Drug Interactions between aspirin / calcium carbonate and Capozide

MONITOR: Some investigators suggest that coadministration with aspirin may attenuate the vasodilator and hypotensive effects of ACE inhibitors. In addition, some have found that the benefits of ACE inhibitors on morbidity and mortality in post-acute myocardial infarction, coronary heart disease, and particularly congestive heart failure may be compromised or even nullified by aspirin. The proposed mechanism is aspirin inhibition of cyclooxygenase, resulting in suppression of prostaglandin synthesis and prostaglandin-mediated hemodynamic effects of ACE inhibitors. However, evidence of a negative interaction is largely contradictory, and interpretation of relevant data has often been complicated by multiple confounding elements as well as the retrospective or post hoc nature of most studies. Available data seem to indicate that low-dose aspirin (less than 236 mg/day, and especially less than 100 mg/day) is unlikely, or at least significantly less likely, to interfere with ACE inhibitor effects, although susceptibility to the interaction may be subject to some degree of interpatient variability.

MANAGEMENT: Based on current data, it is difficult to determine the likelihood of a negative interaction between aspirin and ACE inhibitors and its clinical relevance during long-term therapy, particularly in congestive heart failure. Current recommendations generally do not preclude combination use in patients with cardiovascular diseases or risk factors that might otherwise benefit from the drugs independently. However, patients receiving long-term therapy with the combination should undergo regular blood pressure and other appropriate clinical monitoring such as renal function assessments. The lowest therapeutic dosage of aspirin should be used.

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MONITOR: Although they are frequently combined in clinical practice, diuretics and angiotensin converting enzyme (ACE) inhibitors may have additive effects. Coadministration makes hypotension and hypovolemia more likely than does either drug alone. Some ACE inhibitors may attenuate the increase in the urinary excretion of sodium caused by some loop diuretics. Some patients on diuretics, especially those on dialysis or a dietary salt restriction, may experience acute hypotension with lightheadedness and dizziness after receiving the first dose of the ACE inhibitor. In addition, ACE inhibitors may cause renal insufficiency or acute renal failure in patients with sodium depletion or renal artery stenosis.

MANAGEMENT: Monitoring of blood pressure, diuresis, electrolytes, and renal function is recommended during coadministration. The possibility of first-dose hypotensive effects may be minimized by initiating therapy with small doses of the ACE inhibitor, or either discontinuing the diuretic temporarily or increasing the salt intake approximately one week prior to initiating an ACE inhibitor. Alternatively, the patient may remain under medical supervision for at least two hours after the first dose of the ACE inhibitor, or until blood pressure has stabilized.

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MONITOR: Chronic administration of antacids may reduce serum salicylate concentrations in patients receiving large doses of aspirin or other salicylates. The mechanism involves reduction in salicylate renal tubular reabsorption due to urinary alkalinization by antacids, resulting in increased renal salicylate clearance. In three children treated with large doses of aspirin for rheumatic fever, serum salicylate levels declined 30% to 70% during coadministration with a magnesium and aluminum hydroxide antacid. Other studies have found similar, albeit less dramatic results. Antacids reportedly have no effect on the oral bioavailability of aspirin in healthy adults. However, administration of antacids containing either aluminum and magnesium hydroxide or calcium carbonate two hours before aspirin dosing led to reduced absorption of aspirin in uremic patients.

MANAGEMENT: Patients treated chronically with antacids (or oral medications that contain antacids such as didanosine buffered tablets or pediatric oral solution) and large doses of salicylates (i.e. 3 g/day or more) should be monitored for potentially diminished or inadequate analgesic and anti-inflammatory effects, and the salicylate dosage adjusted if necessary.

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MONITOR: Coadministration of thiazide diuretics with high dosages of calcium and/or vitamin D has been associated with reports of hypercalcemia in some patients. Thiazide diuretics inhibit the renal excretion of calcium and may also enhance responsiveness of bone and renal tubule to parathyroid hormone, thus concurrent use of large amounts of calcium or vitamin D can lead to excessively high plasma levels of calcium. Patients who are particularly susceptible include those with hyperparathyroidism, those being treated for osteoporosis, and those receiving high dosages of vitamin D for hypoparathyroidism. Metabolic alkalosis and the milk-alkali syndrome have been reported during prolonged therapy with thiazide diuretics and calcium.

MANAGEMENT: Patients receiving thiazide diuretic therapy should be cautioned against self-treatment with calcium and vitamin D supplements without first talking to their healthcare provider. Serum calcium should be monitored if thiazide diuretics are coadministered with high dosages of calcium and/or vitamin D. Patients should be advised to seek medical attention if they experience signs and symptoms of hypercalcemia such as dizziness, weakness, lethargy, headache, myalgia, anorexia, nausea, vomiting, and seizures.

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Coadministration with antacids may decrease the oral bioavailability of captopril and other angiotensin converting enzyme (ACE) inhibitors due to delayed gastric emptying and/or elevated gastric pH. In 10 healthy volunteers, 50 mL of an antacid suspension decreased the mean peak plasma concentration (Cmax) and area under the concentration-time curve (AUC) of captopril (50 mg single oral dose) by 50% and 42%, respectively, compared to administration after fasting. The relative bioavailability of captopril was 0.66 with antacid, although its hypotensive activity did not seem to be affected. Based on available data, the clinical significance of this interaction appears to be minor. As a precaution, patients may want to consider separating the administration times of ACE inhibitors and antacids or oral medications that contain antacids (e.g., didanosine buffered tablets or pediatric oral solution) by 1 to 2 hours.

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