| Literature DB >> 2411667 |
Abstract
Anaphylactoid reactions have been reported in association with all of the currently available plasma substitutes. The clinical picture ranges from skin reactions only to severe and life-threatening complications, which can be conveniently classified into four grades of severity. The pathomechanism of these anaphylactoid reactions varies for the different colloids. Anti-dextran antibodies (most likely IgG) seem to be responsible for severe DIAR representing an immune complex anaphylaxis. IgE has not been implicated in reactions of this type. Skin tests seem to be of limited value in the diagnosis of dextran reactions and should be performed with great caution. Administration of a specific hapten (low-molecular-weight dextran) prior to dextran infusion reduces the frequency of DIAR in animals and humans. The principal mediator of anaphylactoid reactions due to gelatin infusion is histamine, and this has been established for urea-linked gelatin. It is likely that the diisocyanate present in some polygeline batches is the histamine-releasing substance. Better purification of polygeline and pretreatment with histamine H1-receptor and H2-receptor antagonists have both substantially reduced the frequency of clinical reactions. Changes in plasma complement levels have been observed in patients with anaphylactoid reactions to HES. Antibodies against HES have been detected in humans, but no correlation has been found between the titer of antibodies and anaphylactoid reactions to HES. A further problem with repeated HES infusions is its potentially irreversible storage. Anaphylactoid reactions to colloids should be treated according to the grade of severity. Epinephrine should only be given in severe (grades III and IV) reactions. The early application of glucocorticosteroids (500-1,000 mg of prednisolone equivalent) also may be helpful.Entities:
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Year: 1985 PMID: 2411667
Source DB: PubMed Journal: Int Anesthesiol Clin ISSN: 0020-5907