Mechanism of contrast allergy

The exact causal mechanism of contrast-induced anaphylactic reactions is still debated. From his extensive research, Elliot Lasser1 has proposed a mechanism in which the large contrast-containing molecule causes an overload effect on the antigen-binding sites on immunoglobulin E (IgE) of mast cells and basophils and does not bind directly to an antigen-specific site. This effect varies with the particular contrast medium. Since the immuno-globulin binding is nonspecific, the resultant reaction depends on the quantity of circulating IgE and mast cells at the time the contrast medium is administered. This nonspecific binding helps explain why patients with strong allergic history are at particular risk and why prior exposure to the contrast agent is not necessary for a reaction to occur.
Other considerations are that direct contact of the contrast agent with the endothelium of blood vessels may activate Factor XII;this substance in turn activates kallikrein; kallikrein activates bradykinin; bradykinin activates prostaglandin and the leucotrienes.1,2 Leucotrienes are similar in their action to histamine, but are multifold more potent and not blocked by antihistamines. Bradykinin can mimic all the significant pathophysiological effects of histamine but is far more potent and, again, this sequence of events would not be blocked by antihistaminic drugs.