Elliott F. Osserman

Markedly increased quantities of lysozyme have been found in the serum and urine (ranging to 2.6 g per day) of ten consecutive cases of monocytic and monomyelocytic leukemia. The enzyme has been isolated from the urine of several cases and physicochemically and immunochemically characterized. It is apparently identical to the lysozyme of normal tears, saliva, leukocytes, and serum, but structurally different from the lysozyme of hen's egg white. The activity of the human enzyme assayed with M. lysodeikticus organisms is 3 to 12 times greater than egg white lysozyme at equivalent concentrations. An agar plate method has been developed for quantitating lysozyme activity in small samples (approximately 25 microl) of serum, urine, or other biological fluids. The range and reproducibility of this method were found to be superior to previously available lysozyme assay procedures. Present evidence indicates that lysozyme is the principal, if not the sole, product of the proliferating monocytes in monocytic and monomyelocytic leukemia, and quantitation of serum and urine lysozyme should be a useful diagnostic procedure for these leukemias.

THE purpose of this article is primarily to review the more recent acquisitions to the knowledge and understanding of the pathophysiology of the plasma-cell dyscrasias. Several comprehensive studies of the clinical, radiographic, pathological and biochemical features of multiple myeloma have been published in the past thirty years.1 2 3 4 5 6 7 8 9 10 11 12 13 Major emphasis in this presentation, however, will be given to specific topics pertaining to plasma-cell neoplasia in which recent progress has been made.The "typical" case of multiple myeloma, if, indeed, such an entity exists, must now be considered as representing just one of several clinical patterns that may arise from a primary . . .

†Faculty Research Associate of the American Cancer Society. ‡Research Trainee of the National Cancer Institute (CRTY-5011).

PERIPHERAL neuropathy has been associated with plasma-cell dyscrasia, 1 but it is not known whether the monoclonal immunoglobulins react with peripheral-nerve antigens. We report on a patient with a peripheral neuropathy associated with an IgMk monoclonal protein, in whom pathological and immunological studies indicated that the IgMk antibody was directed against peripheral-nerve myelin, as shown by complement fixation and immunoabsorption.Case ReportThe patient was a 45-year-old man admitted for evaluation of a slowly progressive sensory-motor neuropathy of 11 years' duration. On examination there was moderate to severe weakness and atrophy of the muscles of the hands and distal parts of . . .

The frequency of monoclonal immunoglobulins and Bence-Jones proteins was studied in 100 cases of amyloidosis classified according to the patterns of distribution of amyloid. Monoclonal immunoglobulins, Bence-Jones proteins (or both) were documented in all 50 Pattern I ("primary-type") cases, nine of 17 Pattern II ("secondary-type") cases, 26 of 30 Mixed Pattern I and II cases and in all three cases of localized amyloidosis. Forty-six per cent of the patients with amyloidosis (all patterns) had Bence-Jones protein only, without a monoclonal immunoglobulin, as compared with 21 per cent of cases of myeloma without associated amyloidosis. There was a higher proportion of λ-type Bence-Jones proteins in the amyloidosis group, and amyloid-related proteins were relatively more anionic than nonamyloid-related proteins. It is postulated that amyloid-related monoclonal immunoglobulins and Bence-Jones proteins may be autoantibodies or fragments of autoantibodies directed against normal tissue constituents. (N Engl J Med 290:473–477, 1974)