Label: saluron- hydroflumenthiazide tablet

Usage In Pregnancy

The routine use of diuretics in an otherwise healthy woman is inappropriate and exposes mother and fetus to unnecessary risk. 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 Warnings 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 the 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.

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, including ACTH.

Interference with adequate oral electrolyte intake will also contribute to hypokalemia. Digitalis therapy may exaggerate the metabolic effects of hypokalemia, especially with respect 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.

Thiazide drugs may increase the responsiveness to tubocurarine.

The antihypertensive effects of the drug may be enhanced in the postsympathectomy patient.

Thiazides may decrease arterial responsiveness to norepinephrine. This diminution is not sufficient to preclude effectiveness of the pressor agent for therapeutic use.

If progressive renal impairment becomes evident, as indicated by rising nonprotein nitrogen 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 Saluron®.

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.

Other antihypertensive medications, especially diazoxide; pre-anesthetic and anesthetic agents used in surgery; 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, including 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.

Diagnostic Interference

With expected physiologic effects.

Blood and urine glucose levels: usually only in patients with a predisposition to glucose intolerance.

Serum bilirubin levels: displacement from albumin binding.

Serum calcium levels: thiazide diuretics should be discontinued before parathyroid function tests are carried out.

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.

Carcinogenesis, Mutagenesis, Impairment of Fertility

No long-term studies in animals have been performed to evaluate carcinogenic or mutagenic potential or impairment of fertility.

Pregnancy

Pregnancy Category D. See "WARNINGS"Section.

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 of 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.