Key Clinical Questions
How do anaphylactic and anaphylactoid reactions differ? How are they treated?
What conditions mimic allergic reactions?
What are the most common types of allergic reactions among hospitalized patients?
Which patients require outpatient referral to an allergist?
Allergic reactions result from an aberrant immune response to an inciting antigen or allergen. The subsequent inflammatory state produces a wide range of clinical symptoms. Anaphylaxis, the most extreme form of allergic reaction, refers to sudden, severe, and potentially fatal hypersensitivity developing in seconds to minutes after exposure.
It is estimated that anaphylaxis accounts for 1 in 2000 ambulance trips and is fatal in as many as 0.7% to 2% of cases. Two epidemiologic studies demonstrated that 1 out of every 2700 to 5100 hospitalizations can be linked to anaphylactic reactions. While the term allergy denotes an immediate hypersensitivity reaction involving immunoglobulin E (IgE) antibody, a large number of severe allergic reactions are not IgE mediated. These “anaphylactoid” reactions are clinically indistinguishable from anaphylaxis and include hypersensitivity to radiocontrast dye, angiotensin-converting enzyme (ACE) inhibitors, and opiates.
Patients experiencing allergic reactions may vary widely in their clinical presentations. Factors affecting the clinical picture include the amount and persistence of antigen, its route of entry, and the end organ response to vasoactive mediators. The majority of allergic reactions manifest as skin findings, such as flushing, pruritus, and transient urticaria. In more severe reactions, a larger number of deep dermal mast cells are recruited, resulting in angioedema.
The onset of anaphylactic reactions can occur minutes to hours after exposure to an allergen and denotes the systemic activation of mast cells. Aside from the cutaneous manifestations, patients may experience respiratory manifestations (hoarseness of voice, dyspnea, wheezing, cough, and chest tightness), gastrointestinal manifestations (nausea, vomiting, colicky abdominal pain, and diarrhea), and cardiovascular manifestations (peripheral vasodilation, reflex tachycardia, and hypotension with resultant cardiovascular collapse).
When the body is exposed to an antigen, a specific IgE antibody is formed that binds to high-affinity receptors, called Fc epsilon type I, located on mast cells and basophils. Upon re-exposure to that allergen cross-linking of cell-bound IgE antibody occurs, resulting in Fc epsilon receptor aggregation and activation. The resultant mast cell degranulation leads to release of inflammatory mediators such as histamine, prostaglandins, tryptase, platelet activation factor, and leukotrienes, all directly contributing to the allergic response through smooth muscle contraction, bronchoconstriction, vasodilation, increased vascular permeability, and edema (Figure 230-1). Allergic reactions mediated by T-helper type 2 (TH2) cells (a subset of CD4+ T cells) preferentially produce interleukins (IL) 4, 5, and 13; all powerful mediators of allergic response. IL-4 promotes B-cell activation and T-cell proliferation and is also responsible for CD4+ T-cell differentiation to TH2 cells. IL-5 recruits and activates eosinophils, contributing to the late phase of allergic ...