) is reported as an ingredient of NasenTropfen-ratiopharm in the following countries:
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Class: Heavy Metal Antagonists
ATC Class: V03AB09
VA Class: AD300
CAS Number: 59-52-9
Brands: BAL in Oil
Dithiol heavy metal antagonist; chelates arsenic, lead, mercury, gold, and other heavy metals.a b
Antidote of choice in treatment of acute arsenic (except arsine), mercury, or gold poisoning following ingestion of salts of these metals or overdosage of therapeutic agents containing these metals.a b
Most effective when administered early in the course of poisoning; administration should be accompanied by appropriate supportive measures.a b
For treatment of acute poisoning by mercury salts, most effective if administered within 1–2 hours following ingestion.a b Does not reverse extensive mercury-induced renal damage.a Minimally effective in chronic mercury poisoning.a b
Usually of no value in the treatment of hypersensitivity reactions to mercury compounds; however, has been used to treat mercury-induced acrodynia (pink disease) in infants and children.a
Usually effective in treatment of chronic poisoning from inorganic or organic arsenicals.a
Consult most recent AAP and CDC recommendations for information regarding chelation therapy.a i
Ineffective in the treatment of poisoning resulting from arsine gas (AsH3).a
May be effective in the treatment of gold-induced dermatitis and gold-induced thrombocytopenia.a
Dermatologic or ocular manifestations of arsenic poisoning have been effectively treated with topical† dimercaprol ointment or oil solution, respectively.a
Used as an adjunct to edetate calcium disodium for chelation of lead in the management of acute lead encephalopathy or symptoms suggestive of encephalopathy and symptomatic lead poisoning in patients with severe lead poisoning (blood lead concentration >100 mcg/dL in adults or >70 mcg/dL in pediatric patients).f g h
Has been used for managing moderate lead poisoning; however, other agents (e.g., edetate calcium disodium, succimer) preferred for managing most cases of moderate lead poisoning.102 103 g h
Consult specialized references for detailed information on the diagnosis and management of suspected or known lead intoxication and on the decision to employ chelation therapy.100 101 102
Not useful in acute poisonings resulting from alkyl lead compounds (e.g., tetraethyl lead).a
Has been used to treat lewisite or mustard-lewisite mixture poisoning† in chemical warfare or terrorism;105 reserve for patients with signs of shock or substantial pulmonary injury.105
Initial management includes respiratory support and immediate decontamination to prevent further absorption by the victim and to prevent contamination of others (e.g., emergency personnel, health-care workers) by direct contact or off-gassing of vapors from contaminated clothing.105
No conclusive evidence regarding efficacy in the treatment of poisonings with other heavy metals† (e.g., antimony, bismuth).a b
Ineffective in treatment of argyria or acute toxicity from thallium, tellurium, or vanadium.a
Should not be used in iron, cadmium, selenium, or uranium poisoning; resulting dimercaprol-metal complexes more toxic than metals alone.a b
Administer at earliest possible time and at adequate doses at frequent intervals for greatest efficacy;a b should always be accompanied by appropriate supportive measures.a b
Consult published protocols and specialized references for dosages of chelating agents, the method and sequence of administration, and specific information on precautions associated with chelation therapy.a i
Maintain alkaline urine during therapy to prevent dissociation of dimercaprol-metal complex and protect the kidneys.105 b f h (See Renal Effects under Cautions.)
Various dosage regimens have been recommended in lead poisoning management;i total dose of chelator depends on patient’s response to, and tolerance of, the select agent,i as well as severity of lead toxicity.i
When source for lead poisoning has been identified, remove patient from that source.102 103 104 g
Chelation therapy can increase absorption of lead from the GI tract; therefore, administer only to patients who reside in environments free of lead both during and after therapy.102 104
Administer in hospital setting; monitor cardiovascular and mental status closely.103 g
Subsequent course(s) of therapy may be required based on clinical symptoms and blood lead concentrations.g In patients with severe lead poisoning, allow ≥2 days without treatment to elapse before a second 5-day course of therapy is considered.103 Assess blood lead concentrations 10–14 days after completion of chelation therapy to allow reequilibration.103 g
Administer by deep IM injection.a b
Has also been administered topically† as a 5% ointment for dermatologic manifestations of arsenic poisoning or as a 5–10% oil solution for ocular manifestations of arsenic poisoning.a
Administer by deep IM injection.a b
Consider prophylactic or therapeutic administration of antihistamines to prevent or relieve mild adverse effects.103 a b
2.5 mg/kg 4 times daily for 2 days; then 2.5 mg/kg twice daily on the third day; then 2.5 mg/kg once daily thereafter for 10 days.a b
3 mg/kg every 4 hours for 2 days; then 3 mg/kg 4 times daily on the third day; then 3 mg/kg twice daily thereafter for 10 daysa b or until recovery is complete.a
2.5 mg/kg every 4 hours for 2 days, then 2.5 mg/kg twice daily for about 1 week.a
Initially, 5 mg/kg.a b Then 2.5 mg/kg once or twice daily for 10 days.a b
Infants and children: 3 mg/kg every 4 hours for 2 days, then 3 mg/kg every 6 hours for 1 day, then 3 mg/kg every 12 hours for 7–8 days.a
Consult most recent published protocols, including those from AAP and CDC, and specialized references for combination therapy dosage recommendations.i
Initially, 4 mg/kga b g or 75 mg/m2.f g Then, at least 4 hours latera (and when adequate urine flow established) begin 4 mg/kga b or 75 mg/m2f g every 4 hours (i.e., 450 mg/m2 daily),g in conjunction with edetate calcium disodium (administered at separate injection sites), a b for at least 3 days (usual duration is 5 days).a f g
Decision to repeat dual therapy should be based on clinical symptoms and blood lead concentrations.g
Initially, 3–4 mg/kgg or 50–75 mg/m2.a Then, at least 4 hours latera (and when adequate urine flow established) begin 3–4 mg/kgb g or 50–75 mg/m2g every 4 hours (i.e., 300–450 mg/m2 daily),g in conjunction with edetate calcium disodium (administered at separate injection sites),a b for 3–5 days.a f g
Decision to repeat dual therapy should be based on clinical symptoms and blood lead concentrations.g
3–5 mg/kg every 4 hours for 4 doses.105 Adjust dosage regimen based on extent of exposure and severity of symptoms.105
Consult most recent published protocols, including those from AAP and CDC, and specialized references for combination therapy dosage recommendations.a i
2.5 mg/kg 4 times daily for 2 days; then 2.5 mg/kg twice daily on the third day; then 2.5 mg/kg once daily thereafter for 10 days.a b
3 mg/kg every 4 hours for 2 days; then 3 mg/kg 4 times daily on the third day; then 3 mg/kg twice daily thereafter for 10 daysa b or until recovery is complete.a
Alternatively, for severe arsenic poisoning, 3 mg/kg every 4 hours for 2 days and then 3 mg/kg twice daily thereafter for 7–10 daysf or 3–5 mg/kg every 4–6 hours for 1 day and then taper dose and frequency, depending on patient’s symptoms.f
2.5 mg/kg every 4 hours for 2 days, then 2.5 mg/kg twice daily for about 1 week.a
100 mg twice daily for 15 days.a
Initially, 5 mg/kg.a b Then 2.5 mg/kg once or twice daily for 10 days.a b
Alternatively, 5 mg/kg initially and then 2.5 mg/kg every 8–12 hours for 1 day, followed by 2.5 mg/kg every 12–24 hours until patient improves, up to a total of 10 days;f or 5 mg/kg every 4 hours for 48 hours, then 2.5 mg/kg every 6 hours for 48 hours, then 2.5 mg/kg every 12 hours for 7 days (total of 10 days).j
Consult most recent published protocols, including those from AAP and CDC, and specialized references for combination therapy dosage recommendations.a
Initially, 4 mg/kga b g or 75 mg/m2.g Then, at least 4 hours later (and when adequate urine flow established) begin 4 mg/kga b or 75 mg/m2g every 4 hours (i.e., 450 mg/m2 daily),g in conjunction with edetate calcium disodium (administered at separate injection sites), a b for at least 3 days (usual duration is 5 days).a
Decision to repeat dual therapy should be based on clinical symptoms and blood lead concentrations.g
Initially, 3–4 mg/kgg or 50–75 mg/m2.a Then, at least 4 hours later (and when adequate urine flow established) begin 3–4 mg/kgb g or 50–75 mg/m2g every 4 hours (i.e., 300–450 mg/m2 daily),g in conjunction with edetate calcium disodium (administered at separate injection sites),a b for at least 3–5 days.a f g
Decision to repeat dual therapy should be based on clinical symptoms and blood lead concentrations.g
3–5 mg/kg every 4 hours for 4 doses.105 Adjust dosage regimen based on extent of exposure and severity of symptoms.105
No special population dosage recommendations at this time.b
Hepatic insufficiency (except for cases of postarsenical jaundice).a b
Known hypersensitivity to peanuts.103 (See Peanut Sensitivity under Sensitivity Reactions.)
Possible injection site pain or sterile abscesses at injection site.a b
Children may experience fever usually starting after second or third dose;a b may persist throughout therapyb until drug discontinued.a
Possible transient reduction of the percentage of polymorphonuclear leukocytes.a b
Dimercaprol injection contains 700 mg of peanut oil per 1 mL of injection solution, which may cause allergic-type reactions in susceptible individuals.b Use with caution in patients with peanut sensitivities; drugs and equipment necessary to treat allergic reactions should be readily available.b
Potentially nephrotoxic.a Chelate rapidly dissociates in acid medium; alkalinization of urine during therapy may prevent dissociation and protect the kidneys.a b
Use with caution and/or reduce dosage in patients with oliguria.a
If acute renal failure develops during therapy, discontinue drug or use very cautiously as serum concentrations of dimercaprol may reach toxic levels.a b
When used in the treatment of severe reactions to gold therapy, may terminate the gold-induced remission of rheumatoid arthritis.a
Potential dose-related rise in SBP and DBP; may be accompanied by tachycardia.a May appear 15–30 minutes following the injection; BP usually returns to normal within 2 hours.a Use with caution in patients with hypertension.a
Repeated high doses may cause capillary damage and loss of protein from the circulation leading to vascular collapse.a Extremely high doses may produce coma and/or seizures.a
Drug has a strong odor and may impart an unpleasant mercaptan-like odor to patient’s breath.a
Possible burning sensation of lips or mouth.a
Erythema and edema usually occur when applied topically.a
May induce hemolysis, including severe forms, in patients with glucose-6-phosphate dehydrogenase deficiency.a Screen high-risk individuals for this deficiency and monitor susceptible patients for hemolysis during therapy.a
Category C.b e
Not known whether dimercaprol is distributed into human milk;b however, breast-feeding is contraindicated in women receiving dimercaprol for treatment of maternal arsenic, gold, mercury, or lead poisoning because of the risk of exposing nursing infant to the toxic heavy metals.e
Fever may occur in 30% of children; usually starts after second or third dose and may persist throughout therapy.a b
Possible transient reduction of the percentage of polymorphonuclear leukocytes.a b
Contraindicated in patients with impaired hepatic function, except postarsenical jaundice.a b (See Contraindications under Cautions.)
Use with extreme caution or discontinue therapy if renal impairment develops during therapy.a b (See Renal Effects under Cautions.)
Dose-related nausea/vomiting, a b BP elevation, tachycardia,a b injection site pain, fever (in children).a
Drug | Interaction | Comments |
|---|---|---|
Iron-containing preparations | Dimercaprol forms a toxic complex with iron103 a | Do not give iron concurrently with dimercaprol; defer iron therapy ≥24 hours after last dimercaprol dosea b |
Peak plasma concentrations attained 30–60 minutes following IM injection.a
Slowly absorbed through the skin following topical application.a
Distributed into all tissues (mainly in the intracellular space) including the brain, with the highest concentrations in the liver and kidneys.a
Dimercaprol (not excreted as the dimercaprol-metal complex) is rapidly metabolized to inactive products.a
Some drug may be excreted as a glucuronide conjugate.a In humans, metabolism and excretion is probably complete within 4 hours.a
Excreted in urine and feces via bile.a
20–25°C.b
Contains sulfhydryl groups that form heterocyclic ring complexes with heavy metals (particularly arsenic, mercury, and gold).a b
These complexes prevent or reverse the binding of metallic cations to body ligands such as essential sulfhydryl-dependent enzymes.a b Does not protect sulfhydryl enzymes from metals, such as selenium, that inhibit such enzymes by an oxidation process.a
If the affinity of the metal for dimercaprol is greater than that for enzymes, a mercaptide is formed, which can be excreted from the body.
Dimercaprol-metal complex can dissociate (particularly in an acid medium or as the level of dimercaprol declines) or be oxidized, thus releasing the metal to exert its toxic effects again.a
Has little affinity for the essential trace metals of the body (except copper); does not usually produce trace metal depletion syndromes.a However, may interfere with normal accumulation of iodine by the thyroid.a
When used for lead poisoning, importance of identifying source of lead poisoning and then removing patient from that source. 102 103 104 Importance of patient residing in an environment free of lead both during and after therapy.102 104
Importance of informing clinician of allergy to peanuts.a
Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.b
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.b
Importance of informing patients of other important precautionary information. (See Cautions.)
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Parenteral | Injection, for IM use only | 100 mg/mL | BAL in Oil | Akorn |
This report on medications is for your information only, and is not considered individual patient advice. Because of the changing nature of drug information, please consult your physician or pharmacist about specific clinical use.
The American Society of Health-System Pharmacists, Inc. and Drugs.com represent that the information provided hereunder was formulated with a reasonable standard of care, and in conformity with professional standards in the field. The American Society of Health-System Pharmacists, Inc. and Drugs.com make no representations or warranties, express or implied, including, but not limited to, any implied warranty of merchantability and/or fitness for a particular purpose, with respect to such information and specifically disclaims all such warranties. Users are advised that decisions regarding drug therapy are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and the information is provided for informational purposes only. The entire monograph for a drug should be reviewed for a thorough understanding of the drug's actions, uses and side effects. The American Society of Health-System Pharmacists, Inc. and Drugs.com do not endorse or recommend the use of any drug. The information is not a substitute for medical care.
AHFS Drug Information. © Copyright, 1959-2011, Selected Revisions October 2009. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.
† Use is not currently included in the labeling approved by the US Food and Drug Administration.
Only references cited for selected revisions after 1984 are available electronically.
100. Piomelli S, Rosen JF, Chisolm JJ Jr et al. Management of childhood lead poisoning. J Pediatr. 1984; 105:523-32. [IDIS 190925] [PubMed 6481529]
101. Pincus D, Saccar CV. Lead poisoning. Am Fam Physician. 1979; 19:120-4. [PubMed 110123]
102. US Department of Health and Human Services. Preventing lead poisoning in young children: a statement by the Centers for Disease Control October 1991. Atlanta, GA: Centers for Disease Control, National Center for Environmental Health and Injury Control 1991-537-304. Available at CDC website.
103. Committee on Drugs, American Academy of Pediatrics. Treatment guidelines for lead exposure in children. Pediatrics. 1995; 96:155-60. [IDIS 349805] [PubMed 7596706]
104. Committee on Environmental Health, American Academy of Pediatrics. Lead poisoning: from screening to primary prevention. Pediatrics. 1993; 92:176-83. [PubMed 8516071]
105. Agency for Toxic Substances and Disease Registry. Medical Management Guidelines for Blister Agents: Lewisite (L) and Mustard-Lewisite Mixture (HL). From the CDC website. Accessed Nov 12, 2001.
a. AHFS Drug Information 2007. McEvoy GK, ed. Dimercaprol. Bethesda, MD: American Society of Health-System Pharmacists; 2007. From AHFS website.
b. Akorn, Inc. BAL in Oil (dimercaprol) injection prescribing information. Decatur, IL; Oct 2006.
c. FDA Public Health Advisory: Edetate disodium (marketed as Endrate and generic products); 2008. From FDA website.
d. MMWR. Deaths associated with hypocalcemia from chelation therapy - Texas, Pennsylvania, and Oregon, 2003-2005. March 2006: 55(08): 204-207. Centers for Disease Control. From CDC website.
e. Briggs GC, Freeman RK, Yaffe SJ. Drugs in pregnancy and lactation.7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2005: 489–491.
f. Howland, MA. Dimercaprol (British Anti-Lewisite or BAL). In: Flomenbaum NE, Goldfrank LR, Hoffman RS et al, eds. Goldfrank’s toxicologic ermergencies. 8th ed. New York: McGraw-Hill; 2006:1265-8.
g. Henretig FM. Lead. In: Flomenbaum NE, Goldfrank LR, Hoffman RS et al, eds. Goldfrank’s toxicologic emergencies. 8th ed. New York: McGraw-Hill; 2006:1308-24.
h. Gracia R, Snodgrass W. Lead toxicity and chelation therapy. Am J Health-Syst Pharm. 2007; 64:45-53. [PubMed 17189579]
i. AHFS Drug Information 2008. McEvoy GK, ed. Edetate Calcium Disodium. Bethesda, MD: American Society of Health-System Pharmacists; 2008. From AHFS website.
j. Young-Jin, S. Mercury. In: Flomenbaum NE, Goldfrank LR, Hoffman RS et al, eds. Goldfrank’s toxicologic emergencies. 8t ed. New York: McGraw-Hill, 2006:1334-44.
Captopril/Hydrochlorothiazide ratiopharm may be available in the countries listed below.
Captopril is reported as an ingredient of Captopril/Hydrochlorothiazide ratiopharm in the following countries:
Hydrochlorothiazide is reported as an ingredient of Captopril/Hydrochlorothiazide ratiopharm in the following countries:
International Drug Name Search
