Current treatments for anti-GM1 ganglioside or antimyelin-associated glycop
rotein (anti-MAG) antibody-associated polyneuropathies are toxic or very co
stly. In this preliminary study the authors treated five patients with neur
opathy and immunoglobulin M antibodies to GM1 ganglioside or MAG by depleti
ng B cells using Rituximab-a monoclonal antibody directed against the B-cel
l surface membrane marker CD20. Within 3 to 6 months after treatment, all f
ive patients had improved function, significantly increased quantitative st
rength measurements, and reduced titers of serum autoantibodies.