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5?h post initiation of infusion. The only person in the cohort not showing a measurable TNF�� increase was a woman caring at home for her brother with full blown AIDS (22). Subcutaneously applied IgG concentrate reaches the circulation slowly and systemic AEs are less frequent compared to IVIG but they are not absent (23�C28) (a case of unintentional i.v. application of SCIG is not considered). In contrast, local mild to moderate AEs are more frequent with SCIG (29). In summary, the intensity of the resulting AEs is depending on the immune status of the recipient, the infusion rate (IR), e.g., how rapidly the active ingredients (the various IgG specificities), the impurities, and the excipients reach the circulation of the recipient. Thus, the i.v. application has the highest chance for the occurrence R428 of AEs. In the early days of IVIG therapy, complement-mediated Crizotinib price ��anaphylactoid�� (i.e., immediate) and ��phlogistic�� (i.e., inflammatory) AEs were distinguished (30, 31). The complement-mediated AEs were considered to be caused by aggregates in the product (��spontaneous complement activation�� or anti-complementary activity or ACA) or by in vivo formation of immune complexes (ICs, patient��s condition related; e.g., subclinical infections or the unnoticed presence of anti-IgA antibodies) and therefore only IgG concentrates with low or absent ACA is accepted by authorities for human use. Below, we present one instructive case of each type of reaction. Immediate adverse events �C the rapid onset of darkness The first reports of rapid onset AEs concerned either the application of complement-activating fractions in an IgG concentrate or the in vivo formation of complement-activating ICs (2�C4). A very rare but potentially fatal condition is the formation of IgA/anti-IgA complexes in patients being initiated on replacement therapy and having serum IgG antibodies against infused IgA not recognized before the start of the IVIG infusion (32). Prerequisite for the presence of anti-IgA antibodies UGT1A7 is the most common primary immunoglobulin defect, i.e., selective IgA deficiency (sIgAD) or IgAD associated with diminution of other immunoglobulin classes. IgAD is defined by serum levels of