Drug Interactions between Symbicort and vigabatrin

GENERALLY AVOID: Theoretical concerns exist that oculotoxic effects of vigabatrin may be additive with those of other drugs that are associated with serious adverse ophthalmic effects. Vigabatrin causes permanent bilateral concentric visual field constriction in 30% or more of patients, with severity ranging from mild to severe. Vigabatrin can also damage the central retina and decrease visual acuity. The onset of vision loss is unpredictable, occurring within weeks of starting treatment to months or even years later. The risk of vision loss increases with increasing dose and cumulative exposure, although there is no dose or exposure known to be risk-free. It is possible that vision loss can worsen even after discontinuation of vigabatrin.

MANAGEMENT: Vigabatrin should generally not be used with other drugs associated with serious adverse ophthalmic effects such as retinopathy or glaucoma unless the benefits clearly outweigh the risks. These drugs may include amiodarone, deferoxamine, ethambutol, quinine derivatives, tamoxifen, and long-term corticosteroids. Vision testing at baseline (no later than 4 weeks after starting vigabatrin) and at least every 3 months during therapy is required for adults. Vision testing is also required about 3 to 6 months after the discontinuation of vigabatrin therapy. Due to the risk of irreversible vision loss, vigabatrin should be withdrawn from patients who fail to show substantial clinical benefit within 3 months of initiation, or sooner if treatment failure becomes obvious. The patient's response and continued need for vigabatrin should be periodically reassessed. The lowest dosage and shortest duration of treatment consistent with clinical objectives should be employed.

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Although they are often combined in clinical practice, the concomitant use of beta-2 adrenergic agonists and corticosteroids may result in additive hypokalemic effects. Since beta-2 agonists can sometimes cause QT interval prolongation, the development of hypokalemia may potentiate the risk of ventricular arrhythmias including torsade de pointes. However, clinical data are limited, and the potential significance is unknown. Patients who are receiving systemic or nebulized formulations of beta-2 agonists, high dosages of inhaled beta-2 agonists, or systemic corticosteroid therapy may be at a greater risk of developing hypokalemia.

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