Defective opsonization in multiple myeloma
BD Cheson, RR Plass and G Rothstein
The mechanisms responsible for the unusual susceptibility of multiple
myeloma (MM) patients to infections are incompletely defined. Since MM is
associated with decreased production of normal serum proteins, we
investigated the possibility that the production of opsonins might also be
impaired. The neutrophil chemiluminescence assay of opsonization was used
to evaluate the ability of serum from patients with MM to opsonize zymosan.
It was found that sera from 18 MM patients exerted only 50% +/- 2.5% (mean
+/- SEM) of the opsonic activity found in 18 control sera (p less than
0.001). In mixture experiments, untreated normal serum completely restored
the opsonic activity of MM serum, suggesting a deficiency of opsonic
factors rather than an inhibitor. In other mixture experiments,
heat-inactivated normal serum only partially corrected the opsonic defect
in MM serum. Serum from three patients had low C3 levels, and treatment of
particles with these resulted in a greater opsonic defect than the patient
population as a whole (p less than 0.02). No correlation between the
opsonic defect and infections was established over an 18-mo period. These
data suggest that MM serum lacks both heat-stable and heat-labile opsonic
activity, the direct clinical significance of which remains to be
clarified. However, these studies support the concept that defective host
resistance in MM may be multifactoral, combining opsonic abnormalities with
other defects previously described.
Volume 55,
Issue 4,
pp. 602-606,
04/01/1980
Copyright © 1980 by The American Society of Hematology
