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June 1986

Acute and Chronic Demyelinating Inflammatory Polyradiculoneuropathy: Association With Autoimmune Diseases and Lymphocyte Response to Human Neuritogenic Protein

Author Affiliations

From the Department of Neurology, Hadassah University Hospital and Hebrew University-Hadassah Medical School, Jerusalem. Dr Korn-Lubetzki is now with the Neuropediatric Diagnostic Unit, Bikur Holim Hospital, Jerusalem.

Arch Neurol. 1986;43(6):604-608. doi:10.1001/archneur.1986.00520060066020

• Of 66 patients (31 female and 35 male) with demyelinating inflammatory polyradiculoneuropathy (DIP), 12% (8/66) had a chronic relapsing and/or progressive course (CR-DIP) and 88% (58/66) had an acute monophasic illness (acute Guillain-Barré syndrome or GBS). Ten (15%) of the 66 had one or more associated putative autoimmune diseases; of these ten, five had CR-DIP and five had GBS. Cell-mediated immune responsiveness (CMI) of 30 cases with DIP was tested in vitro by lymphocyte transformation. Peripheral nervous system neuritogenic protein (NP) and central nervous system encephalitogenic myelin basic protein were the challenge antigens. Eighteen (60%) of the 30 patients had CMI to NP of human peripheral nervous system origin when a stimulation index (SI) of 2 or more was evaluated as positive; eight 27% (1) had CMI to NP when a positive SI was 3 or more. Of the 44 control patients with other neuropathies, only two (4.6%) demonstrated CMI to NP (SI, ≥2). The in vitro response of patients with DIP to myelin basic protein (7/30) was not significantly different from that of the control population (16/44). The high incidence of DIP associated with autoimmune diseases and the CMI to NP in this group suggest that DIP may be an autoimmune disease with NP as one possible major antigen.

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