Cromolyn sodium

Mechanism: Cromolyn sodium stabilizes mast cell membranes, preventing calcium influx required for mast cell degranulation. This blocks release of preformed mediators (histamine, tryptase) and newly synthesized mediators (leukotrienes, prostaglandins) upon antigen exposure, thereby inhibiting both early and late-phase allergic responses. It does not reverse bronchospasm once it has occurred and has no bronchodilator activity.

Clinical use: Historically used for prophylaxis of exercise-induced asthma, allergic asthma, allergic rhinitis, and mastocytosis. Available as inhaled (asthma), intranasal (allergic rhinitis), and ophthalmic (allergic conjunctivitis) formulations, as well as oral for systemic mastocytosis (limited absorption, acts locally on GI mast cells). Must be administered before allergen exposure or exercise for prophylactic effect—not useful for acute exacerbations.

Pharmacokinetics: Poor oral bioavailability, minimal systemic absorption, acts locally at site of administration. Very favorable safety profile due to lack of systemic effects.

Adverse effects: Minimal; may include throat irritation, cough, unpleasant taste with inhaled use. Considered one of the safest respiratory medications, making it historically useful in pediatric populations, though has largely been replaced by leukotriene receptor antagonists and inhaled corticosteroids due to need for frequent dosing (up to 4x/day) and lower efficacy.

Board relevance: Classic distractor answer for asthma pharmacology questions—tests understanding that it is prophylactic only, not for acute attacks, and works via mast cell stabilization rather than bronchodilation or anti-inflammatory corticosteroid mechanisms. Often compared with inhaled corticosteroids and leukotriene modifiers in asthma controller therapy classification.