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Several patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) display polyclonal hypergammaglobulinemia, usually appearing in the first year after onset. Whether this increase in immunoglobulins confers any benefit on the course of CIDP is a matter of debate. The aim of this study was to find out whether in CIDP patients receiving immunoglobulin replacement treatment the polyclonal hypergammaglobulinemia may be due to IgG and IgM substitution for the antibody pool that is defective in CIDP. Serum samples were obtained from six patients with CIDP followed at the ‘S. Giovanni di Dio’ Hospital in Venice, before and during a 3-month immunoglobulin replacement treatment (1 g/kg/month) using human IgG. Serum was investigated for the presence of antineuronal antibodies, anti-myelin-associated glycoprotein antibodies, IgG and IgM anti-aquaporin-4 antibodies, IgM anti-neurofascin antibodies, IgM and IgG anti-ganglioside antibodies and anti-octoclonal IgM or IgG antibodies. Results showed low level of anti-myelin-associated glycoprotein antibodies, IgG anti-aquaporin-4 antibodies, anti-neurofascin antibodies, but not of other antineuronal antibodies in all patients before treatment. Moreover, the polyclonal hypergammaglobulinemia persisted after Ig treatment, as in the majority of CIDP patients already reported in literature. These results add further support to the hypothesis that the polyclonal hypergammaglobulinemia in CIDP is not Ig replacement but a T cell-dependent humoral immune response probably triggered by the loss of tolerance to Schwann cells or by a defective IgG4 switching.Q:

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