Patients with a history of rhinitis (10%), nasal polyps (72%), and nasal mucosal hypertrophy (81.2%) developed asthma after taking aspirin because of episodes of upper sensation and dysmenorrhea.
1,Pathogenesis of AIA The pathogenesis of aspirin-induced asthma has not been fully elucidated so far. It is more recognized that it is related to the imbalance of cyclooxygenase/5-lipoxygenase. Aspirin preferentially blocks cyclooxygenase, thereby inhibiting the production of prostaglandins and thromboxane; however, aspirin does not block 5-lipoxygenase, and a large number of arachidonic acid substrates that are not utilized by cyclooxygenase are generated through lipoxygenase to produce a large number of leukotrienes (LTC4, LTD4, LTE4), which are powerful bronchoconstrictors and pro-secretors, this is the ” shunting hypothesis”. The findings supporting this theory are: (i) increased levels of leukotrienes in nasal secretions, urine, and bronchoalveolar lavage fluid of AIA patients. ② Pre-administration of leukotriene receptor antagonists can partially or even completely prevent aspirin-induced asthma.
2,Pathogenesis of asthma induced by other drugs
(1) Allergic reactions: The mechanism of asthma induced by antibiotics and iodine-containing contrast agents is specific IgE antibody-mediated type I allergic reaction. The mechanism of action of antibiotics and muscle relaxants also belongs to this, but they can also directly cause non-IgE-mediated histamine release.
(2) Normal pharmacological effects: β-blockers, choline agents, and histamines can cause bronchospasm due to their own normal pharmacological effects.
(3) Activation of the complement system: In addition to causing DIA through metabolic reactions, iodine-containing contrast agents can also cause bronchospasm by causing vascular endothelial cell damage, activating the complement system, and thus releasing histamine from mast cell degranulation by releasing allergic reaction toxins.
(4) Local irritation of respiratory mucosa by drugs: various powders such as acetylcysteine (sputum easy to clean), posterior pituitary powder, and sodium cromoglycate powder can cause smooth muscle spasm by irritation of airway mucosa when inhaled.
(5) Structural similarity theory: Many asthma-inducing drugs have a similar benzene ring structure in their molecular structure, and this structure can cause bronchospasm.
(6) Acetylation theory: Some drugs can denature certain proteins in the body through acetylation, and such denatured proteins can stimulate the body to produce antibodies and thus cause allergic reactions.
(7) Increase of endogenous adenosine concentration: Dipyridamole (Pansentin) can block the uptake of endogenous adenosine and increase its level, which is a strong constrictor of bronchial tubes.