The peripheral neuropathy associated with a monoclonal anti-MAG IgM is considered as a specific entity.1-3 The clinical features are different from those seen with monoclonal IgG or IgA, with sensory loss and ataxia more often found. A causal link between the monoclonal IgM and the development of neuropathy is suggested by the antibody activity of the IgM to nerve polypeptides or glycolipids,3-7 the detection of IgM deposits on the myelin sheaths of patients' nerve biopsies,2 8 9 and the induction of the neuropathological process through the transfer of the anti-MAG IgM in animal models.10 11 The low rate (30%) of clinical improvement with chlorambucil (CLB) or plasma exchange in such patients justifies the search for new therapeutic strategies.12 13 In a previous phase II open clinical trial randomly comparing intravenous immunoglobulins (IVIg) and α-interferon (α-IFN), we concluded that IVIg was inefficient but that α-IFN produced a significant clinical improvement in eight out of 10 patients at 6 months and in seven of them at 12 months.14 The mechanism of action of α-IFN was unclear as the concentration of the monoclonal IgM as well as the titre of anti-MAG antibody were unchanged. As the improvement with α-IFN was mainly related to an improvement of sensory symptoms, most of them being subjective, we designed a multicentre, prospective, randomised double blind study of α-IFN versus placebo. Patients included in this study had to fulfill all the following criteria: (1) have had stable or progressive neuropathy for at least 3 months; (2) show the presence of a serum monoclonal IgM with anti-MAG …
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X Mariette (2000) studied this question.