Sabrina Matà1, Stefano Ambrosini2, Domenica Saccomanno3, Tiziana Biagioli4, Marinella Carpo5, Aldo Amantini6, Fabio Giannini7, Alessandro Barilaro2, Lucia Toscani8, Monica Del Mastio2, Giacomo Pietro Comi3, Sandro Sorbi2,9. 1. Department of Neuroscience, Psychology, Drug Research and Child Health, University of Florence, Florence, Italy. masa@unifi.it. 2. Department of Neuroscience, Psychology, Drug Research and Child Health, University of Florence, Florence, Italy. 3. Department of Pathophysiology and Transplantation (DEPT), Neurology Unit, IRCCS Foundation Ca' Granda Ospedale Maggiore Policlinico, University of Milan, Milan, Italy. 4. General Laboratory, Careggi University Hospital, Florence, Italy. 5. Neurology Unit, Ospedale Treviglio, Bergamo, Italy. 6. Department NeuroMuscolar Scheletric and Sensory Organs, SOD Neurophysiology, Florence, Italy. 7. Department of Medical, Surgical and Neurological Sciences, University of Siena, Siena, Italy. 8. Neurology Unit, S.M. Annunziata Hospital, Florence, Italy. 9. IRCCS Fondazione Don Carlo Gnocchi, Florence, Italy.
Abstract
OBJECTIVES: Anti-myelin-associated glycoprotein (MAG) antibody is associated with clinically heterogeneous polyneuropathies. Our purpose was to compare neuropathy phenotypes identified by different anti-MAG tests' results. METHODS: Cohort study: Sera from 40 neuropathy anti-MAG EIA positive patients were tested for anti-MAG by Western blot (WB), for anti-peripheral nerve myelin (PNM) on monkey nerve by immunofluorescence assay (IFA), and for anti-HNK1 on rat CNS slices by IFA. Anti-sulfatide antibodies, for comparison, were also tested by EIA. RESULTS: Among 40 anti-MAG EIA positive sera, 85% also had anti-PNM IFA reactivity and 67.5% bind HNK1 on rat CNS. Anti-HNK1 positive patients had the classical predominantly distal acquired demyelinating symmetric (DADS) neuropathy with a benign course, while anti-PNM positive but anti-HNK1 negative patients had predominantly axonal neuropathy with a high frequency of anti-sulfatide reactivity and the worst long-term prognosis. Anti-MAG EIA positive patients without anti-PNM or anti-HNK1 IFA reactivity had a CIDP-like polyneuropathy. CONCLUSION: Different methods to test for anti-MAG antibodies identify different clinical and electrophysiological findings, as well as long-term outcome. HNK1 reactivity is the strongest marker of DADS.
OBJECTIVES:Anti-myelin-associated glycoprotein (MAG) antibody is associated with clinically heterogeneous polyneuropathies. Our purpose was to compare neuropathy phenotypes identified by different anti-MAG tests' results. METHODS: Cohort study: Sera from 40 neuropathy anti-MAG EIA positive patients were tested for anti-MAG by Western blot (WB), for anti-peripheral nerve myelin (PNM) on monkey nerve by immunofluorescence assay (IFA), and for anti-HNK1 on rat CNS slices by IFA. Anti-sulfatide antibodies, for comparison, were also tested by EIA. RESULTS: Among 40 anti-MAG EIA positive sera, 85% also had anti-PNM IFA reactivity and 67.5% bind HNK1 on rat CNS. Anti-HNK1 positive patients had the classical predominantly distal acquired demyelinating symmetric (DADS) neuropathy with a benign course, while anti-PNM positive but anti-HNK1 negative patients had predominantly axonal neuropathy with a high frequency of anti-sulfatide reactivity and the worst long-term prognosis. Anti-MAG EIA positive patients without anti-PNM or anti-HNK1 IFA reactivity had a CIDP-like polyneuropathy. CONCLUSION: Different methods to test for anti-MAG antibodies identify different clinical and electrophysiological findings, as well as long-term outcome. HNK1 reactivity is the strongest marker of DADS.
Authors: E Nobile-Orazio; P Marmiroli; L Baldini; G Spagnol; S Barbieri; M Moggio; N Polli; E Polli; G Scarlato Journal: Neurology Date: 1987-09 Impact factor: 9.910
Authors: S Erb; F Ferracin; P Fuhr; K M Rösler; C W Hess; T Kuntzer; J Bogousslavsky; R Sztajzel; A J Steck Journal: J Neurol Date: 2000-10 Impact factor: 4.849
Authors: Troy D Jaskowski; Harry E Prince; Ryan W Greer; Christine M Litwin; Harry R Hill Journal: J Neuroimmunol Date: 2007-05-29 Impact factor: 3.478