Abstract
Conclusions and Summary
This report is intended to describe a new observation. Speculation about the ultimate significance of virtually complete inhibition of leukocytic phagocytosis in hypergammaglobulinemic multiple myeloma (M.M.) plasma in vitro is clearly unwarranted at present, but a few tentative conclusions are justified: (1) Depressed phagocytic activity is directly attributable to the γ globulin fraction in M.M. plasma and not to a cellular defect. (2) Plasma from M.M. patients with hyperproteinemia due to increased levels of αR or β globulins, or from patients with hypergammaglobulinemia due to disease other than M.M. does not inhibit leukocyte phagocytic activity. (3) Inhibited phagocytosis appears not to be solely a function of total gamma globulin level. This is most clearly demonstrated by the relatively low levels of γ globulin which inhibit phagocytosis in plasma of M.M. patients without hypergammaglobulinemia or hyperproteinemia; most notably when γ globulin levels are lower than normal. (4) Since the inhibitory effect of hypergammaglobulinemic M.M. plasma may be decreased or abolished by diluting the abnormal plasma with normal plasma or isotonic saline, the effect is not due to a simple deficiency. Specifically, the inhibitory phenomenon appears not to be due to a deficiency of normal gamma globulin. (5) Studies of the phenomenon are continuing.
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