ANAPHYLAKTOIDE REAKTIONEN

Anaphylactoid reactions can occur after infusion of all the presently available colloid solutions. The clinical symptoms observed in 248 patients ranged from mild reactions with urticarial exanthema to severe complications as anaphylactic shock with cardiac and/or respiratory arrest. Thirteen of the cases presented were fatal. In a total of 200,906 infusions of colloidal volume substitutes, the incidence of anaphylactoid reactions was determined: In 1975 it was generally 0.033%. The numbers for the individual colloids were 0.014% for plasma protein, 0.032% for dextran, 0.085% for hydroxyethyl starch, and 0.115% for gelatine infusions. Serious reactions were observed in the following order: 0.038% for gelatine, 0.008% for dextran, 0.006% for hydroxyethyl starch, and 0.003% for allogeneic plasma protein solutions. The majority of dextran reactions was observed in the preoperative phase. Prior to every therapeutic application of xenogeneic sera, sensitization against the protein used has to be excluded. Patients suffering from autoimmune diseases show signs of sensitization and 'unspecific' (i.e., without previous contact with the antigen) sensitization against horse protein more frequently (27%) than do normals (3%). In animal experiments it was shown that antilymphocytic horse IgG is more immunogenic than normal horse IgG. By pretreatment with deaggregated normal horse IgG, it was possible to induce immunologic unresponsiveness in ALG-treated patients. By application of aggregate free antilymphocyte globulin the frequency of adverse side-reactions was further reduced. The pathogenesis of the anaphylactoid reactions is discussed and prophylactic measures are mentioned. The role of immune reactions in anaphylactoid reactions after gelatine and starch infusions is not yet clear. Anti-gelatine-antibodies (1:40) and anti-hydroxytheylstarch-antibodies (1:2) were detected by passive hemagglutination techniques in patients as well as in controls. All laboratory findings obtained from reacting patients must be compared with controls tolerating the individual substances. Studies of 553 control patients undergoing colloid infusions and of 16 volunteers showed that every colloid infusion is followed by a short change in concentration of several immunologic parameters in the plasma, most probably due to dilution. In methodologic studies three classical immunologic techniques were modified: Micromethod of passive hemagglutination using stable, sensitized red cells for detecting antibodies against horse IgG; immunodiffusion technique for determining hemolytic serum complement activity; and passive cutaneous anaphylaxis using radiolabelled antigen (Radio-PCA). From the results of these investigations the following clinically relevant conclusions for the prophylaxis of anaphylactoid reactions after colloid infusions are drawn: The purity of the solutions must be improved (e.g., less aggregates, better stabilizers). If possible, induction of immunologic unresponsiveness should be tried, either by pretreatment with normal deaggregated horse IgG in the case of ALG therapy or by pretreatment with low molecular weight dextran according to the principle of hapten inhibition in preventing dextran incompatibility.