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Pamela Ewan

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date: 24 April 2017

Allergy is common and becoming commoner: it now affects about one-third of the United Kingdom population. This is being driven by environmental changes, which are also leading to an increase in both the complexity and severity of the condition. In addition to the traditional allergic disorders—asthma, rhinitis, and eczema—multisystem allergic disease and reactivity to several allergens are now common; new allergies have appeared, including those due to foods, drugs, and diagnostic agents; and anaphylaxis is increasing.

Where possible, patients with significant allergy should be referred to an allergy specialist who can provide expertise not offered by—and complementary to—that of other specialties. Identifying allergic causes of disease leads to reduction or resolution of its manifestations.

Aetiology and pathogenesis

Mechanism—allergy in its classical form occurs following interaction of allergen with specific IgE antibody bound to high-affinity IgE receptors (Fcε‎RI) on mast cells, which results in mast cell activation, degranulation, and mediator release, but the same clinical presentation can occur as a result of IgE independent mast cell degranulation e.g. idiopathic anaphylaxis. A normal subject has no specific IgE to common allergens and a low or normal total serum IgE level: production of specific IgE antibody requires a change in immunoregulation leading to sensitization (atopic state), with some sensitized subjects progressing to develop clinical allergy.

Allergens—common allergic triggers include (1) inhaled allergens—house dust mite, pollens, and animal danders are the commonest causes of allergic asthma, rhinitis and eczema; (2) foods—commonly egg, milk, peanuts, and tree nuts; mainly cause acute reactions of varying severity, e.g. urticaria, angio-oedema, or anaphylaxis; (3) drugs—particularly antibiotics, aspirin, NSAIDs, and drugs given during general anaesthesia; (4) bee and wasp stings; (5) latex rubber.

Clinical features and diagnosis

Clinical presentation—this can be in various guises acute or chronic, with common manifestations being (1) allergic rhinitis—timing of symptoms indicates the causative allergen; (2) nonallergic rhinitis—some have aspirin sensitivity, rhinosinusitis, nasal polyps, and asthma; (3) conjunctivitis; (4) asthma—timing of symptoms and exacerbations gives clues to aetiology; (5) eczema; (6) urticaria and angio-oedema—severe tongue swelling is a medical emergency and most often drug induced (especially ACE inhibitors) or idiopathic (non-IgE mediated); (7) anaphylaxis—presents with acute dyspnoea or hypotension/collapse, usually with cutaneous features such as erythema or urticaria (see Chapter 17.2).

History taking—a good history is the key to diagnosis: too often the underlying allergic trigger is not identified and disease which could be ameliorated by allergen avoidance continues unchecked; awareness of drug and latex allergy are essential.

Clinical investigation—(1) serum tryptase—may be transiently elevated for up to 4 h following an acute reaction; (2) skin prick tests or serum-specific IgE assays—many patients have positive tests without symptoms, hence performing them in the absence of appropriate clinical information is a common source of error; (3) intradermal and challenge tests—performed by allergy specialists, mainly for diagnosis of drug and food allergy.

Prevention and treatment

Prevention—there are no widely applicable proven methods for primary prevention of allergy.

Acute or chronic disease—management requires (1) allergen avoidance; and may also involve (2) pharmacotherapy—including nonsedative antihistamines and topical corticosteroids (nasal sprays, inhalers, and creams); and, less commonly, (3) immunotherapy (desensitization)—should be offered to patients with poorly controlled allergic rhinitis or venom anaphylaxis.

Anaphylaxis—first-line treatment is intramuscular adrenaline (epinephrine). All patients should subsequently be referred to an allergy specialist for diagnosis and management: allergen or trigger avoidance, e.g. food or drug, reduces further episodes and should be combined with an adrenaline autoinjector for early self-treatment. See Chapter 17.2 for further discussion.

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