Urticaria, commonly referred to as hives, is swelling of the dermis and one of the most common skin conditions seen in clinical practice. Angioedema results from a process similar to urticaria, but the reaction extends below the dermis. Urticaria and angioedema occur in response to the release of inflammatory mediators, including histamine, leukotrienes, platelet-activating factor, prostaglandins, and cytokines from mast cells present in the skin. A variety of stimuli can trigger mast cells and basophils to release their chemical mediators. Typically mast cells degranulate when cross-linking of the membrane-bound IgE occurs. Release of these mediators results in vasodilation, increased vascular leakage, and pruritus. Basophils from the circulatory system also can localize in tissue and release mediators similar to mast cells. Patients with urticaria have elevated histamine content in the skin that is more easily released.
Anaphylaxis is mediated by IgE, whereas anaphylactoid reactions result from mechanisms that are due to nonimmunologic mechanisms. Both reactions are acute, severe, and can be life threatening due to a massive release of inflammatory mediators. Urticaria, angioedema, and anaphylaxis are best considered as symptoms because they have a variety of causes.
Not all mast cell activation is IgE-mediated. Immunologic, nonimmunologic, physical, and chemical stimuli can produce degranulation of mast cells and basophils. Anaphylatoxins,C3a and C5a, can cause histamine release in a non–IgE-mediated reaction. Anaphylatoxins are generated in serum sickness (reactions to blood transfusions) (see Chapter 82) and in infectious, neoplastic, and rheumatic diseases. In addition mast cell degranulation can occur from a direct pharmacologic effect or physical or mechanical activation, such as urticaria after exposure to opiate medications, and dermatographism.
Urticaria/angioedema can be classified into three subcategories: acute, chronic, and physical. By definition acute urticaria and angioedema are hives and diffuse swellingthat last less than 6 weeks. Often the history is quite helpfulin eliciting the cause of the acute reaction (Table 81-1). AnIgE mechanism is more commonly found in acute urticariathan in chronic urticaria. Chronic urticaria and angioedemaare characterized by persistence of symptoms beyond 6 weeks(Table 81-2). Some have daily symptoms of hives and swelling, whereas others have intermittent or recurrent episodes.Chronic urticaria can be idiopathic with unknown causal
Foods Egg, milk, wheat, peanuts, tree nuts, soy, shellfish, fish, strawberries (direct mast cell degranulation)
Medications Suspect all medications, even over-thecounter or homeopathic medications
Insect stings Hymenoptera (honeybee, yellow jacket, hornets, wasp, fire ants), biting insects (papular urticaria)
Infections Bacterial (group A streptococcus pharyngitis, Mycoplasma, sinusitis); viral (hepatitis B, mononucleosis [EBV], coxsackieviruses A and B); parasitic (Ascaris, Ancylostoma, Echinococcus, Fasciola, Filaria, Schistosoma, Strongyloides, Toxocara, Trichinella); fungal (dermatophytes, Candida)
Contact allergy Latex, pollen, animal saliva, nettle plants, caterpillars
Transfusion reactions Blood, blood products, or IVIG administration
From Lasley MV, Kennedy MS, Altman LC: Urticaria and angioedema. In Altman LC, Becker JW, Williams PV, editors: Allergy in Primary Care, Philadelphia, 2000, Saunders, p 232.