Urticaria

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Jan Hed, Clin Immunologist, MD, PhD
Karolinska Institutet, IMPI, Div of Clin Immunology
Huddinge University Hospital, Sweden
 
The statements below are based on conclusions from selected publications. Their intention is to highlight recent research and information that could be beneficial in allergy in vitro testing. They can include seemingly contradictory statements due to differences in selecting patient populations as well as in the study design (for review, see ref. 1 and 2).
  • Urticaria is also called hives or nettle-rash.
     
  • Urticaria is an immediate phase reaction (vascular reaction) in contrast to atopic dermatitis, which is a delayed phase reaction (cellular reaction).
     
  • Urticarias represent a heterogeneous group of disorders with many different triggers and pathophysiological mechanisms.
    Urticaria is a common disease occurring in 15-20% of the population at some stage of their lives (3) and affecting, at a modest estimate, about 1.3% (4) of the population. 
     
  • Urticaria is divided into an acute and a chronic form, the latter defined as daily urticaria more than 6 weeks.
     
  • Acute urticaria can be categorised into allergic, pseudo-allergic (non-allergic, intolerance or anaphylactoid) or idiopathic.
     
  • Allergic IgE-mediated reactions are primarily seen in acute urticaria in children.
     
  • The majority (81%) of acute urticaria in children is associated with infection (5, 6) and only 11% with food, of which about 60% seems to be related to atopy and atopic dermatitis (6).
     
  • The most frequent allergens in acute allergic urticaria are the same as seen in atopic dermatitis, i.e. egg, milk, fish, peanuts, tree-nuts, and shellfish.
     
  • Any drug, food additives, infection or foreign substance should be considered a potential cause in acute pseudo-allergic urticaria.
     
  • Aspirin and other non-steroidal anti-inflammatory drugs are the most common offending drug substances.
     
  • Allergic IgE-mediated reactions are uncommon in adults and chronic urticaria.
     
  • Chronic urticaria may be autoimmune in origin. A large fraction (60%) of patients with chronic urticaria have auto-antibodies directed to the IgE Fc-receptors on mastcells/basophils, and a smaller fraction (10%) have auto-antibodies directed to IgE (7).

References:

    1. Shelley WB, Shelley ED. Advanced Dermatologic Diagnosis. Philadelphia, London, Toronto, Montreal, Sydney, Tokyo: W.B. Saunders Company. 1992:1219-43.
    2. Kobza Black A, Greaves MW. Urticaria and angioedema. In: Kay AB, editor. Allergy and allergic diseases. Oxford: Blackwell Science Ltd. 1997:1586-1607.
    3. Mahmood T. Urticaria. Am Fam Physician. 1995;51:811-6.
    4. Paul E, Greilich KD. (Epidemiology of urticaria diseases). (Article in German). Hautartz. 1991;42:366-75.
    5. Aoki T, Kojima M, Horiko T. Acute urticaria: history and natural course of 50 cases. J Dermatol. 1994;21:73-7.
    6. Mortureux P, Leaute-Labreze C, Legrain-Lifermann V, Lamireau T, Sarlangue J, Taieb A. Acute urticaria in infancy and early childhood: a prospective study. Arch Dermatol. 1998;134:319-23.
    7. Tong LJ, Balakrishnan G, Kochan JP, Kinet JP, Kaplan AP. Assessment of autoimmunity in patients with chronic urticaria. J Allergy Clin Immunol. 1997;99:461-5.