Enter drug's generic or brand name below. Results will appear here. Note: all drug related information obtained on this page is provided by RX List.
Using the RX LIST database:
(1) Enter the drug name in the search box below and hit ENTER
(2) The rx list web site will open here with the drug search completed. Next, scroll down the page to locate the link to the drug you are searching for and then click on the link.
Diucardin (hydroflumethiazide) is an oral thiazide (benzothiadiazide) diuretic-antihypertensive agent.
Diucardin (hydroflumethiazide) is available as 50 mg tablets for oral administration.
Chemical name: 3,4-Dihydro-6-(trifluoromethyl)-2H-1,2,4- benzothiadiazine-7-sulfonamide 1,1-dioxide.
Hydroflumethiazide is an odorless white to cream-colored, finely divided, crystalline powder. It has a melting point between 270° and 275° C. Hydroflumethiazide is freely soluble in acetone, soluble in alcohol, and very slightly soluble in water.
The inactive ingredients contained in Diucardin (hydroflumethiazide) tablets are: lactose, magnesium stearate, microcrystalline cellulose, povidone, and starch.
Diucardin (hydroflumethiazide) is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy.
Diucardin (hydroflumethiazide) has also been found useful in edema due to various forms of renal dysfunction such as: nephrotic syndrome; acute glomerulonephritis; and chronic renal failure.
Diucardin (hydroflumethiazide) is indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effect of other antihypertensive drugs in the more severe forms of hypertension.
USAGE IN PREGNANCY
The routine use of diuretics in an otherwise healthy woman is inappropriate and exposes mother and fetus to unnecessary hazard. Diuretics do not prevent development of toxemia of pregnancy, and there is no satisfactory evidence that they are useful in the treatment of developed toxemia.
Edema during pregnancy may arise from pathological causes or from the physiologic and mechanical consequences of pregnancy. Thiazides are indicated in pregnancy when edema is due to pathologic causes just as they are in the absence of pregnancy (however, see " PRECAUTIONS PREGNANCY" below).
Dependent edema in pregnancy, resulting from restriction of venous return by the expanded uterus, is properly treated through elevation of the lower extremities and use of support hose. Use of diuretics to lower intravascular volume in this case is illogical and unnecessary. There is hypervolemia during normal pregnancy which is harmful to neither the fetus nor the mother (in absence of cardiovascular disease), but which is associated with edema, including generalized edema, in the majority of pregnant women. If this edema produces discomfort, increased recumbency will often provide relief. In rare instances, this edema may cause extreme discomfort which is not relieved by rest. In these cases, a short course of diuretics may provide relief and may be appropriate.
The average adult diuretic dose is 25 to 200 mg per day. The average adult antihypertensive dose is 50 to 100 mg per day.
Therapy should be individualized according to patient response. This therapy should be titrated to gain maximal response as well as the minimal dose possible to maintain that therapeutic response.
Diucardin (hydroflumethiazide) ® Each scored, white oval compressed tablet, inscribed "DIUCARDIN 50," contains 50 mg hydroflumethiazide, in bottles of 100 (NDC 0046-0702-81).
Dispense in a well-closed container as defined in the USP
Caution: Federal law prohibits dispensing without prescription.
Manufactured by:
Ayerst Laboratories Inc.
A Wyeth-Ayerst Company
Philadelphia, PA 19101
The following adverse reactions have been observed, but there is not enough systematic collection of data to support an estimate of their frequency.
GASTROINTESTINAL SYSTEMS
Anorexia, gastric irritation, nausea, vomiting, cramping, diarrhea, constipation, jaundice (intrahepatic cholestatic jaundice), pancreatitis, sialadenitis.
CENTRAL NERVOUS SYSTEM
Dizziness, vertigo, paresthesias, headache, xanthopsia.
HEMATOLOGIC
Leukopenia, agranulocytosis, thrombocytopenia, aplastic anemia, hemolytic anemia.
CARDIOVASCULAR
Orthostatic hypotension (may be aggravated by alcohol, barbiturates, or narcotics).
DERMATOLOGIC HYPERSENSITIVITY
Purpura, photosensitivity, rash, urticaria, necrotizing angiitis (vasculitis, cutaneous vasculitis), fever, respiratory distress including pneumonitis, anaphylactic reactions.
OTHER
Hyperglycemia, glycosuria, hyperuricemia, muscle spasm, weakness, restlessness, transient blurred vision.
Whenever adverse reactions are moderate or severe, thiazide dosage should be reduced or therapy withdrawn.
Anticoagulants, oral
(Effects may be decreased when used concurrently with thiazide diuretics; dosage adjustments may be necessary.)
Antigout medications
(Thiazide diuretics may raise the level of blood uric acid; dosage adjustment of antigout medications may be necessary to control hyperuricemia and gout.)
Antihypertensive medications, other, especially diazoxide, or preanesthetic and anesthetic agents used in surgery or skeletal-muscle relaxants, nondepolarizing, used in surgery
(Effects may be potentiated when used concurrently with thiazide diuretics; dosage adjustments may be necessary.)
Amphotericin B or Corticosteroids or Corticotropin (ACTH)
(Concurrent use with thiazide diuretics may intensify electrolyte imbalance, particularly hypokalemia.)
Cardiac glycosides
(Concurrent use with thiazide diuretics may enhance the possibility of digitalis toxicity associated with hypokalemia.)
Colestipol
(May inhibit gastrointestinal absorption of the thiazide diuretics; administration 1 hour before or 4 hours after colestipol is recommended.)
Hypoglycemics
(Thiazide diuretics may raise blood glucose levels; for adult-onset diabetics, dosage adjustment of hypoglycemic medications may be necessary during and after thiazide diuretic therapy; insulin requirements may be increased, decreased, or unchanged.)
Lithium salts
(Concurrent use with thiazide diuretics is not recommended, as they may provoke lithium toxicity because of reduced renal clearance.)
Methenamine
(Effectiveness may be decreased when used concurrently with thiazide diuretics because of alkalinization of the urine.)
Nonsteroidal anti-inflammatory agents
(In some patients, the steroidal anti-inflammatory agent can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium sparing, and thiazide diuretics. Therefore, when hydroflumethiazide and nonsteroidal anti-inflammatory agents are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained.)
Norepinephrine
(Thiazides may decrease arterial responsiveness to norepinephrine. This diminution is not sufficient to preclude effectiveness of the pressor agent for therapeutic use.)
Tubocurarine
(Thiazide drugs may increase the responsiveness to tubocurarine.)
DIAGNOSTIC INTERFERENCE With expected physiologic effects:
Blood and urine glucose levels (usually only in patients with a predisposition for glucose intolerance) and
Serum bilirubin levels (by displacement from albumin binding) and
Serum calcium levels (thiazide diuretics should be discontinued before parathyroid-function tests are carried out) and
Serum uric acid levels (may be increased)
Serum magnesium, potassium, and sodium levels (may be decreased; serum magnesium levels may increase in uremic patients)
Serum protein-bound iodine (PBI) levels (may be decreased)
Thiazides should be discontinued before carrying out tests for parathyroid function (see " PRECAUTIONS GENERAL, Calcium excretion").
Diucardin (hydroflumethiazide) should be used with caution in severe renal disease. In patients with renal disease, thiazides may precipitate azotemia. Cumulative effects of the drug may develop in patients with impaired renal function.
Thiazides should be used with caution in patients with impaired hepatic function or progressive liver disease, since minor alterations of fluid and electrolyte balance may precipitate hepatic coma.
Thiazides may add to or potentiate the action of other antihypertensive drugs. Potentiation occurs with ganglionic or peripheral adrenergic blocking drugs.
Sensitivity reactions may occur in patients with a history of allergy or bronchial asthma.
The possibility of exacerbation or activation of systemic lupus erythematosus has been reported.
GENERAL
All patients receiving thiazide therapy should be observed for clinical signs of fluid or electrolyte imbalance; namely, hyponatremia, hypochloremic alkalosis, and hypokalemia. Serum and urine electrolyte determinations are particularly important when the patient is vomiting excessively or receiving parenteral fluids. Medication such as digitalis may also influence serum electrolytes. Warning signs, irrespective of cause, are: dryness of mouth, thirst, weakness, lethargy, drowsiness, restlessness, muscle pains or cramps, muscular fatigue, hypotension, oliguria, tachycardia, and gastrointestinal disturbances such as nausea and vomiting.
Hypokalemia may develop with thiazides as with any other potent diuretic, especially with brisk diuresis, when severe cirrhosis is present, or during concomitant use of corticosteroids or ACTH.
Interference with adequate oral electrolyte intake will also contribute to hypokalemia. Digitalis therapy may exaggerate metabolic effects of hypokalemia, especially with reference to myocardial activity.
Any chloride deficit is generally mild and usually does not require specific treatment except under extraordinary circumstances (as in liver disease or renal disease). Dilutional hyponatremia may occur in edematous patients in hot weather; appropriate therapy is water restriction, rather than administration of salt, except in rare instances when the hyponatremia is life-threatening. In actual salt depletion, appropriate replacement is the therapy of choice.
Hyperuricemia may occur or frank gout may be precipitated in certain patients receiving thiazide therapy.
Insulin requirements in diabetic patients may be increased, decreased, or unchanged. Latent diabetes mellitus may become manifested during thiazide administration.
The antihypertensive effects of the drug may be enhanced in the post-sympathectomy patient.
If progressive renal impairment becomes evident, as indicated by a rising creatinine or blood urea nitrogen, a careful reappraisal of therapy is necessary with consideration given to withholding or discontinuing diuretic therapy.
Thiazides may decrease serum PBI levels without signs of thyroid disturbance.
Lithium generally should not be given with diuretics because they reduce its renal clearance and increase the risk of lithium toxicity. Read circulars for lithium preparations before use of such concomitant therapy with Diucardin (hydroflumethiazide) .
Thiazides have been shown to increase the urinary excretion of magnesium; this may result in hypomagnesemia.
Calcium excretion is decreased by thiazides. Pathological changes in the parathyroid gland with hypercalcemia and hypophosphatemia have been observed in a few patients on prolonged thiazide therapy. The common complications of hyperparathyroidism, such as renal lithiasis, bone resorption, and peptic ulceration, have not been seen.
LABORATORY TESTS
Periodic determination of serum electrolytes to detect possible electrolyte imbalance should be performed at appropriate intervals.
DRUG INTERACTIONS
Anticoagulants, oral
(Effects may be decreased when used concurrently with thiazide diuretics; dosage adjustments may be necessary.)
Antigout medications
(Thiazide diuretics may raise the level of blood uric acid; dosage adjustment of antigout medications may be necessary to control hyperuricemia and gout.)
Antihypertensive medications, other, especially diazoxide, or preanesthetic and anesthetic agents used in surgery or skeletal-muscle relaxants, nondepolarizing, used in surgery
(Effects may be potentiated when used concurrently with thiazide diuretics; dosage adjustments may be necessary.)
Amphotericin B or Corticosteroids or Corticotropin (ACTH)
(Concurrent use with thiazide diuretics may intensify electrolyte imbalance, particularly hypokalemia.)
Cardiac glycosides
(Concurrent use with thiazide diuretics may enhance the possibility of digitalis toxicity associated with hypokalemia.)
Colestipol
(May inhibit gastrointestinal absorption of the thiazide diuretics; administration 1 hour before or 4 hours after colestipol is recommended.)
Hypoglycemics
(Thiazide diuretics may raise blood glucose levels; for adult-onset diabetics, dosage adjustment of hypoglycemic medications may be necessary during and after thiazide diuretic therapy; insulin requirements may be increased, decreased, or unchanged.)
Lithium salts
(Concurrent use with thiazide diuretics is not recommended, as they may provoke lithium toxicity because of reduced renal clearance.)
Methenamine
(Effectiveness may be decreased when used concurrently with thiazide diuretics because of alkalinization of the urine.)
Nonsteroidal anti-inflammatory agents
(In some patients, the steroidal anti-inflammatory agent can reduce the diuretic, natriuretic, and antihypertensive effects of loop, potassium sparing, and thiazide diuretics. Therefore, when hydroflumethiazide and nonsteroidal anti-inflammatory agents are used concomitantly, the patient should be observed closely to determine if the desired effect of the diuretic is obtained.)
Norepinephrine
(Thiazides may decrease arterial responsiveness to norepinephrine. This diminution is not sufficient to preclude effectiveness of the pressor agent for therapeutic use.)
Tubocurarine
(Thiazide drugs may increase the responsiveness to tubocurarine.)
DIAGNOSTIC INTERFERENCE With expected physiologic effects:
Blood and urine glucose levels (usually only in patients with a predisposition for glucose intolerance) and
Serum bilirubin levels (by displacement from albumin binding) and
Serum calcium levels (thiazide diuretics should be discontinued before parathyroid-function tests are carried out) and
Serum uric acid levels (may be increased)
Serum magnesium, potassium, and sodium levels (may be decreased; serum magnesium levels may increase in uremic patients)
Serum protein-bound iodine (PBI) levels (may be decreased)
Thiazides should be discontinued before carrying out tests for parathyroid function (see " PRECAUTIONS
GENERAL, Calcium excretion").
CARCINOGENESIS, MUTAGENESIS, IMPAIRMENT OF FERTILITY
No studies have been performed to evaluate carcinogenic or mutagenic potential of Diucardin (hydroflumethiazide) or the potential of Diucardin (hydroflumethiazide) to impair fertility.
PREGNANCY
Teratogenic Effects Pregnancy Category C
Animal reproduction studies have not been conducted with Diucardin (hydroflumethiazide) . It is also not known whether Diucardin (hydroflumethiazide) can cause fetal harm when administered to a pregnant woman or can affect reproduction capacity. Diucardin (hydroflumethiazide) should be given to a pregnant woman only if clearly needed.
Nonteratogenic Effects
Fetal or neonatal jaundice, thrombocytopenia, and possibly other adverse reactions which have occurred in the adult.
NURSING MOTHERS
Thiazides appear in breast milk. If use of the drug is deemed essential, the patient may consider stopping nursing.
PEDIATRIC USE
Safety and effectiveness in children have not been established.
SIGNS AND SYMPTOMS
Diuresis, lethargy progressing to coma, with minimal cardiorespiratory depression and with or without significant serum electrolyte changes or dehydration; GI irritation; hypermotility; transient elevation in BUN level.
TREATMENT
Empty stomach by gastric lavage, taking care to avoid aspiration. Monitor serum electrolyte levels and renal function, and institute supportive measures, as required to maintain hydration, electrolyte balance, respiration, and cardiovascular and renal function. Treat GI effects symptomatically.
Anuria.
Hypersensitivity to this or other sulfonamide-derived drugs.
Hydroflumethiazide is incompletely but fairly rapidly absorbed from the gastrointestinal tract. It appears to have a biphasic biological half-life with an estimated alpha-phase of about 2 hours and an estimated beta-phase of about 17 hours; it has a metabolite with a longer half-life, which is extensively bound to the red blood cells. Hydroflumethiazide is excreted in the urine; its metabolite has also been detected in the urine.
The mechanism of action results in an interference with the renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosage, all thiazides are approximately equal in their diuretic potency. The mechanism whereby thiazides function in the control of hypertension is unknown.
No Information Provided.
