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USMLE – Urticaria

Urticaria (hives) is a common disorder of the skin characterized by localized mast cell degranulation and resultant dermal microvascular hyperpermeability, culminating in pruritic edematous plaques called wheals. Angioedema is closely related to urticaria and is characterized by deeper edema of both the dermis and the subcutaneous fat.

Urticaria most often occurs between the ages of 20 and 40 years, although all age groups are susceptible. Individual lesions develop and fade within hours (usually less than 24 hours), and episodes may last for days or persist for months. Lesions vary from small, pruritic papules to large edematous plaques. Individual lesions may coalesce to form annular, linear, or arciform configurations. Sites of predilection for urticarial eruptions include any area exposed to pressure, such as the trunk, distal extremities, and ears. Persistent urticaria may simply be the result of inability to eliminate the causative antigen or may herald underlying disease (e.g., collagen vascular disorders, Hodgkin disease).

The histologic features of urticaria may be so subtle that many biopsy specimens at first resemble normal skin. There is usually a sparse superficial perivenular infiltrate consisting of mononuclear cells and rare neutrophils. Eosinophils may also be present. Collagen bundles are more widely spaced than in normal skin, a result of superficial dermal edema fluid that does not stain in routinely prepared tissue. Superficial lymphatic channels are dilated in an attempt to accommodate this transudated edema fluid.

In most cases, urticaria results from antigen-induced release of vasoactive mediators from mast cell granules through sensitization with specific immunoglobulin E (IgE) antibodies. This IgE-dependent degranulation can follow exposure to a number of antigens (pollens, foods, drugs, insect venom) and specifically results from bridging between mast cell-bound IgE molecules by multivalent ligand. IgE-independent urticaria may result from substances that in certain individuals directly incite the degranulation of mast cells, such as opiates, certain antibiotics, curare, and radiographic contrast media. Another cause of IgE-independent urticaria is exposure to chemicals, such as aspirin, that suppress prostaglandin synthesis from arachidonic acid. Hereditary angioneurotic edema is the result of an inherited deficiency of C1 activator (C1 esterase inhibitor) that results in uncontrolled activation of the early components of the complement system (so-called complement-mediated urticaria).

Lillian Thompson By Lillian Thompson

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