Drug Interactions between cholecalciferol / lactobacillus reuteri and nifurtimox

CONTRAINDICATED: Use of alcohol or products containing alcohol during therapy with nitrofurans may result in a disulfiram-like reaction in some patients. The presumed mechanism is inhibition of aldehyde dehydrogenase (ALDH) by nitrofurans in a manner similar to disulfiram. Following ingestion of alcohol, inhibition of ALDH results in increased concentrations of acetaldehyde, the accumulation of which can produce an unpleasant physiologic response referred to as the 'disulfiram reaction'. Symptoms include flushing, throbbing in head and neck, throbbing headache, respiratory difficulty, nausea, vomiting, sweating, thirst, chest pain, palpitation, dyspnea, hyperventilation, tachycardia, hypotension, syncope, weakness, vertigo, blurred vision, and confusion. Severe reactions may result in respiratory depression, cardiovascular collapse, arrhythmia, myocardial infarction, acute congestive heart failure, unconsciousness, convulsions, and death.

ADJUST DOSING INTERVAL: Food enhances the oral bioavailability of nifurtimox. When a single 120 mg oral dose of nifurtimox was administered with a high-fat meal (800 to 1000 calories; approximately 60% fat) in adult Chagas patients, nifurtimox peak plasma concentration (Cmax) and systemic exposure (AUC) increased by 68% and 71%, respectively, compared to administration under fasted conditions. Nifurtimox was administered with food in clinical trials.

MANAGEMENT: Consumption of alcohol is considered contraindicated during nifurtimox therapy. To ensure maximal oral absorption, nifurtimox should be administered with food.

MONITOR: Additive effects and possible toxicity (e.g., hypercalcemia, hypercalciuria, and/or hyperphosphatemia) may occur when patients using vitamin D and/or vitamin D analogs ingest a diet high in vitamin D, calcium, and/or phosphorus. The biologically active forms of vitamin D stimulate intestinal absorption of calcium and phosphorus. This may be helpful in patients with hypocalcemia and/or hypophosphatemia. However, sudden increases in calcium or phosphorus consumption due to dietary changes could precipitate hypercalcemia and/or hyperphosphatemia. Patients with certain disease states, such as impaired renal function, may be more susceptible to toxic side effects like ectopic calcification. On the other hand, if dietary calcium is inadequate for the body's needs, the active form of vitamin D will stimulate osteoclasts to pull calcium from the bones. This may be detrimental in a patient with reduced bone density.

MANAGEMENT: Given the narrow therapeutic index of vitamin D and vitamin D analogs, the amounts of calcium, phosphorus, and vitamin D present in the patient's diet may need to be taken into consideration. Specific dietary guidance should be discussed with the patient and regular lab work should be monitored as indicated. Calcium, phosphorus, and vitamin D levels should be kept within the desired ranges, which may differ depending on the patient's condition. Patients should also be counseled on the signs and symptoms of hypervitaminosis D, hypercalcemia, and/or hyperphosphatemia.