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Anti–myelin‐associated glycoprotein IgM antibody titers in neuropathy associated with macroglobulinemia
Author(s) -
NobileOrazio E.,
Francomano E.,
Daverio R.,
Barbieri S.,
Marmiroli P.,
Manfredini E.,
Carpo M.,
Moggio M.,
Legname G.,
Baldini L.,
Scarlato G.
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410260408
Subject(s) - macroglobulinemia , gammopathy , immunology , titer , immunoglobulin m , antibody , myelin associated glycoprotein , medicine , polyneuropathy , antigen , autoantibody , peripheral neuropathy , immunoglobulin g , myelin , monoclonal , monoclonal antibody , endocrinology , multiple myeloma , diabetes mellitus , central nervous system
Abstract Twenty‐seven patients with neuropathy and IgM monoclonal gammopathy were tested for antigen specificity of the M‐protein and for anti–myelin‐associated glycoprotein (MAG) IgM levels by immunoblot. In 16 patients (59.2%) the M‐protein reacted with MAG and with cross‐reactive glycoconjugates. Anti‐MAG IgM titers in these patients ranged between 1 : 12,800 and 1 : 100,000. A fainter IgM reactivity with MAG and related glycoconjugates was detected in 3 additional patients with neuropathy, but also in 8 of 24 patients with IgM M‐protein without neuropathy (33.3%). This reactivity was not due to the M‐protein and corresponded to antibody titers of 1:400 or less in all but 1 patient with a titer of 1 : 3,200. Low titers of anti‐MAG IgM (1 : 200 or less) were also detected in 17 of 101 control patients without IgM M‐proteins (16.8%), while 1 patient with neuropathy of unknown cause had anti‐MAG IgMk titers of 1 : 25,600. In 1 patient with neuropathy and IgM M‐protein that was not anti‐MAG, the M‐protein bound to other antigens in nerve, while in 6, other possible causes or mechanisms for the neuropathy were found. In this study, high titers of anti‐MAG IgM antibodies were always associated with neuropathy. The presence of low levels of anti‐MAG IgM in a significant proportion of controls suggests that monoclonal expansion of naturally occurring B‐cell clones secreting anti‐MAG IgM may be responsible for the high incidence of this antigen specificity of the M‐protein.