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M R MacKenzie

Publications and source records attributed to M R MacKenzie.

50 records · Page 3Linked to original sources

The hyperviscosity syndrome. I. In IgG myeloma. The role of protein concentration and molecular shape.

The hyperviscosity syndrome is an uncommon complication in IgG myeloma. Its occurrence has been ascribed to the presence in the serum of high molecular weight polymers of the IgG proteins. Three patients with IgG myeloma and the clinical hyperviscosity syndrome were investigated, none of whom had IgG polymers in the serum by analytical ultracentrifugation. Relative serum viscosity in these patients ranged from 10 to 17.4 (normal 1.4-1.8). The total serum proteins ranged from 14 to 19 g/100 ml of which 10 to 17 g/100 ml was IgG globulin. Physicochemical studies of two of the isolated myeloma proteins indicated that they were of normal molecular weight (near 158,000 and 162,000). Protein Ca had a normal molecular radius (52.2 A) and configuration, (intrinsic viscosity of 5.5 cc/g, frictional ratio 1.48), but was present in very high concentration in the serum. Protein Pur had an increased molecular radius (58.2 A) and was asymmetrical (intrinsic viscosity 10.2 cc/g, frictional ratio 1.63). These results indicate that the concentration and molecular configuration of the myeloma protein are important determinants of the presence or absence of the hyperviscosity syndrome.

Blood Proteins↗

Non-random chromosomal aberrations associated with multiple myeloma.

Myelomatous tissue from 30 patients was assessed for cytogenetic abnormalities and one-third showed chromosomal deletions, additions, and/or rearrangements. Evidence is presented that those cases with only normal cytogenetics represent metaphase cells of nonmyelomatous tissue. The findings of our abnormal cases when added to the 18 reported in two series by others show unique cytogenetic patterns are present in this disease. From analysis of these 27 banded cases of myeloma, we conclude: (1) cytogenetic abnormalities of myeloma are not random; (2) clonal evolution may be associated with disease progression, however the abnormalities identified late in the disease are similar to those found in early myeloma; (3) cytogenetic aberrations of multiple myeloma differ considerably from those of chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and acute lymphocytic and nonlymphocytic leukemia; and (4) the myeloma karyotype often exhibits one or more of the following: rearrangements involving chromosome 1 and 14, trisomy 3, 5, 7, 9 and 11, and monosomy 8 and 13. These findings have great importance for molecular biologic studies of multiple myeloma.

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