The pathomechanism of acetylsalicylic acid intolerance. A hypothesis.
In a number of individuals suffering from chronic asthma or chronic urticaria, acetylsalicylic acid and structurally unrelated non-steroidal anti-inflammatory agents and other compounds, e.g. tartrazine, elicit an intolerance syndrome that mimics the signs and symptoms of an immediate-type allergic (anaphylactic) reaction. An immunological basis for this reaction could be excluded. It is assumed that the eliciting agents activate complement and that the intolerant individuals lack plasma carboxypeptidase B, that normally inactivates C3a and C5a in statu nascendi. The anaphylatoxins, if not immediately inactivated, release the endogenous mediators of the anaphylactic reaction from the tissue mast cells.
D001241:Aspirin / Q000009:adverse effects*; D002268:Carboxypeptidases / Q000097:blood; D003165:Complement System Proteins / Q000378:metabolism; D004361:Drug Tolerance; D006636:Histamine Release; D006801:Humans
D003165:Complement System Proteins; D002268:Carboxypeptidases; D001241:Aspirin