Immediate hypersensitivity: Difference between revisions

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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."<ref name="MeSH">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?term=Immediate+hypersensitivity |title=Hypersensitivity, immediate  |accessdate=2008-01-16 |author=Anonymous |authorlink= |coauthors= |date= |format= |work= |publisher=National Library of Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref>
'''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."<ref name="MeSH">{{cite web |url=http://www.nlm.nih.gov/cgi/mesh/2008/MB_cgi?term=Immediate+hypersensitivity |title=Hypersensitivity, immediate  |accessdate=2008-01-16 |author=Anonymous |authorlink= |coauthors= |date= |format= |work= |publisher=National Library of Medicine |pages= |language= |archiveurl= |archivedate= |quote=}}</ref>


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


;Examples include:
==Examples==
*Allergic [[asthma]]
*Allergic [[asthma]]
*Allergic [[conjunctivitis]]
*Allergic [[conjunctivitis]]

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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]

Pathogenesis

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.

Examples

  • 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
  • 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]

Treatment

There are minimal randomized controlled trials to guide treatment, especially for treating anaphylaxis.[6][7]

One protocol that successfully treated 241 drug hypersensitivity reactions is:[8]

  • 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 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:[9]

  • 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).[10]
  • Antihistamines (H2) were not studied in this review.
  • Glucocorticoids parenterally are recommended by all but two guidelines.

References

  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. 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.
  7. Anonymous. Cochrane Reviews - by topic 'Anaesthesia'. Cochrane Collaboration. Retrieved on 2008-01-16.
  8. 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]
  9. 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.
  10. Brown SG, Mullins RJ, Gold MS (2006). "Anaphylaxis: diagnosis and management". Med. J. Aust. 185 (5): 283–9. PMID 16948628[e]