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

Citation
H. Kessary-shoham et al., In vivo administration of intravenous immunoglobulin (IVIg) can lead to enhanced erythrocyte sequestration, J AUTOIMMUN, 13(1), 1999, pp. 129-135
Citations number
21
Categorie Soggetti
Immunology
Journal title
JOURNAL OF AUTOIMMUNITY
ISSN journal
08968411 → ACNP
Volume
13
Issue
1
Year of publication
1999
Pages
129 - 135
Database
ISI
SICI code
0896-8411(199908)13:1<129:IVAOII>2.0.ZU;2-D
Abstract
Enhanced erythrocyte sequestration is one of the very few major adverse eff ects of intravenous immunoglobulin (IVIg). Mg contains high molecular weigh t IgG complexes (similar to 300 kDa) which, in the presence of serum, mimic immune complexes by activating complement, binding to CR1 of red blood cel ls (RBC) (CD35) and mediating erythrophagocytosis. Four of seven patients u ndergoing Mg therapy showed significant drops in haematocrit and haemoglobi n that were not due to isoantibodies in the Mg. Prior to treatment, patient s' RBC carried IgG and complement (C') 3d that were not bound as immune com plexes via CR1 (CD35). The patients whose RBC bound immune complex-like moi eties and showed drops in haematocrit and haemoglobin subsequent to Mg were young adults (22-35 years); older patients (50-69 years) showed no ill eff ects. In the presence of complement, RBC of young patients bound Mg complex es in vitro while those of older patients did not. It is not the absolute l evels of erythrocyte-associated IgG or C'3 fragments, neither pre- nor post -therapy, which are predictive of Mg associated decreases in haematocrit an d haemoglobin levels. Patient age and RBC inability to bind the Mg immune c omplex-like moieties in vitro both appear to be predictors of resistance to sequestration after in vivo treatment with Mg. (C) 1999 Academic Press.