Description
Anaphylactoid reaction induced by IgG anti-IgA antibodies may occur in individuals with IgA deficiency. The incidence of IgA deficiency is quite common in the population, with its frequency reaching nearly 1:400. Formation of immunocomplexes of antibodies (IgG anti-IgA) with antigen (IgA) leads to complement activation. Anaphylactoid reaction that release vasoactive anaphylatoxins (C3a, C4a, C5a) is a serious complication in transfusions or immunoglobuline replacement therapy. Like anaphylactic reaction, it is accompanied by hives, hypotension, dispnoea with bronchospasm or stridor.
Anti-IgA antibodies are found in patients with undetectable IgA levels. In about 10% of patients with IgA deficiency (IgAD) and with common variable immunodeficiency (CVID), anti-IgA antibodies are present. A causal relationship has been between IgG anti-IgA antibodies and the development of anaphylactoid reactions has been demonstrated, especially for cases when anti?IgA antibodies are in higher concentrations.
Patients with IgA deficiency who need a blood transfusion or blood derivatives substitution should receive negative IgA blood components or an autotransfusion should be performed. Measurement of anti-IgA antibodies should be carried out in patients requiring this treatment.
The recommendation for subjects with known anaphylactoid reaction is to perform the test for anti-IgA at the interval of at least ten days after the response (the onset of antibodies production). Alternative subcutaneous immunoglobulin replacement therapy (SCIG) may be considered if anaphylactoid reactions to intravenous gammaglobulin therapy (IVIG) have occured and if anti?IgA antibodies are present