Drug Interactions between Dual-Action Acid Controller Complete and Hecoria

MONITOR: Famotidine may cause QTc prolongation. Theoretically, coadministration with other agents that can prolong the QT interval may result in additive effects and increased risk of ventricular arrhythmias including torsade de pointes and sudden death. According to the manufacturer, prolongation of the QT interval has been reported very rarely in patients with impaired renal function whose dose/dosing interval of famotidine may not have been adjusted appropriately. In general, the risk of an individual agent or a combination of these agents causing ventricular arrhythmia in association with QT prolongation is largely unpredictable but may be increased by certain underlying risk factors such as congenital long QT syndrome, cardiac disease, and electrolyte disturbances (e.g., hypokalemia, hypomagnesemia). In addition, the extent of drug-induced QT prolongation is dependent on the particular drug(s) involved and dosage(s) of the drug(s).

MANAGEMENT: Caution and clinical monitoring are recommended if famotidine is used in combination with other drugs that can prolong the QT interval. Patients should be advised to seek prompt medical attention if they experience symptoms that could indicate the occurrence of torsade de pointes such as dizziness, lightheadedness, fainting, palpitation, irregular heart rhythm, shortness of breath, or syncope.

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MONITOR: Coadministration with aluminum-magnesium hydroxide may increase tacrolimus blood concentrations in vivo. The mechanism of interaction is unknown. In a single-dose study, administration of tacrolimus with aluminum-magnesium hydroxide in healthy volunteers resulted in a 10% and 21% increase in tacrolimus peak concentration (Cmax) and systemic exposure (AUC), respectively, compared to administration without aluminum-magnesium hydroxide. This finding contradicts the results from an in vitro study, which showed that tacrolimus incubated in 100 mL simulated gastric fluid with the equivalent of 500 mg of various antacids resulted in loss of tacrolimus, due presumably to a pH-mediated degradation of tacrolimus. Specifically, Mylanta caused a 14% loss of tacrolimus in 24 hours, magnesium oxide caused a 98% loss in 12 hours, and calcium carbonate caused a 30% loss in 24 hours. In contrast, aluminum hydroxide gel caused an immediate 35% loss of tacrolimus (within 2 minutes) and no further loss for 24 hours, suggesting adsorption of tacrolimus.

MANAGEMENT: Given the narrow therapeutic index and the large interindividual variability in the pharmacokinetics of tacrolimus, caution is advised if the drug is used in combination with aluminum and/or magnesium hydroxide. Pharmacologic response and tacrolimus blood levels should be monitored more closely whenever aluminum/magnesium hydroxide is added to or discontinued from therapy, and the immunosuppressant dosage adjusted as necessary. Patients should be advised to contact their doctor if they experience potential signs and symptoms of tacrolimus toxicity such as fever, infection, diarrhea, tremor, headache, fatigue, lethargy, and changes in motor function, mental status, or sensory function.

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Antacids and some aluminum, calcium, and magnesium salts may decrease the plasma concentrations of H2-receptor antagonists during oral coadministration. The mechanism of interaction is unknown, but may involve reduced oral absorption due to increased gastric pH. Study data vary, with no changes to nearly 60% reductions in systemic exposures (AUCs) reported for cimetidine, famotidine, and ranitidine. The clinical significance has not been established. As a precaution, patients may consider taking H2-receptor antagonists one to two hours before antacids.

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Antacids and some aluminum, calcium, and magnesium salts may decrease the plasma concentrations of H2-receptor antagonists during oral coadministration. The mechanism of interaction is unknown, but may involve reduced oral absorption due to increased gastric pH. Study data vary, with no changes to nearly 60% reductions in systemic exposures (AUCs) reported for cimetidine, famotidine, and ranitidine. The clinical significance has not been established. As a precaution, patients may consider taking H2-receptor antagonists one to two hours before antacids.

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In vitro data suggest that the presence of antacids may reduce the bioavailability of tacrolimus. An in vitro study showed that tacrolimus incubated in 100 mL simulated gastric fluid with the equivalent of 500 mg of various antacids resulted in loss of tacrolimus, due presumably to a pH-mediated degradation of tacrolimus. Specifically, aluminum-magnesium hydroxide caused a 14% loss of tacrolimus in 24 hours, magnesium oxide caused a 98% loss in 12 hours, and calcium carbonate caused a 30% loss in 24 hours. In contrast, aluminum hydroxide gel caused an immediate 35% loss of tacrolimus (within 2 minutes) and no further loss for 24 hours, suggesting adsorption of tacrolimus. Whether these effects occur in vivo, and to what extent, are unknown. Sodium bicarbonate has been reported to cause widely variable trough plasma levels and reduced blood concentrations of tacrolimus when given close to the time of administration of tacrolimus. No other details were available in the report. However, in a single-dose study, administration of tacrolimus with aluminum-magnesium hydroxide in healthy volunteers resulted in a 10% and 21% increase (not decrease) in tacrolimus peak concentration (Cmax) and systemic exposure (AUC), respectively, compared to administration without aluminum-magnesium hydroxide.

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