Excerpt from Papular Urticaria

Synonyms, Key Words, and Related Terms: insect bites, type I hypersensitivity reaction, id reaction

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Background

Papular urticaria is a common and often annoying disorder manifested by chronic or recurrent papules caused by a hypersensitivity reaction to the bites of mosquitoes, fleas, bedbugs, and other insects. Individual papules may surround a wheal and display a central punctum (Stibich, 2001). Papular urticaria tends to be evident during spring and summer months. However, in some climates, such as in San Francisco, the hometown of one of the authors, this condition may affect children throughout the year.

Pathophysiology

The histopathologic pattern in papular urticaria consists of mild subepidermal edema, extravasation of erythrocytes, interstitial eosinophils, and exocytosis of lymphocytes. These findings suggest a pathophysiologic process that is immunologically based (Stibich, 2001). Papular urticaria is generally regarded to be the result of a hypersensitivity or id reaction to bites from insects, such as mosquitoes, gnats, fleas, mites, and bedbugs (Jordaan, 1997). Varicella vaccines have also been implicated (Bronstein, 2005).

Morphologic and immunohistochemical evidence suggest that a type I hypersensitivity reaction plays a central role in the pathogenesis of papular urticaria. The reaction is thought to be caused by a hematogenously disseminated antigen deposited by an arthropod bite in a patient who is sensitive. This theory is supported by the fact that these lesions can and often do occur in areas away from the bites. The putative antigen is unknown.

The presence of immunoglobulin and complement deposits in the skin of some patients with papular urticaria suggests that the lesions may be due to a cutaneous vasculitis (Heng, 1984). The deposits were most frequently seen in lesions within 24 hours of their development. The presence of granular deposits of Clq, C3, and immunoglobulin M (IgM) in superficial dermal blood vessel walls suggests that immune complexes (IgM aggregates) may be primarily involved in the pathogenesis, with complement activation initiated by Clq through the classical pathway.

Frequency

United States

The incidence is unknown.

International

The incidence is unknown.

Mortality/Morbidity

The main morbidity is the discomfort due to localized pruritus.

Race

No racial predisposition is known, although certain ethnic groups, specifically Asians, may be more predisposed to more intense reactions.

Sex

No sexual predisposition is known.

Age

This eruption occurs primarily in children, but they eventually outgrow this disease, probably through desensitization after multiple arthropod exposures (Steen 2004). This condition, however, can also occur in adults, albeit at a much lower rate.