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    Chapter 38:: Urticaria and Angioedema:: Allen P. Kaplan

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    Syamsi Kubangun
    Urticaria and angioedema are common conditions, occurring in 20% of the population at some point. Acute cases are usually caused by drugs, foods, or infections and involve immunoglobulin E-dependent mechanisms. Chronic cases have an autoimmune cause 45% of the time. Treatment of acute cases relies on antihistamines and short term corticosteroids to identify and remove triggers. Treatment of chronic cases includes antihistamines, low dose corticosteroids, or cyclosporine. The mast cell is the primary cell involved, releasing mediators that cause localized swelling in urticaria and deeper swelling in angioedema.

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    Chapter 38:: Urticaria and Angioedema:: Allen P. Kaplan

    Uploaded by

    Syamsi Kubangun
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    Urticaria and angioedema are common conditions, occurring in 20% of the population at some point. Acute cases are usually caused by drugs, foods, or infections and involve immunoglobulin E-dependent mechanisms. Chronic cases have an autoimmune cause 45% of the time. Treatment of acute cases relies on antihistamines and short term corticosteroids to identify and remove triggers. Treatment of chronic cases includes antihistamines, low dose corticosteroids, or cyclosporine. The mast cell is the primary cell involved, releasing mediators that cause localized swelling in urticaria and deeper swelling in angioedema.

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    Urticaria and angioedema are common conditions, occurring in 20% of the population at some point. Acute cases are usually caused by drugs, foods, or infections and involve immunoglobulin E-dependent mechanisms. Chronic cases have an autoimmune cause 45% of the time. Treatment of acute cases relies on antihistamines and short term corticosteroids to identify and remove triggers. Treatment of chronic cases includes antihistamines, low dose corticosteroids, or cyclosporine. The mast cell is the primary cell involved, releasing mediators that cause localized swelling in urticaria and deeper swelling in angioedema.

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    © All Rights Reserved
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    Download as docx, pdf, or txt
    56 views2 pages

    Chapter 38:: Urticaria and Angioedema:: Allen P. Kaplan

    Uploaded by

    Syamsi Kubangun
    Urticaria and angioedema are common conditions, occurring in 20% of the population at some point. Acute cases are usually caused by drugs, foods, or infections and involve immunoglobulin E-dependent mechanisms. Chronic cases have an autoimmune cause 45% of the time. Treatment of acute cases relies on antihistamines and short term corticosteroids to identify and remove triggers. Treatment of chronic cases includes antihistamines, low dose corticosteroids, or cyclosporine. The mast cell is the primary cell involved, releasing mediators that cause localized swelling in urticaria and deeper swelling in angioedema.

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    © All Rights Reserved
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    Chapter 38 :: Urticaria and Angioedema

    :: Allen P. Kaplan
    .IJRTJCARIA AND ANGIOEDEMA
    ATA GLANCE
    Occurs acutely at some time in 20% of the population; incidence of chronic urticaria/ angloedeina is approximately 0.5%.
    Acute Ur&aria/angjoede is caused by drugs, foods, occasionaily infection in association with immunoglobulin E-dependent
    mechajms (allergy), or metabolic factors.
    Chronic urticaria/a.ngioedema is an
    autoimmune disorder in 45% of patients.
    In the absence of urticaria, angioedema can be due to overproduction or impaired breakdown of bradykinin.
    Treatment of acute urticaria/angioedema relies on antihjstamjne and short courses of corticosteroids, and identification and
    elimination of endogenous and exogenous causes.
    Treatment of Cl inhibitor deficiency includes androgenic agents, antifibrinolytic agents, and Cl inhibitor (Cl INH)
    concentrates, a kallikrejn inhibitor, and bradykinin receptor antagonist.
    Treatment of physical Urticaria/angioedema includes high-dose antthistan-jne prophylaxis, except for delayed pressure
    urticaria.
    Treatment of chronic idiopathic or
    autoim.mune urticaria/angioedema includes antihistamines (nonsedating preparations primarily), low-dose daily or alternate
    day corticosteroids, or cyclosporine.
    Urticaria is defined as a skin lesion consisting of a wheal-and-flare reactiOn in which localized intracutan eous edema
    (wheal) is surrounded by an area of redn ess (erythema) that is typically pruritic. Individual hives can last as briefly as 30
    minutes to as long as 36 hours. They can be as small as a millimeter or 68 inches in diameter (giant urticaria). They blanch
    with pressure as the dilated blood vessels are compressed, which also accounts for the central pallor of the wheal. The dilated
    blood vessels and increased permeability that characterize urticaria are present in the superficial dermis and involves the
    venular plexus in that locat ion. Angioedema can be caused by the same pathog enic mechanisms as urticaia but the
    pathology is in

    the deep dermis and subcutaneous tissue and swelling is the major manifestation. The overlying skin may be erythematous or
    normal. There is less pruritus (fewer type C nerve endings at the deeper Cutaneous levels) but there may be pain or burning.

    EPIDEMIOLOGY
    Urticaria and angioedema are common. Age, race, sex, occupation, geographic location, and season of the year may be
    implicated in urticaria and angioedema only insofar as they may contribute to exposure to an elici ting agent. Of a group of
    college students, 15%20% reported having experienced urticaria, while 1 %3% of the patients referred to hospital
    dermatology clini cs in the United Kingdom noted urticaria and angio edema. In the National Ambulatory Medical Care
    Survey data from 1990 to 1997 in the United States, women accounted for 69% of patient visits. There was a bimodal age
    distribution in patients aged birth to 9 years and 30-40 years.1
    Urticaria/angioedema is considered to be acute if it lasts less than 6 weeks. Most acute episodes are due to adverse reactions
    to medications or foods and in child ren, to viral illnesses. Episodes of urticaria/angjo edema persisting beyond 6. weeks are
    considered chronic and are divided into two major subgroups: (1) chronic autojmmujje urticarja (45%) and (2) chronic
    idiopathic urticaria (55%) with a combined incid ence in the general population of Q5%2 Physically induced
    urticaria/angioedema is not included in the definition. Various types of physical urticaria/angio edema may last for years, but
    the individual lesions last fewer than 2 hours (except delayed pressure urtic aria) and are intermittent. Whereas 85% of
    children experience urticaria in the absence of angioedema, 40% of adult patients with urticaria also experience angioedema.

    Approximately 50% of patients with chronic urtic aria (with or without angioedema) are free of lesions within 1 year, 65%
    within 3 years, and 85% within 5 years; fewer than 5% have lesions that last for more than 10 years. Angioedema alters the
    natural history, and only 25% of patients experience resolution of lesions within 1 year. There are no data regarding the
    remission rate in patients with only angioedema, The hereditary group is considered to be life long once the diagnosis
    becomes clinically manifest.
    PATHOGENESIS
    The mast cell is the major effector cell in most forms of urticaria and angioedema, although other cell types undoubtedl.y
    contribute. Cutaneous mast cells adhere

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