Disease relevance of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• At autopsy old CNS demyelination consistent with MS was found as well as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with onion bulb formation in hypertrophic nerves [1].
• In 4 (2 with multiple sclerosis, 1 with chronic progressive myelopathy, and 1 with chronic inflammatory polyradiculoneuropathy) of these 12, the antibodies that were all directed to p19 were determined to be specific by homologous competitive inhibition [2].
• Four patients with chronic inflammatory demyelinating polyneuropathy (CIDP) who were refractory to conventional treatment were treated with high-dose cyclophosphamide (200 mg/kg over 4 days) [3].
• RESULTS: Nine HNPP subjects, 22 with CIDP and 49 with diabetic polyneuropathy [4].
• Heterozygous P0 knockout mice develop a peripheral neuropathy that resembles chronic inflammatory demyelinating polyneuropathy (CIDP) [5].

High impact information on Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• P0 protein is a target antigen in chronic inflammatory demyelinating polyradiculoneuropathy [6].
• Randomized controlled trial of intravenous immunoglobulin versus oral prednisolone in chronic inflammatory demyelinating polyradiculoneuropathy [7].
• These results show that P0 is an autoantigen in some patients with CIDP [6].
• Prednisone improves chronic inflammatory demyelinating polyradiculoneuropathy more than no treatment [8].
• Because the myelinating BB-1-positive Schwann cells expressed HLA-DR antigen, the findings indicate that, in CIDP, Schwann cells possess the necessary markers to function as antigen-presenting cells [9].

Chemical compound and disease context of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• Chronic nephrotoxicity complicating cyclosporine treatment of chronic inflammatory demyelinating polyradiculoneuropathy [10].
• Pulse cyclophosphamide therapy in CIDP [11].
• Twenty-seven patients with static or worsening chronic inflammatory-demyelinating polyradiculoneuropathy were randomly assigned to alternate day decremental prednisone therapy alone or with azathioprine (2 mg/kg) for 9 months [12].
• Procainamide-induced chronic inflammatory demyelinating polyradiculoneuropathy [13].
• BACKGROUND: Classic chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) patients have prominent proximal and distal weakness [14].

Biological context of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• Thirty-one chronic idiopathic demyelinating polyradiculoneuropathy (CIDP) patients have been typed for HLA-A, -B and -C antigens serologically and for HLA-DR, -DQ and -DP class II genes by RFLP analysis [15].
• The 38-year-old patient had elevated CSF-protein, slow nerve conduction velocities, sural nerve biopsy revealed mixed axon loss with demyelination and CIDP white matter lesions were observed in magnetic resonance imaging, the GM1- and GM3-autoantibodies may play a role in the pathogenesis of CIDP in SLE [16].
• The diagnosis of CIDP was based on the research criteria proposed by the Ad Hoc Subcommittee of the American Academy of Neurology AIDS Task Force. The nerve pathology in these patients comprised macrophage-associated active demyelination and subsequent remyelination of various proportions [17].
• The acute lesions of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) consist of endoneurial foci of chemokine and chemokine receptor expression and T cell and macrophage activation [18].

Anatomical context of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• Twelve patients (5 with multiple sclerosis, 1 with chronic progressive myelopathy, 2 with chronic inflammatory polyradiculoneuropathy, 2 with myasthenia gravis, and 2 with motor neuron disease) had low-titer HTLV-I antibodies that reacted with a single gag protein, p19 or p24, on Western blot assay [2].
• In biopsies from CIDP and vasculitic neuropathy patients, but not in those from healthy controls, Schwann cells expressed the adhesion/T-cell stimulatory molecule CD58 (LFA-3) [19].
• High-dose cyclophosphamide without stem-cell rescue for refractory CIDP [3].
• In vitro studies showed that IgG from pooled normal donors (IV-IgG) inhibits the reaction between serum from a CIDP patient and the NBL cell line [20].
• RESULTS: The production of MMP-2 and MMP-9 is increased in nerve tissue in CIDP and NSVN compared with NIN [21].

Gene context of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• T cells are the predominant source of MMP-2 and MMP-9 in CIDP and NSVN, whereas macrophages contribute only to a minor extent [21].
• Expression of MMP-3 and MMP-7 was not detectable in CIDP or NSVN [21].
• CXCL9, CXCL10, and CCL3 were raised in the CSF in CIDP compared with controls and non-demyelinating neuropathies (p < 0.001) [22].
• From a panel of 25 Guillain-Barré syndrome (GBS) and 24 chronic inflammatory demyelinating polyneuropathy (CIDP) patients, only two patients showed reactivity towards Cx32 and P(0) [23].
• CSF levels of MCP-1 and IP-10 correlated with the CSF:plasma albumin ratio in both GBS and CIDP patients [24].

Analytical, diagnostic and therapeutic context of Polyradiculoneuropathy, Chronic Inflammatory Demyelinating

• CONCLUSION: Cystatin C levels in CSF measured by ELISA may help the physician recognize GBS, CIDP, and MS [25].
• DESIGN: A retrospective medical record review between 1992 and 2003 of outcomes in CIDP, comparing patients in 3 cohorts depending on whether their primary treatment was IVMP, IVIg, or oral immunosuppression with prednisone or cyclosporine [26].
• Induction of suppression, presumably through favorable modifications of the cytokine network or other humoral mediators, might be one, among others, of the mechanisms through which prednisone and plasma exchange are effective in CIDP [27].
• Immunoelectrophoresis and immunofixation, respectively, detected IgM M-protein in 6 (35%) and 13 (76%) of the 17 CIDP patients [28].
• Suggestive preliminary evidence from controlled 3-month clinical trials that prednisone improves chronic inflammatory polyradiculoneuropathy [29].

References