Antileukotriene agents compared to inhaled corticosteroids

Our clinical experience with montelukast has been mixed at best. And when effective, the effect has been mild. It is a medication that we will use in patients with CRS and nasal polyps with either allergic rhinitis and/or asthma. We also utilize anti-leukotrienes as a steroid sparing medication. In some patients, we have found a synergistic effect of montelukast with zileuton. Given the short half life of montelukast, the effect of montelukast can be determined within a couple of days. In addition, we have observed on a handful of patients a peripheral elevation of eosinophils with the addition of anti-leukotrienes. Consequently, we follow patients’ peripheral eosinophil counts.

Leukotrienes are eicosanoids derived from arachidonic acid, which is present in cell membranes. The cysteinyl leukotrienes, which are elaborated by bronchopulmonary mast cells, eosinophils, and probably alveolar macrophages, have been shown to mediate bronchoconstriction induced by exercise, hyperventilation in cold air, aspirin, and inhaled allergens. They act by stimulating a specific receptor, known as cysteinyl leukotriene receptor type 1 (CysLT1). Antileukotrienes having clinical usefulness in asthma include zileuton, which inhibits 5-lipoxygenase, an enzyme critical in the biosynthesis of leukotrienes, and leukotriene receptor antagonists (cinalukast, montelukast, zarirlukast, and others). Antileukotrienes reverse bronchconstriction in asthma to a lesser degree than β 2 -adrenergic agonists, but their effects are additive to those of the latter agents. In chronic asthma, antileukotrienes improve peak flow and FEV 1 and reduce the frequency and severity of acute asthmatic attacks, the need for β 2 -agonists, and the need for corticosteroid rescue. They are particularly effective in the prophylaxis of asthma induced by exercise and aspirin. In contrast, many people with allergic asthma show little or no response. Antileukotrienes are not indicated in the treatment of an acute asthmatic attack or in mild, intermittent asthma controlled adequately with occasional use of inhaled β 2 -agonists. They have not been recommended as a substitute for inhaled corticosteroids in prophylaxis of asthma. Antileukotrienes are administered orally or by inhalation. Both onset and waning of clinical effects are gradual. Side-effects are minimal, but drug interactions may occur because of interference with cytochrome P-450 enzymes. Rare transitory elevations of hepatic aminotransferase have been reported with some agents.

Churg-Strauss syndrome / Delayed / Incidence not known
vasculitis / Delayed / Incidence not known
erythema multiforme / Delayed / Incidence not known
Stevens-Johnson syndrome / Delayed / Incidence not known
toxic epidermal necrolysis / Delayed / Incidence not known
pancreatitis / Delayed / Incidence not known
erythema nodosum / Delayed / Incidence not known
anaphylactoid reactions / Rapid / Incidence not known
angioedema / Rapid / Incidence not known
suicidal ideation / Delayed / Incidence not known
seizures / Delayed / Incidence not known

Antileukotriene agents compared to inhaled corticosteroids

antileukotriene agents compared to inhaled corticosteroids

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