Relationship between Paraprotein Polymerization and Clinical Features in IgA Myeloma

P. J. Roberts‐Thomson, D. Y. Mason, I. C.M. MacLennan

Research output: Contribution to journalArticlepeer-review

28 Citations (Scopus)


The clinical manifestations of IgA multiple myeloma are usually not considered distinguishable from those of IgG myeloma despite the fact that IgA differs from IgG in several characteristics, particularly molecular size heterogeneity. The clinical and laboratory features of 25 patients with IgA myeloma seen during a 5 year period are presented. The degree of paraprotein polymerization was observed to vary greatly in these patients but remained chronologically constant in six individuals studied on several occasions over this period. The patients were divided into two groups on the basis of the degree of paraprotein polymerization. The first group comprised those patients in whom the IgA paraprotein was greater than 50% polymerized, whilst in the second group the paraprotein was predominantly monomeric. No clinical or pathological differences were seen between the ‘polymeric’ and ‘monomeric’ groups of myeloma apart from that directly attributable to the physicochemical effect of the paraprotein polymerization. Thus, five patients out of 11 of the ‘polymeric’ group had developed the hyperviscosity syndrome, whilst no patients in the ‘monomeric’ group had developed this complication. The concentration of the paraprotein during the course of the disease was comparable in both groups. This syndrome is considered to be relatively common in IgA myeloma and adds to the morbidity and mortality of the disease. Its anticipation and treatment may improve the quality and survival of patients likely to develop this complication.

Original languageEnglish
Pages (from-to)117-130
Number of pages14
JournalBritish Journal of Haematology
Issue number1
Publication statusPublished - May 1976
Externally publishedYes


Dive into the research topics of 'Relationship between Paraprotein Polymerization and Clinical Features in IgA Myeloma'. Together they form a unique fingerprint.

Cite this