Torsemide (tablet)

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Torsemide (tablet)
Adult Indications & Dosage
Pediatric Indications & Dosage
Contraindications
Warnings & Precautions
Adverse Reactions
Drug Interactions
Use in Specific Populations
Administration & Monitoring
Overdosage
Pharmacology
Clinical Studies
How Supplied
Images
Patient Counseling Information
Precautions with Alcohol
Brand Names
Look-Alike Names

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Adeel Jamil, M.D. [2]

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Overview

Torsemide (tablet) is a loop diuretic that is FDA approved for the treatment of edema associated with congestive heart failure, renal disease, or liver disease. Torsemide is also indicated for the treatment of hypertension, alone or in combination with other antihypertensive agents. Common adverse reactions include polyuria and rhinitis.

Adult Indications and Dosage

FDA-Labeled Indications and Dosage (Adult)

Edema Associated with Congestive Heart Failure
  • Dosing Information
  • 10–20 mg PO qd
  • If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.
Edema Associated with Chronic Renal Failure
  • Dosing Information
  • 20 mg PO qd
  • If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 200 mg have not been adequately studied.
Edema Associated with Hepatic Cirrhosis
  • Dosing Information
  • If the diuretic response is inadequate, the dose should be titrated upward by approximately doubling until the desired diuretic response is obtained. Single doses higher than 40 mg have not been adequately studied.
Hypertension
  • Dosing Information
  • 5mg PO qd
  • If the 5 mg dose does not provide adequate reduction in blood pressure within 4 to 6 weeks, the dose may be increased to 10 mg once daily. If the response to 10 mg is insufficient, an additional antihypertensive agent should be added to the treatment regimen.

Off-Label Use and Dosage (Adult)

Guideline-Supported Use

There is limited information regarding Off-Label Guideline-Supported Use of Torsemide (tablet) in adult patients.

Non–Guideline-Supported Use

There is limited information regarding Off-Label Non–Guideline-Supported Use of Torsemide (tablet) in adult patients.

Pediatric Indications and Dosage

FDA-Labeled Indications and Dosage (Pediatric)

  • Safety and effectiveness in pediatric patients have not been established.

Off-Label Use and Dosage (Pediatric)

Guideline-Supported Use

There is limited information regarding Off-Label Guideline-Supported Use of Torsemide (tablet) in pediatric patients.

Non–Guideline-Supported Use

There is limited information regarding Off-Label Non–Guideline-Supported Use of Torsemide (tablet) in pediatric patients.

Contraindications

Warnings

Hepatic Disease With Cirrhosis and Ascites
Ototoxicity
  • Tinnitus and hearing loss (usually reversible) have been observed after rapid intravenous injection of other loop diuretics and have also been observed after oral Demadex. It is not certain that these events were attributable to Demadex. Ototoxicity has also been seen in animal studies when very high plasma levels of torsemide were induced.
Volume and Electrolyte Depletion

Precautions

Laboratory Values
Calcium
  • Single doses of Demadex increased the urinary excretion of calcium by normal subjects, but serum calcium levels were slightly increased in 4- to 6-week hypertension trials. In a long-term study of patients with congestive heart failure, the average 1-year change in serum calcium was a decrease of 0.10 mg/dL (0.02 mmol/L). Among 426 patients treated with Demadex for an average of 11 months, hypocalcemia was not reported as an adverse event.
Magnesium
  • Single doses of Demadex caused healthy volunteers to increase their urinary excretion of magnesium, but serum magnesium levels were slightly increased in 4- to 6-week hypertension trials. In long-term hypertension studies, the average 1-year change in serum magnesium was an increase of 0.03 mg/dL (0.01 mmol/L). Among 426 patients treated with Demadex for an average of 11 months, one case of hypomagnesemia (1.3 mg/dL [0.53 mmol/L]) was reported as an adverse event.
  • In a long-term clinical study of Demadex in patients with congestive heart failure, the estimated annual change in serum magnesium was an increase of 0.2 mg/dL (0.08 mmol/L), but these data are confounded by the fact that many of these patients received magnesium supplements. In a 4-week study in which magnesium supplementation was not given, the rate of occurrence of serum magnesium levels below 1.7 mg/dL (0.70 mmol/L) was 6% and 9% in the groups receiving 5 mg and 10 mg of Demadex, respectively.
Blood Urea Nitrogen (BUN), Creatinine and Uric Acid
  • Demadex produces small dose-related increases in each of these laboratory values. In hypertensive patients who received 10 mg of Demadex daily for 6 weeks, the mean increase in blood urea nitrogen was 1.8 mg/dL (0.6 mmol/L), the mean increase in serum creatinine was 0.05 mg/dL (4 mmol/L), and the mean increase in serum uric acid was 1.2 mg/dL (70 mmol/L). Little further change occurred with long-term treatment, and all changes reversed when treatment was discontinued.
  • Symptomatic gout has been reported in patients receiving Demadex, but its incidence has been similar to that seen in patients receiving placebo.
Glucose
  • Hypertensive patients who received 10 mg of daily Demadex experienced a mean increase in serum glucose concentration of 5.5 mg/dL (0.3 mmol/L) after 6 weeks of therapy, with a further increase of 1.8 mg/dL (0.1 mmol/L) during the subsequent year. In long-term studies in diabetics, mean fasting glucose values were not significantly changed from baseline. Cases of hyperglycemia have been reported but are uncommon.
Serum Lipids
  • In the controlled short-term hypertension studies in the United States, daily doses of 5 mg, 10 mg, and 20 mg of Demadex were associated with increases in total plasma cholesterol of 4, 4, and 8 mg/dL (0.10 to 0.20 mmol/L), respectively. The changes subsided during chronic therapy.
  • In the same short-term hypertension studies, daily doses of 5 mg, 10 mg and 20 mg of Demadex were associated with mean increases in plasma triglycerides of 16, 13 and 71 mg/dL (0.15 to 0.80 mmol/L), respectively.
  • In long-term studies of 5 mg to 20 mg of Demadex daily, no clinically significant differences from baseline lipid values were observed after 1 year of therapy.
Other

Adverse Reactions

Clinical Trials Experience

  • To report SUSPECTED ADVERSE REACTIONS, contact Meda Pharmaceuticals Inc. at 1-800-526-3840 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.
  • At the time of approval, Demadex had been evaluated for safety in approximately 4000 subjects: over 800 of these subjects received Demadex for at least 6 months, and over 380 were treated for more than 1 year. Among these subjects were 564 who received Demadex during United States-based trials in which 274 other subjects received placebo.
  • The reported side effects of Demadex were generally transient, and there was no relationship between side effects and age, sex, race, or duration of therapy. Discontinuation of therapy due to side effects occurred in 3.5% of United States patients treated with Demadex and in 4.4% of patients treated with placebo. In studies conducted in the United States and Europe, discontinuation rates due to side effects were 3.0% (38/1250) with Demadex and 3.4% (13/380) with furosemide in patients with congestive heart failure, 2.0% (8/409) with Demadex and 4.8% (11/230) with furosemide in patients with renal insufficiency, and 7.6% (13/170) with Demadex and 0% (0/33) with furosemide in patients with cirrhosis.
  • The most common reasons for discontinuation of therapy with Demadex were (in descending order of frequency) dizziness, headache, nausea, weakness, vomiting, hyperglycemia, excessive urination, hyperuricemia, hypokalemia, excessive thirst, hypovolemia, impotence, esophageal hemorrhage, and dyspepsia. Dropout rates for these adverse events ranged from 0.1% to 0.5%.
  • The side effects considered possibly or probably related to study drug that occurred in United States placebo-controlled trials in more than 1% of patients treated with Demadex are shown in Table 1.
This image is provided by the National Library of Medicine.
  • The daily doses of Demadex used in these trials ranged from 1.25 mg to 20 mg, with most patients receiving 5 mg to 10 mg; the duration of treatment ranged from 1 to 52 days, with a median of 41 days. Of the side effects listed in the table, only “excessive urination” occurred significantly more frequently in patients treated with Demadex than in patients treated with placebo. In the placebo-controlled hypertension studies whose design allowed side-effect rates to be attributed to dose, excessive urination was reported by 1% of patients receiving placebo, 4% of those treated with 5 mg of daily Demadex, and 15% of those treated with 10 mg. The complaint of excessive urination was generally not reported as an adverse event among patients who received Demadex for cardiac, renal, or hepatic failure.
  • Serious adverse events reported in the clinical studies for which a drug relationship could not be excluded were atrial fibrillation, chest pain, diarrhea, digitalis intoxication, gastrointestinal hemorrhage, hyperglycemia, hyperuricemia, hypokalemia, hypotension, hypovolemia, shunt thrombosis, rash, rectal bleeding, syncope, and ventricular tachycardia.
  • Angioedema has been reported in a patient exposed to Demadex who was later found to be allergic to sulfa drugs.
  • Of the adverse reactions during placebo-controlled trials listed without taking into account assessment of relatedness to drug therapy, arthritis and various other nonspecific musculoskeletal problems were more frequently reported in association with Demadex than with placebo, even though gout was somewhat more frequently associated with placebo. These reactions did not increase in frequency or severity with the dose of Demadex. One patient in the group treated with Demadex withdrew due to myalgia, and one in the placebo group withdrew due to gout.

Postmarketing Experience

  • The following adverse reactions have been identified during the post approval use of Demadex. Because these reactions are reported voluntarily from a population of uncertain size, it is not always possible to reliably estimate their frequency or establish a causal relationship to drug exposure. Adverse reactions reported include the following: leucopenia, thrombocytopenia.
  • Serious skin reactions (i.e., Stevens-Johnson syndrome, toxic epidermal necrolysis) have been reported in association with torsemide use.
  • Pancreatitis has been reported in association with torsemide use.

Drug Interactions

  • In patients with essential hypertension, Demadex has been administered together with beta-blockers, ACE inhibitors, and calcium-channel blockers. In patients with congestive heart failure, Demadex has been administered together with digitalis glycosides, ACE inhibitors, and organic nitrates. None of these combined uses was associated with new or unexpected adverse events.
  • Torsemide does not affect the protein binding of glyburide or of warfarin, the anticoagulant effect of phenprocoumon (a related coumarin derivative), or the pharmacokinetics of digoxin or carvedilol (a vasodilator/beta-blocker). In healthy subjects, coadministration of Demadex was associated with significant reduction in the renal clearance of spironolactone, with corresponding increases in the AUC. However, clinical experience indicates that dosage adjustment of either agent is not required.
  • Because Demadex and salicylates compete for secretion by renal tubules, patients receiving high doses of salicylates may experience salicylate toxicity when Demadex is concomitantly administered. Also, although possible interactions between torsemide and nonsteroidal anti-inflammatory agents (including aspirin) have not been studied, coadministration of these agents with another loop diuretic (furosemide) has occasionally been associated with renal dysfunction.
  • The natriuretic effect of Demadex (like that of many other diuretics) is partially inhibited by the concomitant administration of indomethacin. This effect has been demonstrated for Demadex under conditions of dietary sodium restriction (50 mEq/day) but not in the presence of normal sodium intake (150 mEq/day).
  • The pharmacokinetic profile and diuretic activity of torsemide are not altered by cimetidine or spironolactone. Coadministration of digoxin is reported to increase the area under the curve for torsemide by 50%, but dose adjustment of Demadex is not necessary.
  • Concomitant use of torsemide and cholestyramine has not been studied in humans but, in a study in animals, coadministration of cholestyramine decreased the absorption of orally administered torsemide. If Demadex and cholestyramine are used concomitantly, simultaneous administration is not recommended.
  • Coadministration of probenecid reduces secretion of Demadex into the proximal tubule and thereby decreases the diuretic activity of Demadex.
  • Other diuretics are known to reduce the renal clearance of lithium, inducing a high risk of lithium toxicity, so coadministration of lithium and diuretics should be undertaken with great caution, if at all. Coadministration of lithium and Demadex has not been studied.
  • Other diuretics have been reported to increase the ototoxic potential of aminoglycoside antibiotics and of ethacrynic acid, especially in the presence of impaired renal function. These potential interactions with Demadex have not been studied.

Use in Specific Populations

Pregnancy

Pregnancy Category (FDA):

  • Pregnancy Category B
  • There was no fetotoxicity or teratogenicity in rats treated with up to 5 mg/kg/day of torsemide (on a mg/kg basis, this is 15 times a human dose of 20 mg/day; on a mg/m2 basis, the animal dose is 10 times the human dose), or in rabbits, treated with 1.6 mg/kg/day (on a mg/kg basis, 5 times the human dose of 20 mg/kg/day; on a mg/m2 basis, 1.7 times this dose). Fetal and maternal toxicity (decrease in average body weight, increase in fetal resorption and delayed fetal ossification) occurred in rabbits and rats given doses 4 (rabbits) and 5 (rats) times larger. Adequate and well-controlled studies have not been carried out in pregnant women. Because animal reproduction studies are not always predictive of human response, this drug should be used during pregnancy only if clearly needed.


Pregnancy Category (AUS):

  • Australian Drug Evaluation Committee (ADEC) Pregnancy Category

There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Torsemide (tablet) in women who are pregnant.

Labor and Delivery

  • The effect of Demadex on labor and delivery is unknown.

Nursing Mothers

  • It is not known whether Demadex is excreted in human milk. Because many drugs are excreted in human milk, caution should be exercised when Demadex is administered to a nursing woman.

Pediatric Use

Geriatic Use

  • Of the total number of patients who received Demadex in United States clinical studies, 24% were 65 or older while about 4% were 75 or older. No specific age-related differences in effectiveness or safety were observed between younger patients and elderly patients.

Gender

There is no FDA guidance on the use of Torsemide (tablet) with respect to specific gender populations.

Race

There is no FDA guidance on the use of Torsemide (tablet) with respect to specific racial populations.

Renal Impairment

There is no FDA guidance on the use of Torsemide (tablet) in patients with renal impairment.

Hepatic Impairment

There is no FDA guidance on the use of Torsemide (tablet) in patients with hepatic impairment.

Females of Reproductive Potential and Males

There is no FDA guidance on the use of Torsemide (tablet) in women of reproductive potentials and males.

Immunocompromised Patients

There is no FDA guidance one the use of Torsemide (tablet) in patients who are immunocompromised.

Administration and Monitoring

Administration

  • Oral
  • Demadex tablets may be given at any time in relation to a meal, as convenient. Special dosage adjustment in the elderly is not necessary.

Monitoring

Electrolytes
  • Periodic monitoring of serum potassium and other electrolytes is advised in patients treated with Demadex.

IV Compatibility

There is limited information regarding IV Compatibility of Torsemide (tablet) in the drug label.

Overdosage

Acute Overdose

Signs and Symptoms

Management

  • No data are available to suggest physiological maneuvers (e.g., maneuvers to change the pH of the urine) that might accelerate elimination of torsemide and its metabolites. Torsemide is not dialyzable, so hemodialysis will not accelerate elimination.

Chronic Overdose

There is limited information regarding Chronic Overdose of Torsemide (tablet) in the drug label.

Pharmacology

Template:Px
Template:Px
Torsemide (tablet)
Systematic (IUPAC) name
N-[(isopropylamino)carbonyl]-4-[(3-methylphenyl)amino]pyridine-3-sulfonamide
Identifiers
CAS number 56211-40-6
ATC code C03CA04
PubChem 41781
DrugBank DB00214
Chemical data
Formula Template:OrganicBox atomTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox atomTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBoxTemplate:OrganicBox 
Mol. mass 348.421 g/mol
SMILES eMolecules & PubChem
Pharmacokinetic data
Bioavailability 80-90%
Protein binding Highly bound (>99%).
Metabolism Hepatic (80%)
Half life 3.5 hours; Cirrhosis: 7-8 hours
Excretion ?
Therapeutic considerations
Pregnancy cat.

C(US)

Legal status

[[Prescription drug|Template:Unicode-only]](US)

Routes Oral, IV

Mechanism of Action

  • Micropuncture studies in animals have shown that torsemide acts from within the lumen of the thick ascending portion of the loop of Henle, where it inhibits the Na+/K+/2CI--carrier system. Clinical pharmacology studies have confirmed this site of action in humans, and effects in other segments of the nephron have not been demonstrated. Diuretic activity thus correlates better with the rate of drug excretion in the urine than with the concentration in the blood.
  • Torsemide increases the urinary excretion of sodium, chloride, and water, but it does not significantly alter glomerular filtration rate, renal plasma flow, or acid-base balance.

Structure

  • Demadex® (torsemide) is a diuretic of the pyridine-sulfonylurea class. Its chemical name is 1-isopropyl-3-[(4-m-toluidino-3-pyridyl) sulfonyl] urea and its structural formula is:
This image is provided by the National Library of Medicine.
  • Its empirical formula is C16H20N4O3S, its pKa is 7.1, and its molecular weight is 348.43.
  • Torsemide is a white to off-white crystalline powder. The tablets for oral administration also contain lactose NF, crospovidone NF, povidone USP, microcrystalline cellulose NF, and magnesium stearate NF.

Pharmacodynamics

There is limited information regarding Pharmacodynamics of Torsemide (tablet) in the drug label.

Pharmacokinetics

  • The bioavailability of Demadex tablets is approximately 80%, with little intersubject variation; the 90% confidence interval is 75% to 89%. The drug is absorbed with little first-pass metabolism, and the serum concentration reaches its peak (Cmax) within 1 hour after oral administration. Cmax and area under the serum concentration-time curve (AUC) after oral administration are proportional to dose over the range of 2.5 mg to 200 mg. Simultaneous food intake delays the time to Cmax by about 30 minutes, but overall bioavailability (AUC) and diuretic activity are unchanged. Absorption is essentially unaffected by renal or hepatic dysfunction.
  • The volume of distribution of torsemide is 12 liters to 15 liters in normal adults or in patients with mild to moderate renal failure or congestive heart failure. In patients with hepatic cirrhosis, the volume of distribution is approximately doubled.
  • In normal subjects the elimination half-life of torsemide is approximately 3.5 hours. Torsemide is cleared from the circulation by both hepatic metabolism (approximately 80% of total clearance) and excretion into the urine (approximately 20% of total clearance in patients with normal renal function). The major metabolite in humans is the carboxylic acid derivative, which is biologically inactive. Two of the lesser metabolites possess some diuretic activity, but for practical purposes metabolism terminates the action of the drug.
  • Because torsemide is extensively bound to plasma protein (>99%), very little enters tubular urine via glomerular filtration. Most renal clearance of torsemide occurs via active secretion of the drug by the proximal tubules into tubular urine.
  • In patients with decompensated congestive heart failure, hepatic and renal clearance are both reduced, probably because of hepatic congestion and decreased renal plasma flow, respectively. The total clearance of torsemide is approximately 50% of that seen in healthy volunteers, and the plasma half-life and AUC are correspondingly increased. Because of reduced renal clearance, a smaller fraction of any given dose is delivered to the intraluminal site of action, so at any given dose there is less natriuresis in patients with congestive heart failure than in normal subjects.
  • In patients with renal failure, renal clearance of torsemide is markedly decreased but total plasma clearance is not significantly altered. A smaller fraction of the administered dose is delivered to the intraluminal site of action, and the natriuretic action of any given dose of diuretic is reduced. A diuretic response in renal failure may still be achieved if patients are given higher doses. The total plasma clearance and elimination half-life of torsemide remain normal under the conditions of impaired renal function because metabolic elimination by the liver remains intact.
  • In patients with hepatic cirrhosis, the volume of distribution, plasma half-life, and renal clearance are all increased, but total clearance is unchanged.
  • The pharmacokinetic profile of torsemide in healthy elderly subjects is similar to that in young subjects except for a decrease in renal clearance related to the decline in renal function that commonly occurs with aging. However, total plasma clearance and elimination half-life remain unchanged.

Nonclinical Toxicology

  • No overall increase in tumor incidence was found when torsemide was given to rats and mice throughout their lives at doses up to 9 mg/kg/day (rats) and 32 mg/kg/day (mice). On a body-weight basis, these doses are 27 to 96 times a human dose of 20 mg; on a body-surface-area basis, they are 5 to 8 times this dose. In the rat study, the high-dose female group demonstrated renal tubular injury, interstitial inflammation, and a statistically significant increase in renal adenomas and carcinomas. The tumor incidence in this group was, however, not much higher than the incidence sometimes seen in historical controls. Similar signs of chronic non-neoplastic renal injury have been reported in high-dose animal studies of other diuretics such as furosemide and hydrochlorothiazide.
  • No mutagenic activity was detected in any of a variety of in vivo and in vitro tests of torsemide and its major human metabolite. The tests included the Ames test in bacteria (with and without metabolic activation), tests for chromosome aberrations and sister chromatid exchanges in human lymphocytes, tests for various nuclear anomalies in cells found in hamster and murine bone marrow, tests for unscheduled DNA synthesis in mice and rats, and others.
  • In doses up to 25 mg/kg/day (75 times a human dose of 20 mg on a body-weight basis; 13 times this dose on a body-surface-area basis), torsemide had no adverse effect on the reproductive performance of male or female rats.

Clinical Studies

  • With oral dosing, the onset of diuresis occurs within 1 hour and the peak effect occurs during the first or second hour and diuresis lasts about 6 to 8 hours. In healthy subjects given single doses, the dose-response relationship for sodium excretion is linear over the dose range of 2.5 mg to 20 mg. The increase in potassium excretion is negligible after a single dose of up to 10 mg and only slight (5 mEq to 15 mEq) after a single dose of 20 mg.
Congestive Heart Failure
  • Demadex has been studied in controlled trials in patients with New York Heart Association Class II to Class IV congestive heart failure. Patients who received 10 mg to 20 mg of daily Demadex in these studies achieved significantly greater reductions in weight and edema than did patients who received placebo.
Nonanuric Renal Failure
  • In single-dose studies in patients with nonanuric renal failure, high doses of Demadex (20 mg to 200 mg) caused marked increases in water and sodium excretion. In patients with nonanuric renal failure, severe enough to require hemodialysis, chronic treatment with up to 200 mg of daily Demadex has not been shown to change steady-state fluid retention. When patients in a study of acute renal failure received total daily doses of 520 mg to 1200 mg of Demadex, 19% experienced seizures. Ninety-six patients were treated in this study; 6/32 treated with torsemide experienced seizures, 6/32 treated with comparably high doses of furosemide experienced seizures, and 1/32 treated with placebo experienced a seizure.
Hepatic Cirrhosis
  • When given with aldosterone antagonists, Demadex also caused increases in sodium and fluid excretion in patients with edema or ascites due to hepatic cirrhosis. Urinary sodium excretion rate relative to the urinary excretion rate of Demadex is less in cirrhotic patients than in healthy subjects (possibly because of the hyperaldosteronism and resultant sodium retention that are characteristic of portal hypertension and ascites). However, because of the increased renal clearance of Demadex in patients with hepatic cirrhosis, these factors tend to balance each other, and the result is an overall natriuretic response that is similar to that seen in healthy subjects. Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.
Essential Hypertension
  • In patients with essential hypertension, Demadex has been shown in controlled studies to lower blood pressure when administered once a day at doses of 5 mg to 10 mg. The antihypertensive effect is near maximal after 4 to 6 weeks of treatment, but it may continue to increase for up to 12 weeks. Systolic and diastolic supine and standing blood pressures are all reduced. There is no significant orthostatic effect, and there is only a minimal peak-trough difference in blood pressure reduction.
  • The antihypertensive effects of Demadex are, like those of other diuretics, on the average greater in black patients (a low-renin population) than in nonblack patients.
  • When Demadex is first administered, daily urinary sodium excretion increases for at least a week. With chronic administration, however, daily sodium loss comes into balance with dietary sodium intake. If the administration of Demadex is suddenly stopped, blood pressure returns to pretreatment levels over several days, without overshoot.
  • Demadex has been administered together with β-adrenergic blocking agents, ACE inhibitors, and calcium-channel blockers. Adverse drug interactions have not been observed, and special dosage adjustment has not been necessary.

How Supplied

  • Demadex for oral administration is available as white, scored tablets containing 5 mg, 10 mg, 20 mg, or 100 mg of torsemide. The tablets are supplied in bottles of 100 as follows:
This image is provided by the National Library of Medicine.
  • Each tablet is debossed on the scored side with the Boehringer Manheim logo and 102, 103, 104, or 105 (for 5 mg, 10 mg, 20 mg, or 100 mg, respectively). On the opposite side, the tablet is debossed with 5, 10, 20, or 100 to indicate the dose.
  • Storage
  • Store at 15° to 30°C (59° to 86°F).

Storage

There is limited information regarding Torsemide (tablet) Storage in the drug label.

Images

Drug Images

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Package and Label Display Panel

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Patient Counseling Information

There is limited information regarding Patient Counseling Information of Torsemide (tablet) in the drug label.

Precautions with Alcohol

  • Alcohol-Torsemide (tablet) interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.

Brand Names

Look-Alike Drug Names

Drug Shortage Status

Price

References

The contents of this FDA label are provided by the National Library of Medicine.

  1. ↑ "Demadex (torsemide) tablet".
  2. ↑ "http://www.ismp.org". External link in |title= (help)

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