Anamnestic response

The bleeding potential is similar among the agents. However, thrombocytopenia, particularly profound thrombocytopenia (platelet count <50,000 mrrT3) occurs with a two-to four-fold higher frequency with abciximab (0.4— 1.0%) compared with eptifibatide (0-0.2%) or tirofiban (0,1 —0.3%) (6), The exact mechanism of this difference is not clear, However, immune complex-mediated reaction (due to an anamnestic response to the humanized chimeric antibody) may contribute to rapid precipitation of thrombocytopenia with abciximab (6), Platelet counts should, therefore, be measured early (within the first one to four hours) after administration of these agents and followed for the duration of therapy. Platelet transfusion should be considered for profound thrombocytopenia with or without serious bleeding (6). 

Delayed reactions are difficult to prevent. Incompatibility may not be demonstrable before transfusion, and at the time of the reaction the relevant antibodies may not be detectable. Post-transfusion blood samples must therefore be subjected to repeated serological testing. Delayed reactions usually occur as a result of a secondary anamnestic response within 3-21 days after the transfusion of apparently compatible blood, at a time when the antibody concentration has risen sufficiently to bring about hemolysis of the donor s erythrocytes. A primary immune response can also evoke this kind of reaction (61). 

Patients with bleeding disorders are at risk of developing antibodies against the protein that is absent, present in reduced amounts, or present in an inactive form in their blood. Such coagulation inhibitors make treatment very difficult. Inhibitors of factor VIII are the most common and develop in 5-20% of patients with hemophiha A. Inhibitors of factor IX develop in 1-4% of patients with hemophilia B (3,4). Patients with factor VIII inhibitors present clinically either as high responders who show a strong anamnestic response and a sharp rise in inhibitor concentrations after exposure to factor VIII, or low responders, who show little or no anamnestic response (5). 

The risk of thrombocjdopenia is increased in patients with a history of previous heparin therapy (44). Thrombocjdopenia and/or thromboembohc comphcations can occur sooner in patients with a history of previous exposure to heparin, suggesting an anamnestic response (28,43). 

Anamnestic response following second administration of antigen. Primary response following initial antigen dose has a lag phase in which no antibody is detected (4"C5 d). This is followed by a lag phase in which antibody is produced. 

If no further exposure occurs, or the immunogen is removed by the mammal, a low level of IgM and IgG can be detected. If reexposure occurs, a similar peak of IgM antibody is produced that declines in a similar kinetic manner to the primary IgM response, but the IgG response is not only more rapid (over time) but also reaches higher serum levels that persist for a longer period of time. This IgG response to reexposure is known as the anamnestic response. This is illustrated in Fig. 7. 

Anamnestic response Prompt immune response due to recall by memory cells. See secondary response. 

The likelihood of elicitation of an IgE response to an antigen is enhanced by inoculation into the footpads (126-128). As indicated earlier, certain parasites induce the formation of relatively high titers of the homocytotropic antibody. Reports vary as to the possibility of elicitation of an anamnestic response. 

Kenney B, Tormey CA. Acute vancomycin-dependent immune thrombocytopenia as an anamnestic response. Platelets 2008 19(5) 379-83. 

The following experiments were conducted in order to ascertain the effects of a pantothenic acid deficiency upon the various phases of the anamnestic response to diphtheria toxoid (Pruzansky and Axelrod, 1954). Pantothenic acid-deficient rats and their respective controls were immunized as described above. Three weeks later the antibody response to this primary injection was determined, and the rats were given a secondary injection of the toxoid. A week later, the anamnestic response to this secondary injection was determined. As previously noted, the antibody response to the primary injection of toxoid was very poor in the deficient rats in contrast with the good responses of the controls. No anamnestic response to the secondary injection was observed in the deficient rats, whereas the controls displayed a very marked anamnesis. An anamnestic response in the deficient rats could not be elicited despite the simultaneous administration of large amounts of pantothenic acid immediately following the secondary injection of toxoid. In contrast, the growth effect of the vitamin was immediate and profound. Thus, the deleterious... 

In order to investigate further the specificity of these vitamin effects, these studies were extended to include purified diphtheria toxoid as the antigen. Again, the marked impairment of antibody response in various vitamin deficiency states was evident (Pruzansky and Axelrod, 1955). With the exception of the deleterious action of a vitamin D deficiency, the trends observed with diphtheria toxoid were similar to those noted when red blood cells served as the antigen. Later studies clearly demonstrated the inhibitory effects of the nutritional deficiency states upon the anamnestic process, with impairment of the secondary response being most pronounced (Figure 1.) (Axelrod, 1958). The conclusion was drawn that the successful attainment and maintenance of a satisfactory anamnestic response to diphtheria toxoid in the albino rat requires a state of adequate nutriture during both the primary and secondary phases of this process. 

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