Abstract
It is a pleasure and privilege to present the Memorial Fund Lecture for 1957, and I should like to express my appreciation to Dr. Virden, Dr. Frederick O'Brien, and to the members of the Memorial Fund Committee for their invitation to address your Society on this occasion. Multiple myeloma is a disease which has been of major interest to radiologists since the introduction of the technics of diagnostic roentgenography to medicine, and several comprehensive radiographic studies of the disease are available (1–7). Certainly for this audience there is no need to review the various roentgenologic patterns of multiple myeloma. Rather, it is the purpose of this presentation to describe some recent clinical and laboratory studies which support the theses that radiographically evident disease is usually disease which has already progressed to an advanced stage, and that the diagnosis of a proliferative disorder of plasma-cell origin is frequently possible by biochemical technics before roentgen changes are demonstrable. At the outset, an examination of terminology seems appropriate. The term “myeloma” properly denotes a tumor of the marrow, which might be due to any one of a variety of infiltrations. The designation “plasma-cell myeloma” is more precise, but this still implies the presence of tumefaction, i.e., the destruction of bone by a plasmacell tumor. Several clinical studies, however, have made it clear that tumor formation and skeletal destruction may at times be a relatively late and insignificant feature of primary plasmacell proliferation. It is recognized that a certain number of patients will exhibit profound anemia, renal insufficiency, para-amyloidosis, or manifestations secondary to cryoglobulinemia as the predominating features of their clinical picture, with skeletal manifestations playing a minor or even negligible role. These cases are usually called “multiple myeloma” even if a fatal outcome ensues before any skeletal damage is evident. The designation “primary plasmacell proliferation” has been suggested as being more inclusive of the several clinical variants which we now recognize. This term could be used with the understanding that the majority, but not all, of these cases will ultimately exhibit skeletal destruction, true “myeloma,” at some stage in the progression of protein metabolism, presently to be defined, which appear to be unique and distinctive to this disease, or group of diseases. In the course of the past four years, we have had the privilege of studying a group of 24 patients whose sera were discovered to contain an abnormal protein of the myeloma type, but who displayed neither symptomatic nor radiographic evidence of osseous disease. Some of these patients were under medical observation for unrelated conditions.

This publication has 0 references indexed in Scilit: