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Urticaria. An updated review.

E W Monroe, H E Jones

    Archives of Dermatology
    |January 1, 1977
    PubMed
    Summary
    This summary is machine-generated.

    Urticaria pathogenesis involves diverse immunologic and nonimmunologic factors converging on mast cells. Key mediators like histamine, released from these cells, increase vascular permeability, causing hives.

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    Area of Science:

    • Immunology
    • Dermatology
    • Pathogenesis of Urticaria

    Background:

    • Urticaria (hives) can be triggered by various stimuli.
    • Pathogenesis involves both immunologic and nonimmunologic pathways.
    • Type I hypersensitivity mediated by immunoglobulin E (IgE) is a primary immunologic mechanism.

    Purpose of the Study:

    • To review the multifaceted pathogenesis of urticaria.
    • To explore the roles of various mediators in urticarial lesion development.
    • To emphasize the significance of histamine and its regulation.

    Main Methods:

    • Review of existing literature on urticaria pathogenesis.
    • Analysis of immunologic and nonimmunologic factors.
    • Examination of mediator roles, including histamine, kinins, and anaphylatoxins.

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    Main Results:

    • Multiple factors (immunologic, nonimmunologic, genetic) converge on mast cells and basophils.
    • Release of mediators like histamine, kinins, serotonin, and anaphylatoxins increases vascular permeability.
    • These mediators contribute to the formation of wheals characteristic of urticaria.

    Conclusions:

    • Urticaria results from a complex interplay of factors leading to mediator release.
    • Histamine is a crucial mediator, and its release from mast cells and basophils is tightly regulated.
    • Understanding these mechanisms is vital for diagnosis and treatment of urticaria.