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
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.