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Anti-myelin-associated glycoprotein IgM antibody titers in neuropathy associated with macroglobulinemia.

Authors :
Nobile Orazio, E
Francomano, E
Daverio, R
Barbieri, S
Marmiroli, P
Manfredini, E
Carpo, M
Moggio, M
Legname, G
Baldini, L
MARMIROLI, PAOLA LORENA
Baldini, L.
Nobile Orazio, E
Francomano, E
Daverio, R
Barbieri, S
Marmiroli, P
Manfredini, E
Carpo, M
Moggio, M
Legname, G
Baldini, L
MARMIROLI, PAOLA LORENA
Baldini, L.
Publication Year :
1989

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.

Details

Database :
OAIster
Notes :
STAMPA, English
Publication Type :
Electronic Resource
Accession number :
edsoai.on1308904113
Document Type :
Electronic Resource