• Urticaria (hives): well-circumscribed erythematous wheals with raised serpiginous borders and blanched centers that may coalesce to become giant wheals. Limited to the superficial portion of the dermis. • Angioedema: similar eruptions to urticaria but with larger, well-demarcated edematous areas that involve subcutaneous structures as well as the dermis. • Chronic versus acute: recurrent episodes of urticaria and/or angioedema of less than 6 weeks’ duration are considered acute, whereas attacks persisting beyond this period are designated chronic. • Special forms: special forms have characteristic features—dermographism, cholinergic urticaria, solar urticaria, cold urti-caria. • Three distinct sources of mediators: — Preformed mediators: contained in granules and released immediately — Secondarily formed mediators: generated immediately or within minutes by interaction of primary mediators and nearby cells and tissues — Granule matrix–derived mediators: preformed but slowly dissociate from granule after discharge and remain in tissues for hours • Most common immunologic mechanism is mediated by IgE. • Early vascular changes arise from mast cells—histamine and end products of arachidonic acid. Wheal and flare occur within minutes of initiation and last 30-60 minutes. • Prolonged and delayed reactions represent leukocytic infiltration in response to mast cell chemotactic factors. They develop over time—erythema, edema, and induration beginning within 2 hours and lasting 12-24 hours. Leukocyte infiltration may induce second wave of mast cell activation or release toxic lysosomal enzymes and mediators. • Events triggered by mediators depend on type of mediator and tissues where they are released. • Lesions start within 1-2 minutes of contact: erythema, replaced within 3-5 minutes by edema and surrounding reflex urticaria. Maximal edema occurs within 10-15 minutes. Erythema regresses within an hour; edema persists up to 3 hours. • Associated with other diseases: parasitosis, insect bites, neuropsychiatric disorders, hormonal changes, thyroid disorders, pregnancy, menopause, diabetes, immunologic alterations, other urticarias, during or after drug therapy, Candida albicans, angioedema, hypereosinophilia. • Cholinergic urticaria: heat reflex urticaria is the second most frequent physical urticaria. These lesions involve stimulation of sweat glands by cholinergic afferent fibers. Lesions are pinpoint wheals surrounded by reflex erythema. Wheals arise at or between follicles, preferentially on upper trunk and arms. • Three basic types of stimuli: passive overheating, physical exercise, and emotional stress. • Eliciting activities: physical exercise, warm bath or sauna, eating hot spices, drinking alcohol. • Lesions: arise within 2-10 minutes and last 30-50 minutes. • Systemic symptoms: suggest generalized mast cell release beyond skin—headache, periorbital edema, lacrimation and burning of eyes, nausea and vomiting, abdominal cramps, diarrhea, dizziness, hypotension, and asthmatic attacks. • Cold urticaria: urticarial and/or angioedematous reaction of skin making contact with cold objects, water, or air. Lesions are restricted to area of exposure. Develop within a few seconds to minutes after removal of cold object and rewarming of skin. The colder the object or element, the faster the reaction. Widespread local exposure and generalized urticaria are accompanied by flushing, headache, chills, dizziness, tachycardia, abdominal pain, nausea, vomiting, myalgia, shortness of breath, wheezing, unconsciousness. — Cold urticaria accompanies a variety of clinical conditions, including viral infections, parasitic infestations, syphilis, multiple insect bites, penicillin injections, dietary changes, stress. Children with cold urticaria have higher risk of anaphylaxis, especially triggered by swimming. — Associated with infectious mononucleosis, cryoglobulinemia, and myeloma, in which cold urticaria may precede diagnosis by several years. • A minority of cases of chronic urticaria have an autoimmune basis, involving autoantibodies to IgE or the Fc • Autoimmunity is linked to bowel permeabilities. Subclinical impairments of small bowel red blood cell function may induce higher sensitivity to histamine in the gastrointestinal tract. Naturopathic approach treats overt and subclinical gastrointestinal permeability to decrease systemic inflammatory responses to endotoxins. • Leading cause of urticaria in adults. In children, attributable to foods, food additives, or infections. Most drugs are small molecules incapable of inducing antigenic or allergenic activity by themselves. Typically they act as haptens binding to endogenous macromolecules, inducing hapten-specific antibodies. Alternatively, they interact directly with mast cells, inducing degranulation. Many drugs produce urticaria, most commonly penicillin and aspirin. • Penicillin: antibiotics are most common cause of drug-induced urticaria. Population rate of allergenicity of penicillin is 10%, with 25% of these displaying urticaria, angioedema, or anaphylaxis. Penicillin cannot be destroyed by boiling or steam distillation and is undetected in foods. Penicillin in milk is more allergenic than in meat; penicillin can be degraded into more allergenic compounds in the presence of carbohydrate and metals. • Aspirin (ASA) and nonsteroidal antiinflammatory drugs (NSAIDs): Urticaria is a more common indicator of ASA sensitivity than asthma (Textbook, “Asthma”). Incidence of ASA sensitivity in patients with chronic urticaria is 20 times greater than normal control subjects. From 2%-67% of patients with chronic urticaria are sensitive to ASA. Aspirin inhibits cyclooxygenase by shunting eicosanoids towards leukotriene synthesis and increasing smooth muscle contraction and vascular permeability. ASA and other NSAIDs increase gut permeability and may alter normal handling of antigens. Dosage of 650 mg ASA q.d. for 3 weeks may desensitize patients and reduce responsiveness to foods that typically cause a reaction. Effect also occurs in patients with asthma but disappears within 9 days after stopping treat ment from a loss of effect or possible placebo response. NSAIDs are associated with prolonged and more pronounced autoreactivity in urticaria.
Urticaria
DIAGNOSTIC SUMMARY
PATHOPHYSIOLOGY
CAUSES OF URTICARIA
Physical
Autoimmune Urticaria
RIα subunit of high-affinity IgE mast cell receptor. Autoimmune antibodies are found in 24%-76% of patients with chronic urticaria. They have a more severe, prolonged course of disease. Middle-aged women have higher rates of urticaria and autoimmunity, particularly for thyroid disease. Thyroid autoantibodies are found more frequently in patients with IgE-receptor autoantibodies (see thyroid section below).
Drugs
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Urticaria
