-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.
INDICATIONS AND USAGE
DEMADEX is indicated for the treatment of edema associated with congestive heart failure, renal disease, or hepatic disease. Use of torsemide has been found to be effective for the treatment of edema associated with chronic renal failure. Chronic use of any diuretic in hepatic disease has not been studied in adequate and well-controlled trials.
DEMADEX is indicated for the treatment of hypertension alone or in combination with other antihypertensive agents.
CONTRAINDICATIONS
DEMADEX is contraindicated in patients with known hypersensitivity to DEMADEX or to sulfonylureas.
DEMADEX is contraindicated in patients who are anuric.
WARNINGS
Hepatic Disease With Cirrhosis and Ascites
DEMADEX should be used with caution in patients with hepatic disease with cirrhosis and ascites, since sudden alterations of fluid and electrolyte balance may precipitate hepatic coma. In these patients, diuresis with DEMADEX (or any other diuretic) is best initiated in the hospital. To prevent hypokalemia and metabolic alkalosis, an aldosterone antagonist or potassium-sparing drug should be used concomitantly with DEMADEX.
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
Patients receiving diuretics should be observed for clinical evidence of electrolyte imbalance, hypovolemia, or prerenal azotemia. Symptoms of these disturbances may include one or more of the following: dryness of the mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, nausea, and vomiting. Excessive diuresis may cause dehydration, blood-volume reduction, and possibly thrombosis and embolism, especially in elderly patients. In patients who develop fluid and electrolyte imbalances, hypovolemia, or prerenal azotemia, the observed laboratory cha |
