Based on differing underlying mechanisms, doctors usually divide drug allergies into four main types: immediate hypersensitivity allergies, immune complex disease, cytotoxic responses, and delayed hypersensitivity reactions.
Generally occurring anywhere from instantly to within the first six hours after exposure to the culprit medication, immediate hypersensitivity drug reactions involve IgE antibodies, mast cells, and the release of large amounts of chemical mediators that are responsible for the symptoms. These reactions may be severe and even life-threatening. Penicillin, when administered either intramuscularly or intravenously, is perhaps the best known cause of this type of severe reaction, but by no means the sole cause. Many other types of antibiotics, adrenocorticotropic hormone (ACTH), insulin, flu vaccine, tetanus toxoid, and gamma globulin may also provoke immediate hypersensitivity drug reactions and profound shock.
Immune-complex disease, once called serum sickness disease, is a second kind of drug-induced allergy. In this type of reaction, small-sized drug-antibody molecular complexes float in the bloodstream until they are deposited in the tiny blood vessels of many important organs. Once there, they attract other blood proteins and initiate a cascade of events, culminating in significant inflammation and damage to the surrounding tissues and organs. Symptoms include fever, rash, hives, tender black-and-blue nodules in the skin, swollen glands, and joint pains. Drugs commonly linked to this type of allergy include penicillin, sulfa drugs, phenytoin (Dilantin), aspirin, streptomycin, hydralazine (Apresoline), procainamide (Pronestyl), isoniazid (INH), propylthiouracil, and chlorpromazine (Thorazine).
Cytotoxic reactions (which literally mean those that are poisonous to cells) are a third kind of drug allergy. In simplest terms, the offending drug alone or the drug bound to an antibody attaches to the surface of specific target cells for example, red blood cells and initiates their destruction. Drugs that may precipitate anemia (a low blood count) in this manner include penicillin, quinidine (Quinaglute), quinine, aspirin, and cephalosporin antibiotics (Keflex, Velosef, and Duricef). Destruction of platelets, the cells needed for normal blood coagulation, has been reported with quinine, quinidine, acetaminophen (Tylenol), and sulfa drugs. And lastly, white blood cell destruction has been linked to phenylbutazone (Butazolidin), phenothiazines (for example, Thorazine), sulfa drugs, phenytoin (Dilantin), and tolbutamide (Orinase), among others.
Finally, drugs may cause allergy by a fourth immunologic mechanism known as delayed hypersensitivity, which involves the participation of sensitized lymphocytes. Within the skin, delayed reactions manifest themselves as allergic contact dermatitis. Neomycin, bacitracin, parabens, propylene glycol, and PABA are examples of common ingredients found in many OTC and prescription items that are known to cause contact allergies. Although it occurs less often, a delayed hypersensitivity reaction may also involve other organs. For example, nitrofurantoin (Furadantin), penicillin, and phenytoin (Dilantin) have been known to cause delayed hypersensitivity inflammation in the lungs.
