What causes papular urticaria?

Updated: Feb 12, 2021
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Papular urticaria is generally regarded to be the result of a hypersensitivity or id reaction to bites from insects, [10] such as mosquitoes, gnats, fleas, [11, 12] mites, [13, 14] bedbugs, [15, 16] caterpillars, [17] and moths. [17] Varicella vaccines have also been implicated. [18] However, it is unusual to identify an actual culprit in any given patient. [19, 20] One specific mite causing it is Peymotes ventricosus, and it is also known as the “grain itch”, “barley itch”, “straw itch”, “hay itch”, “prairie itch”, “mattress itch”, and “cotton seed itch”, sometimes evident occupationally in farmers, bakers, antique dealers, [21] dock workers, packers, and indoor workers. These mites are invisible to the naked eye. [22]

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. [1]

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. [23] 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 classic pathway. A T helper 2 (Th2) shift may be present, similar to what is observed in atopy. [12]

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