Drug Interaction Report

MONITOR: Concomitant use of aminolevulinate topical preparations with other known photosensitizing agents may enhance the phototoxic reaction to photodynamic therapy. These agents have each been individually associated with photosensitivity reactions and may have additive effects if administered concurrently. Medicinal products with known phototoxic or photoallergic potential include fluoroquinolones, phenothiazines, retinoids, sulfonamides, sulfonylureas, tetracyclines, thiazide diuretics, griseofulvin, and hypericin extracts (e.g., St John's Wort).

MANAGEMENT: Caution is advised and pharmacologic response to photodynamic therapy should be carefully monitored if concomitant use of other photosensitizing agents cannot be avoided. Patients should be advised to avoid exposure of treated areas to sunlight or bright indoor lights (e.g., examination lamps, operating room lamps, tanning beds, lights at close proximity) during the period between application of aminolevulinic acid or methyl aminolevulinate and photoactivation, and for 48 hours post-illumination. As sunscreen is not effective in protecting treated areas of skin, patients should be counseled to wear protective apparel, such as a wide-brimmed hat, long sleeve shirt, and gloves to protect themselves. Concomitant use with other topical medicinal products should be avoided. Some authorities recommend avoiding use of hypericin-containing products for 2 weeks prior to treatment with topical aminolevulinic acid.

GENERALLY AVOID: Concurrent use of ethanol and phenothiazines may result in additive CNS depression and psychomotor impairment. Also, ethanol may precipitate dystonic reactions in patients who are taking phenothiazines. The two drugs probably act on different sites in the brain, although the exact mechanism of the interaction is not known.

MANAGEMENT: Patients should be advised to avoid alcohol during phenothiazine therapy.

MONITOR: Smoking cessation may lead to elevated plasma concentrations and enhanced pharmacologic effects of drugs that are substrates of CYP450 1A2 (and possibly CYP450 1A1) and/or certain drugs with a narrow therapeutic index (e.g., flecainide, pentazocine). One proposed mechanism is related to the loss of CYP450 1A2 and 1A1 induction by polycyclic aromatic hydrocarbons in tobacco smoke; when smoking cessation agents are initiated and smoking stops, the metabolism of certain drugs may decrease leading to increased plasma concentrations. The mechanism by which smoking cessation affects narrow therapeutic index drugs that are not known substrates of CYP450 1A2 or 1A1 is unknown. The clinical significance of this interaction is unknown as clinical data are lacking.

MANAGEMENT: Until more information is available, caution is advisable if smoking cessation agents are used concomitantly with drugs that are substrates of CYP450 1A2 or 1A1 and/or those with a narrow therapeutic range. Patients receiving smoking cessation agents may require periodic dose adjustments and closer clinical and laboratory monitoring of medications that are substrates of CYP450 1A2 or 1A1.