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Mouse model links macroglobulinemia to cerebral microcirculatory dysfunction; leaves open whether findings translate to human hyperviscosity symptoms or therapy.
THE natural history of human macroglobulinemia includes transient neurological symptoms ranging from headache to dizziness, dysequilibria, and focal motor weakness.¹⁻³In many cases these symptoms are associated with a rise in serum viscosity and are ameliorated by plasmaphoresis which reduces the concentration of macroglobulin (IgM) and the serum viscosity. These symptoms form a portion of the "hyperviscosity syndrome"¹and are often accompanied by "beading" or the presence of "box-car" deformities in retinal vessels.¹,⁴⁻⁶An experimental model of macroglobulinemia is provided by Balb/c mice, bearing a plasma cell tumor, (MOPC-104E), which secretes large amounts of IgM into the blood stream.⁷,⁸Like their human counterparts¹,⁹,¹⁰these mice display an elevated blood viscosity which is a function of the concentration of IgM in the plasma, and which also depends upon the viscosity of the plasma, and the hematocrit level.⁸Erythrocytes from these mice displayed a marked
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William I. Rosenblum (1968) studied this question.
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