So one of the most common problems that we encounter in the treatment of myeloma is the risk of infection. And it really derives from two things. One, patients with myeloma are inherently at risk of infection. As you see clonal expansion, you see a decrease in the number of polyclonal normal immunoglobulins and immunoparesis. In addition, many of our therapies also cause further reduction of our total globulins, which are part of our antibody-mediated infection-fighting capabilities...
So one of the most common problems that we encounter in the treatment of myeloma is the risk of infection. And it really derives from two things. One, patients with myeloma are inherently at risk of infection. As you see clonal expansion, you see a decrease in the number of polyclonal normal immunoglobulins and immunoparesis. In addition, many of our therapies also cause further reduction of our total globulins, which are part of our antibody-mediated infection-fighting capabilities. And so what we’ve done in the past couple of years in an ad hoc fashion is we’ve treated patients with immunoglobulin replacement therapy, specifically intravenous immunoglobulin G, IVIG, as a way to combat some of the hypogammaglobulinemia that we see. So what we did in our study is we did a retrospective longitudinal observational study of the patients seen through MGB in our research patient data repository, which is kind of a data vault that we’re able to do different research projects from. And we identified about over 6,000 patients with multiple myeloma who had had immunoglobulin data measured and as well had identified a cohort of about 7% of those patients who had received IVIG at some point over the course of their therapy. And what the really important finding was, so we set a threshold of hypogammaglobulinemia of 500 milligrams per deciliter. And we identified patients who had received IVIG. And what we showed in terms of the risk of infection, particularly severe infections and antimicrobial use, were significantly reduced with the introduction of IVIG. And in addition to that, when patients do receive IVIG, they have not surprisingly significantly less hypogammaglobulinemia. And so I think this is particularly important now as we have therapies like CAR T-cell and bispecific T-cell engagers that cause even greater reductions in the gamma globulin production. And we know that these patients have significantly increased risk of infection compared to even prior. So it’s really nice to have something that supports what we’re doing in clinical practice.
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