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Immediate hypersensitivity

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Immediate hypersensitivity is defined as "hypersensitivity reactions which occur within minutes of exposure to challenging antigen due to the release of histamine which follows the antigen-antibody reaction and causes smooth muscle contraction and increased vascular permeability."[1]


Type 1 hypersensitivity is an allergic reaction provoked by re-exposure to a specific type of antigen referred to as an allergen. Exposure may be by ingestion, inhalation, injection, or direct contact. The difference between a normal immune response and a type I hypersensitive response is that plasma cells secrete IgE. This class of antibodies binds to Fc receptors on the surface of tissue mast cells and blood basophils. Mast cells and basophils coated by IgE are "sensitized." Later exposure to the same allergen, cross-links the bound IgE on sensitized cells resulting in degranulation and the secretion of pharmacologically active mediators such as histamine, leukotriene, and prostaglandin that act on the surrounding tissues. The principal effects of these products are vasodilation and smooth-muscle contraction.

The reaction may be either local or systemic. Symptoms vary from mild irritation to death.


  • Allergic asthma
  • Allergic conjunctivitis
  • Allergic rhinitis ("hay fever")
  • Anaphylaxis. Anaphaxis has no universally accepted definition[2], but is defined by the U.S. National Library of Medicine as "may include rapidly progressing urticaria, respiratory distress, vascular collapse, systemic shock."[3]
  • Angioedema which is defined as "swelling involving the deep dermis, subcutaneous, or submucosal tissues, representing localized edema. Angioedema often occurs in the face, lips, tongue, and larynx."[4]
  • Eosinophilia. An elevated total eosinophil count, or an increased percentage of eosinophils among other leukocytes.
  • Urticaria (hives) which is defined as "a vascular reaction of the skin characterized by erythema and wheal formation due to localized increase of vascular permeability. The causative mechanism may be allergy, infection, or stress."[5]
  • Food hypersensitivity, which may be overdiagnosed.[6]


There are minimal randomized controlled trials to guide treatment, especially for treating anaphylaxis.[7][8]

Clinical practice guidelines for advanced cardiac life support by the American Heart Association provide treatment algorithms that are available at[9]

One protocol that successfully treated 241 drug hypersensitivity reactions is:[10]

  • First, for patients who report reactions to beta-lactam antibioics, give skin tests and do not challenge patients with positive skin tests.[11]
  • Reactions without a decrease in blood pressure. Give 40 to 60 mg of prednisolone and then 10 mg of loratadine or cetirizine for 2 days.
  • Reactions with anaphylaxis. Give 0.25 µg [sic? should this be 0.25 mg] of intramuscular epinephrine in addition to prednisolone or antihistamine. Repeat epinephrine every 15 minutes if necessary.
  • Reactions with hypotension. Give plasma expanders as needed.

For treating anaphylaxis, in the absence of empiric evidence a review of six clinical practice guidelines found that:[12]

  • Epinephrine intramuscularly at doses ranging from 0.01 mg/kg up to 0.5 mg is recommended by all guidelines.
  • Antihistamines (H1) are recommended by all but one guideline. Most recommended diphenhydramine while one guideline recommended chlorphenamine. The one dissenting guideline is from Australia where the only parenteral antihistamine is promethazine. While this guideline does not recommend antihistamines, it allows oral, non-drowsiness-inducing antihistamines that do not act on other receptors for other amines (such as serotonin or catecholamines).[13]
  • Antihistamines (H2) were not studied in this review.
  • Glucocorticoids parenterally are recommended by all but two guidelines.


  1. Anonymous. Hypersensitivity, immediate. National Library of Medicine. Retrieved on 2008-01-16.
  2. Sampson HA, Muñoz-Furlong A, Campbell RL, et al (2006). "Second symposium on the definition and management of anaphylaxis: summary report--Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium". J. Allergy Clin. Immunol. 117 (2): 391–7. DOI:10.1016/j.jaci.2005.12.1303. PMID 16461139. Research Blogging.
  3. Anonymous. Anaphylaxis. National Library of Medicine. Retrieved on 2008-01-16.
  4. Anonymous. Angioedema. National Library of Medicine. Retrieved on 2008-01-16.
  5. Anonymous. Urticaria. National Library of Medicine. Retrieved on 2008-01-16.
  6. Chafen, Jennifer J. Schneider; Sydne J. Newberry, Marc A. Riedl, Dena M. Bravata, Margaret Maglione, Marika J. Suttorp, Vandana Sundaram, Neil M. Paige, Ali Towfigh, Benjamin J. Hulley, Paul G. Shekelle (2010-05-12). "Diagnosing and Managing Common Food Allergies: A Systematic Review". JAMA 303 (18): 1848-1856. DOI:10.1001/jama.2010.582. Retrieved on 2010-05-12. Research Blogging.
  7. Sheikh A, Ten Broek V, Brown SG, Simons FE (2007). "H1-antihistamines for the treatment of anaphylaxis: Cochrane systematic review". Allergy 62 (8): 830–7. DOI:10.1111/j.1398-9995.2007.01435.x. PMID 17620060. Research Blogging.
  8. Anonymous. Cochrane Reviews - by topic 'Anaesthesia'. Cochrane Collaboration. Retrieved on 2008-01-16.
  9. (December 2005) "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: Part 10.6: Anaphylaxis". Circulation 112 (24 Suppl): IV1–203. DOI:10.1161/CIRCULATIONAHA.105.166550. PMID 16314375. Research Blogging.
  10. Messaad D, Sahla H, Benahmed S, Godard P, Bousquet J, Demoly P (2004). "Drug provocation tests in patients with a history suggesting an immediate drug hypersensitivity reaction". Ann. Intern. Med. 140 (12): 1001–6. PMID 15197017[e]
  11. Brockow K, Romano A, Blanca M, Ring J, Pichler W, Demoly P. General considerations for skin test procedures in the diagnosis of drug hypersensitivity. Allergy. 2002;57:45-51. PMID 11991289
  12. Alrasbi M, Sheikh A (2007). "Comparison of international guidelines for the emergency medical management of anaphylaxis". Allergy 62 (8): 838–41. DOI:10.1111/j.1398-9995.2007.01434.x. PMID 17620061. Research Blogging.
  13. Brown SG, Mullins RJ, Gold MS (2006). "Anaphylaxis: diagnosis and management". Med. J. Aust. 185 (5): 283–9. PMID 16948628[e]