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What is Demadex (torsemide)?
Demadex (torsemide) is a “loop” diuretic (water pill) used to treat edema (water retention) due to congestive heart failure, kidney disease, chronic kidney failure, or liver disease. Demadex also is used alone or combined with other antihypertensive medications to treat high blood pressure (hypertension).
Demadex causes a profound increase in urine output (diuresis) by preventing the kidney from retaining water. It blocks the reabsorption back into the blood of sodium and water that has been filtered out of the blood by the kidneys.
The potent diuretic effect of Demadex can cause the loss of large amounts of body water leading to dehydration as well as the loss of electrolytes (for example, sodium, potassium, magnesium, and calcium). Careful medical supervision is necessary during treatment.
Common side effects of Demadex include:
- excessive urination,
- runny nose,
- ECG abnormality,
- joint pain,
- stomach upset,
- sore throat,
- muscle pain,
- fluid retention (edema), and
Serious side effects of Demadex include:
- atrial fibrillation,
- chest pain,
- gastrointestinal bleeding,
- high blood sugar (hyperglycemia),
- increased uric acid,
- low blood potassium (hypokalemia),
- low blood pressure (hypotension),
- dehydration (symptoms include dry mouth, thirst, weakness, drowsiness, reduced kidney function, heart arrhythmias, muscle aches and pains, nausea, vomiting),
- blood clot in shunt,
- rectal bleeding,
- fast heart rate,
- serious skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis),
- allergic reactions,
- reduced number of white blood cells and platelets, and
- ringing in the ears (tinnitus) and reversible hearing loss.
Combining Demadex with other diuretics can exaggerate the losses of potassium and magnesium.
The body’s ability to eliminate lithium may decrease when taken with Demadex.
Use of Demadex and aminoglycosides may increase the risk of hearing impairment.
Probenecid decreases the diuretic effect of Demadex by reducing secretion of torsemide into the kidney tubules.
What are the important side effects of Demadex (torsemide)?
Potent medication like torsemide can cause low blood levels of potassium, magnesium, sodium, and calcium. Additionally, fluid losses may lead to dehydration. The symptoms of dehydration may include:
- Dry mouth
- Reduced kidney function
- Heart arrhythmias
- Muscle aches and pains
Possible side effects of this medication reported often include:
- Excessive urination
- Runny nose
- ECG abnormality
- Joint pain
- Stomach upset
- Sore throat
- Muscle pain
Possible serious side effects and adverse effects include:
- Atrial fibrillation
- Chest pain
- Gastrointestinal bleeding
- High blood sugar (hyperglycemia)
- Increased uric acid (hyperuricemia)
- Low blood potassium (hypokalemia)
- Low blood pressure (hypotension)
- Dehydration (symptoms listed previously)
- Shunt thrombosis
- Rectal bleeding
- Ventricular tachycardia
- Serious skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis)
- Allergic reactions
- Reduced number of white blood cells and platelets
Demadex can cause dehydration and loss of potassium and other electrolytes. Low potassium levels (hypokalemia) can cause abnormal heartbeats especially in people with heart disease or those taking the medicine digoxin (Lanoxin). Levels of potassium and other electrolytes should be monitored during medical treatment with this medicine.
Demadex (torsemide) side effects list for healthcare professionals
The following risks are discussed in more detail in others sections:
Clinical Trials 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.
In pre-approval studies, Demadex has 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.
Discontinuation of therapy due to adverse reactions occurred in 3.5% of United States patients treated with Demadex and in 4.4% of patients treated with placebo.
In United States placebo-controlled trials excessive urination occurred in 6.7% of patients compared with 2.2% of patients receiving placebo. 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.
In the placebo-controlled hypertension studies excessive urination was dose related; 1% of patients receiving placebo, 4% of those treated with 5 mg of daily Demadex, and 15% of those treated with 10 mg. Excessive urination was generally not reported as an adverse event among patients who received Demadex for cardiac, renal, or hepatic failure.
There was no effect of age or sex on the incidence of adverse reactions.
In controlled studies in the United States, Demadex was administered to hypertensive patients at doses of 5 mg or 10 mg daily. After 6 weeks at these doses, the mean decrease in serum potassium was approximately 0.1 mEq/L. The percentage of patients who had a serum potassium level below 3.5 mEq/L at any time during the studies was 1.5% on Demadex and 3% on placebo.
In patients followed for 1 year, there was no progressive change in mean serum potassium levels. In patients with congestive heart failure, hepatic cirrhosis, or renal disease treated with Demadex at doses higher than those studied in United States antihypertensive trials, hypokalemia was observed with greater frequency, in a dose-related manner.
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.
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.
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 estimate their frequency reliably or establish a causal relationship to drug exposure.
Gastrointestinal system: Pancreatitis, abdominal pain
Hepatobiliary: Increase in liver transaminases, gamma-glutamyltransferase
Metabolism: Thiamine (vitamin B1) deficiency
Skin/hypersensitivity: Stevens-Johnson syndrome, toxic epidermal necrolysis, photosensitivity reaction, pruritus
Urogenital: Acute urinary retention
What drugs interact with Demadex (torsemide)?
Nonsteroidal Anti-Inflammatory Drugs
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.
Concomitant use of nonsteroidal anti-inflammatory drugs (NSAIDs) and torsemide has been associated with the development of acute renal failure. The antihypertensive and diuretic effects of Demadex can be reduced by NSAIDs.
Partial inhibition of the natriuretic effect of Demadex by concomitant administration of indomethacin 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).
Cytochrome P450 2C9 Inhibitors And Inducers
Torsemide is a substrate of CYP2C9. Concomitant use of CYP2C9 inhibitors (e.g., amiodarone, fluconazole, miconazole, oxandrolone) can decrease torsemide clearance and increase torsemide plasma concentrations. Concomitant use of CYP2C9 inducers (e.g., rifampin) increase torsemide clearance and decrease plasma torsemide concentrations. Monitor diuretic effect and blood pressure when used in combination with CYP2C9 inhibitor or inducer. Adjust torsemide dose if necessary.
Because of its inhibition of CYP2C9 metabolism, torsemide may affect the efficacy and safety of sensitive CYP2C9 substrates, such as celecoxib, or of substrates with a narrow therapeutic range, such as warfarin or phenytoin. Monitor patients and adjust dosages if 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 should be coadministered, administer Demadex at least one hour before or 4 to 6 h after cholestyramine administration.
Organic Anion Drugs
Coadministration of organic anion drugs (e.g., probenecid) that undergo significant renal tubular secretion have the potential to reduce secretion of Demadex into the proximal tubule and thereby decreases the diuretic activity of Demadex. Monitor diuretic effect and blood pressure during coadministration.
Like other diuretics, torsemide reduces the renal clearance of lithium, inducing a high risk of lithium toxicity. Monitor lithium levels periodically when torsemide is coadministered.
Loop diuretics increase the ototoxic potential of other ototoxic drugs, including aminoglycoside antibiotics and ethacrynic acid. This effect has been reported with concomitant use of torsemide and gentamycin. Avoid concomitant use of Demadex and aminoglycoside antibiotics, if possible.
Coadministration of Demadex with ACE inhibitors or angiotensin receptor blockers can increase the risk of hypotension and renal impairment.
Demadex can increase the risk of renal toxicity related to administration of radiocontrast agents.
Corticosteroids And ACTH
Concomitant use with Demadex may increase risk of hypokalemia
Demadex (torsemide) is a “loop” diuretic (water pill) used to treat edema (water retention) due to congestive heart failure, kidney disease, chronic kidney failure, or liver disease. Demadex also is used alone or combined with other antihypertensive medications to treat high blood pressure (hypertension). Common side effects of Demadex include headache, excessive urination, dizziness, runny nose, weakness, diarrhea, ECG abnormality, cough, constipation, nausea, joint pain, stomach upset, sore throat, muscle pain, insomnia, fluid retention (edema), and nervousness. The safety of Demadex in pregnant women has not been established. It is unknown if Demadex is excreted in human milk.
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High Blood Pressure (Hypertension) Signs, Causes, Diet, and Treatment
High blood pressure (hypertension) is a disease in which pressure within the arteries of the body is elevated. About 75 million people in the US have hypertension (1 in 3 adults), and only half of them are able to manage it. Many people do not know that they have high blood pressure because it often has no has no warning signs or symptoms. Systolic and diastolic are the two readings in which blood pressure is measured. The American College of Cardiology released new guidelines for high blood pressure in 2017. The guidelines now state that blood normal blood pressure is 120/80 mmHg. If either one of those numbers is higher, you have high blood pressure. The American Academy of Cardiology defines high blood pressure slightly differently. The AAC considers 130/80 mm Hg. or greater (either number) stage 1 hypertension. Stage 2 hypertension is considered 140/90 mm Hg. or greater. If you have high blood pressure you are at risk of developing life threatening diseases like stroke and heart attack.REFERENCE: CDC. High Blood Pressure. Updated: Nov 13, 2017.
Pulmonary hypertension is elevated pressure in the pulmonary arteries that carry blood from the lungs to the heart. The most common symptoms are fatigue and difficulty breathing. If the condition goes undiagnosed, more severe symptoms may occur. As pulmonary hypertension worsens, some people with the condition have difficulty performing any activities that require physical exertion. While there is no cure for pulmonary hypertension, it can be managed and treated with medications and supplemental oxygen to increase blood oxygen levels.
Congestive Heart Failure (CHF) Symptoms, Treatment, and Life Expectancy
Congestive heart failure (CHF) refers to a condition in which the heart loses the ability to function properly. Heart disease, high blood pressure, diabetes, myocarditis, and cardiomyopathies are just a few potential causes of congestive heart failure. Signs and symptoms of congestive heart failure may include fatigue, breathlessness, palpitations, angina, and edema. Physical examination, patient history, blood tests, and imaging tests are used to diagnose congestive heart failure. Treatment of heart failure consists of lifestyle modification and taking medications to decrease fluid in the body and ease the strain on the heart. The prognosis of a patient with congestive heart failure depends on the stage of the heart failure and the overall condition of the individual.
Pseudotumor Cerebri (Idiopathic Intracranial Hypertension)
Pseudotumor Cerebri (intracranial hypertension) is a condition where there is an increase in pressure of fluid surrounding the brain and spinal cord (cerebrospinal fluid or CSF) mimicing a brain tumor. The cause is unknown. The most common symptom is headache but also include eye-pain, vision loss and double vision. Pseudotumor cerebri is diagnosed with MRI or CAT scans and treated by discontinuing offending medications (if applicable), weight loss and diuretic medications. The condition can also be helped by repeated drainage of spinal fluid using the lumbar puncture.
Preeclampsia (Pregnancy Induced Hypertension)
Preeclampsia is related to increased blood pressure and protein in the mother's urine. Preeclampsia typically begins after the 20th week of pregnancy. When preeclampsia causes seizures, it is termed "eclampsia" and is the second leading cause of maternal death of in the US. Preeclampsia is the leading cause of fetal complications. Risk factors for preeclampsia include high blood pressure, obesity, multiple births, and women with preexisting medical conditions such as diabetes, kidney disease, rheumatoid arthritis, lupus, or scleroderma. Pregnancy planning and lifestyle changes may reduce the risk of preeclampsia during pregnancy.
Kidney (Renal) Failure
Kidney failure can occur from an acute event or a chronic condition or disease. Prerenal kidney failure is caused by blood loss, dehydration, or medication. Some of the renal causes of kidney failure include sepsis, medications, rhabdomyolysis, multiple myeloma, and acute glomerulonephritis. Post renal causes of kidney failure include bladder obstruction, prostate problems, tumors, or kidney stones.Treatment options included diet, medications, or dialysis.
Portal hypertension is most commonly caused by cirrhosis, a disease that results from scarring of the liver. Other causes of portal hypertension include blood clots in the portal vein, blockages of the veins that carry the blood from the liver to the heart, and a parasitic infection called schistosomiasis. Symptoms of portal hypertension include varices (enlarged veins), vomiting blood, blood in the stool, black and tarry stool, ascites (abnormal fluid collection within the peritoneum, the sac that contains the intestines within the abdominal cavity), confusion and lethargy, splenomegaly or enlargement of the spleen, and decreased white blood cell counts.
Hypertensive Kidney Disease
High blood pressure can damage the kidneys and is one of the leading causes of kidney failure (end-stage renal kidney disease). Kidney damage, like hypertension, can be unnoticeable and detected only through medical tests. If you have kidney disease, you should control your blood pressure. Other treatment options include prescription medications.
Heart failure (congestive) is caused by many conditions including coronary artery disease, heart attack, cardiomyopathy, and conditions that overwork the heart. Symptoms of heart failure include congested lungs, fluid and water retention, dizziness, fatigue and weakness, and rapid or irregular heartbeats. There are two types of congestive heart failure, systolic or left-sided heart failure; and diastolic or right-sided heart failure. Treatment, prognosis, and life-expectancy for a person with congestive heart failure depends upon the stage of the disease.
Drug-Induced Liver Disease
Drug-induced liver diseases are diseases of the liver that are caused by: physician-prescribed medications, OTC medications, vitamins, hormones, herbs, illicit (recreational) drugs, and environmental toxins. Read about the signs and symptoms of drug-induced liver disease like hepatitis (inflammation of the liver cells), liver disease treatment, and types.
Liver disease can be cause by a variety of things including infection (hepatitis), diseases, for example, gallstones, high cholesterol or triglycerides, blood flow obstruction to the liver, and toxins (medications and chemicals). Symptoms of liver disease depends upon the cause and may include nausea, vomiting, upper right abdominal pain, and jaundice. Treatment depends upon the cause of the liver disease.
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Medications & Supplements
Report Problems to the Food and Drug Administration
You are encouraged to report negative side effects of prescription drugs to the FDA. Visit the FDA MedWatch website or call 1-800-FDA-1088.
Professional side effects and drug interactions sections courtesy of the U.S. Food and Drug Administration.