LYCOS RETRIEVER 
Hydrochlorothiazide: Diuretics
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Hydrochlorothiazide may increase the toxicity of digitalis glycosides by depleting serum-potassium concentrations. Due to the potassium depletion it may enhance the neuromuscular blocking action of competitive muscle relaxants such as tubocurarine or gallamine triethiodide (Ellenhorn & Barceloux, 1988). It may increase the effect of anti-hypertensive agents such as guanethidine sulfate, methyldopa, or a ganglionic blocking agent (Ellenhorn & Barceloux, 1988; Reynolds, 1989). The postural hypotension due to thiazide diuretic therapy may be increased by concomitant ingestion of alcohol, barbiturates, or opiates (Reynolds, 1989; Barnhart, 1987). The potassium-depleting effect of thiazide diuretic may be enhanced by corticosteroids, corticotrophin, carbenoxolone, and amphotericin (Ellenhorn & Barceloux, 1988). Hydrochlorothiazide has been reported to reduce the response to pressor amines, such as noradrenaline, but the clinical significance of this effect is uncertain.
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Duration of diuretic activity and effective dosage range of the hydrochlorothiazide and triamterene components of Hydrochlorothiazide/triamterine are similar. Onset of diuresis with Hydrochlorothiazide/triamterine takes place within one hour, peaks at two to three hours and tapers off during the subsequent seven to nine hours.
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Hydrochlorothiazide is generally a very safe diuretic, as the distance between therapeutically effective and frankly toxic doses is large (Gosselin, 1984). Clinical toxicity is relatively infrequent and may result from overdosage, adverse reactions or unexpected hypersensitivity. Main risks Electrolytes imbalances that may lead to cardiac arrhythmias and orthostatic hypotension. Metabolic disturbances, such as hyperglycaemia and hyperuricaemia. Aggravation of hepatic and/or renal insufficiency Hypersensitivity reactions. Blood dyscrasias.
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