Biphasic Anaphylaxis: Review of Incidence, Clinical Predictors, and Observation Recommendations
Section snippets
Historical review
In 1902, Portier and Richet [1] attempted prophylaxis by means of immunization of dogs to sea anemone venom. The sensitized dogs had fatal reactions to subsequent nonlethal doses of the venom, however. This unexpected adverse outcome was termed by Portier and Richet [1] as anaphylaxis. Although a biphasic anaphylactic reaction was described by Duke [2] in 1925 and in two textbooks published in 1983 [3], [4], it was Popa and Lerner [5] who described the first case reports in 1984 and coined the
Clinical characteristics of the biphasic response
There have been several biphasic anaphylactic reaction studies and case reports [9], [10], [11], [12], [13], [14], [15], [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26]. These evaluations are summarized in Table 1.
Popa and Lerner [5] reported three patients who developed systemic anaphylactic symptoms after exposure to rabies vaccine, rye grass extract immunotherapy, or yellow jacket sting. These patients were treated and had improved until 3.5 to 4 hours later, when they
Theories of biphasic pathogenesis
Several potential pathogenic mechanisms have been proposed as listed in Box 2.
The biphasic response was originally thought to be attributable to a temporarily ablated initial reaction, and therefore the result of insufficient treatment [3], [4], [5]. It was later hypothesized that the biphasic anaphylactic response, like that in the skin and respiratory tract, was the result of the secondary influx of cells into the site(s) of the reaction [5]. There are several lines of evidence that mitigate
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