Drug Interactions between budesonide / formoterol and etrasimod

GENERALLY AVOID: Coadministration of etrasimod with antineoplastic, immunosuppressive, or other immune-modulating therapies may increase the risk of unintended additive immunosuppressive effects. Etrasimod causes reversible sequestration of lymphocytes in lymphoid tissues. When administered daily for 52 weeks, etrasimod produced a mean reduction in peripheral blood lymphocyte count to 45% of baseline values, which may increase the risk of infections. Life-threatening and rare fatal infections have occurred in association with other sphingosine 1-phosphate (S1P) receptor modulators. Decreased lymphocyte counts persist during chronic daily dosing and generally return to normal within 4 to 5 weeks after stopping the medication.

MANAGEMENT: The safety and efficacy of etrasimod in combination with antineoplastic, immunosuppressive, or immune-modulating agents have not been evaluated. Because its pharmacodynamic effects may persist for up to 5 weeks after treatment discontinuation, concomitant use during and within 5 weeks following the last dose of etrasimod with antineoplastic, immunosuppressive, or immune-modulating agents should generally be avoided. If concomitant use within this period is considered necessary, patients should be monitored for infectious complications during this extended period. When switching from drugs with prolonged immune effects to etrasimod, the half-life and mode of action of these drugs must also be considered to avoid unintended additive immunosuppressive effects.

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MONITOR: Beta-2 adrenergic agonists can cause dose-related prolongation of the QT interval and potassium loss. Theoretically, coadministration with other agents that can prolong the QT interval may result in additive effects and increased risk of ventricular arrhythmias including torsade de pointes and sudden death. In general, the risk of an individual agent or a combination of 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 drug(s). Clinically significant prolongation of QT interval and hypokalemia occur infrequently when beta-2 agonists are inhaled at normally recommended dosages. However, these effects may be more common when the drugs are administered systemically or when recommended dosages are exceeded.

MANAGEMENT: Caution is recommended if beta-2 agonists are used in combination with other drugs that can prolong the QT interval. 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 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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