Drug desensitization: Difference between revisions
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imported>Howard C. Berkowitz No edit summary |
imported>Howard C. Berkowitz No edit summary |
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| journal = Wake Forest School of Medicine}}</ref> | | journal = Wake Forest School of Medicine}}</ref> | ||
It is primarily directed at Type I, or [[ | It is primarily directed at Type I, or [[Immunoglobulin E|immunoglobulin E]]-mediated, in the [[Gell and Coombs classification of immune reactions]]. The interaction of these with the drug causes degranulation of [[basophil]]s and [[mast cell]]s, which release or produce immune mediators such as [[histamine]], [[prostaglandin]]s, and [[leukotriene]]s. <ref>{{citation | ||
| title = Hypersensitivity Reactions, Immediate | |||
| author = Miriam K Anand and John M Route | journal = eMedicine | |||
| date = 21 April 2010 | |||
| url = http://emedicine.medscape.com/article/136217-overview}}</ref> | |||
==References== | |||
{{reflist}} | |||
Revision as of 21:39, 24 September 2010
Drug desensitization is a technique for suppressing dangerous immune reactions to specific drugs, such that the drug may be used for treatment. It uses different approaches than allergy desensitization, intended to produce long-term effects. [1]
It is primarily directed at Type I, or immunoglobulin E-mediated, in the Gell and Coombs classification of immune reactions. The interaction of these with the drug causes degranulation of basophils and mast cells, which release or produce immune mediators such as histamine, prostaglandins, and leukotrienes. [2]
References
- ↑ "Drug Desensitization", Wake Forest School of Medicine
- ↑ Miriam K Anand and John M Route (21 April 2010), "Hypersensitivity Reactions, Immediate", eMedicine