摘要
To investigate the therapeutic potential of high dose immunoglobulin (HIG) in experimental allergic neuritis (EAN) to provide a theoretical basis of its clinical use in the treatment of human inflammatory demyelinating neuropathies Methods Female Lewis rats were induced to EAN, and divided into experimental and control groups The rats were treated with either 0 3?g/kg·day 1 of IgG or an equivalent volume of 0 15?mol/L glycine Clinical, electrophysiologic, and histologic evaluations were carried out in a blind fashion Results Clinically, rats treated with IgG had significantly less severe symptoms ( P <0 001) and slower progression ( P <0 001) than controls Electrophysiologically, the mean conduction latency of the experimental group was significantly shorter than controls ( P <0 05) Histologically, rats treated with IgG prepared from normal Lewis rats had a significantly lower percentage of demyelinated fibers ( P =0 01) and total abnormal fibers ( P <0 001) than controls Statistically, clinical, electrophysiologic and morphologic data were all significantly correlated Conclusions The EAN animal model is reliable for observation of HIG effects, and useful to provide data for clinical work HIG has a significant therapeutic effect in EAN when given soon after disease onset It can reduce clinical disease severity and decrease the number of demyelinated fibers as well as the number of total abnormal fibers For the current controversy over whether HIG is effective, the results of this research support the clinical use of HIG in human demyelinating neuropathy
To investigate the therapeutic potential of high dose immunoglobulin (HIG) in experimental allergic neuritis (EAN) to provide a theoretical basis of its clinical use in the treatment of human inflammatory demyelinating neuropathies Methods Female Lewis rats were induced to EAN, and divided into experimental and control groups The rats were treated with either 0 3?g/kg·day 1 of IgG or an equivalent volume of 0 15?mol/L glycine Clinical, electrophysiologic, and histologic evaluations were carried out in a blind fashion Results Clinically, rats treated with IgG had significantly less severe symptoms ( P <0 001) and slower progression ( P <0 001) than controls Electrophysiologically, the mean conduction latency of the experimental group was significantly shorter than controls ( P <0 05) Histologically, rats treated with IgG prepared from normal Lewis rats had a significantly lower percentage of demyelinated fibers ( P =0 01) and total abnormal fibers ( P <0 001) than controls Statistically, clinical, electrophysiologic and morphologic data were all significantly correlated Conclusions The EAN animal model is reliable for observation of HIG effects, and useful to provide data for clinical work HIG has a significant therapeutic effect in EAN when given soon after disease onset It can reduce clinical disease severity and decrease the number of demyelinated fibers as well as the number of total abnormal fibers For the current controversy over whether HIG is effective, the results of this research support the clinical use of HIG in human demyelinating neuropathy
