Drug Interactions between Omeclamox-Pak and propofol

MONITOR: Treatment with propofol may lead to prolongation of the QT interval; however, the extent of prolongation and its clinical impact is difficult to determine. A retrospective single-center cohort study in patients treated at the Mayo clinic over 17 years (n=628,784) concluded that torsade de pointes (TdP) after propofol administration occurred at an annual incidence of 1.93 per million; however, it was often associated with other risk factors, including concomitant QT-prolonging medications, low serum potassium levels (<3.5 mmol/L), and low serum magnesium levels (<1.8 mg/dL). Other studies have reported that propofol has no effect or that it decreases the QTc interval and may offset QTc prolongation due to other coadministered anesthetic medications. Theoretically, concurrent use of two or more drugs that can cause QT interval prolongation may result in additive effects and increased risk of ventricular arrhythmias including TdP and sudden death. 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 drugs. Data from formal QT/QTc studies on propofol are lacking.

MANAGEMENT: Caution and clinical monitoring is recommended if propofol is used concomitantly with other agents associated with QT interval prolongation. 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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Although some in vitro data indicate synergism between macrolide antibiotics and penicillins, other in vitro data indicate antagonism. When these drugs are given together, neither has predictable therapeutic efficacy. Data are available for erythromycin, although theoretically this interaction could occur with any macrolide. Except for monitoring of the effectiveness of antibiotic therapy, no special precautions appear to be necessary.

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Clarithromycin may increase and prolong the omeprazole plasma concentration. The mechanism may be related to clarithromycin inhibition of hepatic cytochrome P450 enzymes responsible for omeprazole metabolism. Coadministration of omeprazole may result in an increase in clarithromycin and 14-(R)-hydroxyclarithromycin plasma concentrations. These increases may be due to the effect of omeprazole on gastric pH.

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