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The authors retrospectively examined the anti-ganglioside antibody (AGA) IgM level changes from 14 patients with chronic dysimmune neuropathy (5 with multifocal motor neuropathy and 9 with chronic inflammatory demyelinating polyneuropathy) treated with maintenance doses of intravenous immunoglobulins (IVIg). The median follow-up was 5 years. At last follow-up, 93% of the patients had an increment of AGA levels, and five patients with initial AGA values within normal range became positive during follow-up. Overall, median AGA titers significantly increased from the first to the last samples, despite a substantial clinical stability after the initial improvement with IVIg. The AGA increment rate was inversely correlated with IVIg infusions interval necessary to maintain therapeutic efficacy. Thus, antibody testing in the follow-up of patients with dysimmune neuropathies may be helpful to predict the decline of IVIg efficacy and to identify those patients who eventually take advantage from an increase in infusion frequency.

A child with Guillain-Barre syndrome treated with intravenous immune globulin (IVIG) developed neutropenia (absolute neutrophil count — 390), which resolved 3 days after completion of the therapy. Potential mechanisms for the development of neutropenia during the use of IVIG therapy are discussed. In this case, testing of the IVIG used revealed the presence of a high concentration of anti-neutrophil antibodies compared to other samples. It is recommended that white blood cell and neutrophil counts be monitored daily during the use of such therapy.

Experimental autoimmune neuritis (EAN) is an animal model for Guillain-Barre syndrome (GBS). Intravenous immunoglobulins (IVIg) are an effective treatment for GBS, but their mechanism of action is not well understood. Here we tested whether IVIg treatment, a potent modulator of proinflammatory assaults, reduces inflammation in EAN. The evaluation of IVIg treatment failed to demonstrate a salutary effect in different models of EAN. IVIg appears not to suppress the acute inflammatory insult on the peripheral nerve, but may have beneficial long-term effects not looked for in the present investigation.

Patients with chronic inflammatory demyelinating polyneuropathy (CIDP) and with a chronic polyneuropathy (non-CIDP) were studied for the presence of anti-GM1 antibodies. In pretreatment sera of CIDP patients, we found IgG anti-GM1 antibodies in 23%, IgM in 7%, and IgA in 14%. Predominantly motor involvement was associated with IgG and IgM anti-GM1 antibodies in CIDP patients (P = 0.002). Improvement after intravenous immunoglobulin (IVIg) therapy was not associated with anti-GM1 antibody titer before or after treatment. Anti-GM1 antibody titers before onset of treatment was not related to poor clinical outcome, although large clinical improvements after IVIg therapy were observed less often (P = 0.057) in patients with high titer anti-GM1 antibodies before treatment.