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Effects of plasmapheresis on peripheral blood mononuclear cell populations from patients with macroglobulinemia
Author(s) -
Paglieroni Teresa,
Caggiano Vincent,
Mackenzie Malcolm R.
Publication year - 1987
Publication title -
journal of clinical apheresis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.697
H-Index - 46
eISSN - 1098-1101
pISSN - 0733-2459
DOI - 10.1002/jca.2920030403
Subject(s) - plasmapheresis , medicine , peripheral blood mononuclear cell , immunology , macroglobulinemia , hyperviscosity syndrome , leukapheresis , flow cytometry , lymphocyte , waldenstrom macroglobulinemia , b cell , monocyte , in vitro , antibody , biology , stem cell , multiple myeloma , cd34 , biochemistry , genetics , lymphoma
Abstract Effects of plasmapheresis on peripheral blood T‐cell, B‐cell, monocyte, and natural‐killer‐cell populations were studied in ten macroglobulinemia patients with hyperviscosity syndrome. Following plasmapheresis, there was a transient decrease in the number of T4 + helper cells and a longer‐lasting decrease in the number of Leu‐7 + natural killer cells and Mo2+ monocytes. In addition, there was a greater than 50% decrease in the in vitro ingestion capacity of monocytes. Although no significant changes in the numbers of IgM +, B1+, B4 +, or PCA + B cells (P > .05) were detected, there was a highly significant (P < .01) increase in I2 antigen density on the surface of IgM + B cells and in the bromodeoxyuridine uptake by these cells 7‐9 days after plasmapheresis. These findings suggest that following plasmapheresis, IgM+ B cells are activated. Using flow cytometry to determine when maximum IgM+ B cell activation occurs by measuring I2 antigen density on the cell surface may be useful in determining the postplasmapheresis timing of chemotherapy in macroglobulinemia patients with hyperviscosity syndrome who require more aggressive treatment.