In vivo administration of intravenous immunoglobulin (IVIg) can lead to enhanced erythrocyte sequestration

H. Kessary-Shoham, Y. Levy, Y. Shoenfeld, M. Lorber, H. Gershon*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Enhanced erythrocyte sequestration is one of the very few major adverse effects of intravenous immunoglobulin (IVIg). IVIg contains high molecular weight IgG complexes (~300 kDa) which, in the presence of serum, mimic immune complexes by activating complement, binding to CR1 of red blood cells (RBC) (CD35) and mediating erythrophagocytosis. Four of seven patients undergoing IVIg therapy showed significant drops in haematocrit and haemoglobin that were not due to isoantibodies in the IVIg. Prior to treatment, patients' RBC carried IgG and complement (C') 3d that were not bound as immune complexes via CR1 (CD35). The patients whose RBC bound immune complex-like moieties and showed drops in haematocrit and haemoglobin subsequent to IVIg were young adults (22-35 years); older patients (50-69 years) showed no ill effects. In the presence of complement, RBC of young patients bound IVIg complexes in vitro while those of older patients did not. It is not the absolute levels of erythrocyte-associated IgG or C'3 fragments, neither pre- nor post-therapy, which are predictive of Wig associated decreases in haematocrit and haemoglobin levels. Patient age and RBC inability to bind the IVIg immune complex-like moieties in vitro both appear to be predictors of resistance to sequestration after in vivo treatment with IVIg.

Original languageEnglish
Pages (from-to)129-135
Number of pages7
JournalJournal of Autoimmunity
Volume13
Issue number1
DOIs
StatePublished - Aug 1999

Funding

FundersFunder number
Weisz Gerontology Research Fund/WD

    Keywords

    • Aging
    • Anaemia
    • Autoimmunity
    • Erythrocyte sequestration
    • IVIg

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