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Clinical and Laboratory Features in Anti-NF155 Autoimmune Nodopathy.

Lorena Martín-Aguilar1, Cinta Lleixà1, Elba Pascual-Goñi1

  • 1From the Neuromuscular Diseases Unit (L.M.-A., C.L., E.P.-G., M.C.-Á., R.R.-G., E.C.-V., J.T.-S., E.N.-O., I.I., L.Q.), Department of Neurology, Hospital de La Santa Creu I Sant Pau, Universitat Autònoma de Barcelona; Biomedical Research Institute Sant Pau (IIB Sant Pau) (L.M.-A., C.L., E.P.-G., M.C.-Á., J.D.-M., E.C.-V., X.S.-C., E.G.); Immunology Department (L.M.-M.), Hospital de La Santa Creu I Sant Pau, Universitat Autònoma de Barcelona, Spain; Centro para La Investigación Biomédica en Red en Enfermedades Raras (CIBERER) (J.D.-M., R.R.-G., E.C.-V., N.L., X.S.-C., E.G., I.I., L.Q.); University Hospital Birmingham (Y.R., S.S.), UK; Erasmus Medical Center (B.C.J., A.B.), Rotterdam, the Netherlands; IRCCS Mondino Foundation (Andrea Cortese, E.V.), Pavia, Italy; Department of Neurology (R.H., F.Z.), Medical University of Vienna; Paracelsus Medical University (C.R.), Salzburg, Austria; IRCCS Humanitas Research Hospital (G.L.), Milan University, Rozzano, Italy; Kuala Lumpur General Hospital (F.L.H.), Jalan Pahang, Kuala Lumpur, Malaysia; Hospital Universitari Germans Trias I Pujol (A.M.-P.), Badalona; Hospital Universitario Virgen de Las Nieves (Alejandra Carvajal), Granada, Spain; Hospital Universitario Clínico San Cecilio (R.P.-M.), Granada; Hospital Son Llàtzer (M.U.-M.), Palma de Mallorca; Hospital San Jorge (O.A.), Huesca, España; Hospital San Pedro (M.Á.L.-P.), Logroño; Hospital Universitari Josep Trueta (F.M.), Girona; Hospital Clínico Universitario de Santiago (J.P.-F.), Santiago de Compostela; Hospital Universitario Virgen Del Rocío (L.M.-D., M.C.-S.), Sevilla; Hospital Universitari Sant Joan (N.O.), Reus; Complejo Asistencial de Ávila (M.B.), Ávila, Spain; Akdeniz University (Ö.D.), Antalya, Turkey; Toronto General Hospital (V.B.), University Health Network, University of Toronto, Canada; Instituto Nacional de Ciencias Neurológicas. Lima (D.S.-C.), Perú; St. Josef-Hospital (K.P.), Ruhr-University Bochum; and Sant Joseph Hospital (C.S.), Berlin, Germany.

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|November 3, 2021
PubMed
Summary

Autoimmune nodopathy (AN) associated with antineurofascin-155 (NF155) antibodies shows a distinct clinical profile. Rituximab treatment demonstrated significant patient response, with autoantibody titers and serum neurofilament light (NfL) levels aiding disease monitoring.

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Area of Science:

  • Neurology
  • Immunology
  • Autoimmune Diseases

Background:

  • Autoimmune nodopathy (AN) is a rare neurological disorder.
  • Antineurofascin-155 (NF155) antibodies are implicated in certain autoimmune neuropathies.

Purpose of the Study:

  • To delineate the clinical and laboratory characteristics of anti-NF155 antibody-positive autoimmune nodopathy (AN).
  • To assess treatment responses and identify reliable biomarkers for disease monitoring.

Main Methods:

  • Retrospective analysis of 40 patients with detected anti-NF155 antibodies.
  • Collection of clinical data, functional scales (mRS, I-RODS), autoantibody titers, and serum neurofilament light (NfL) levels.
  • Evaluation of treatment efficacy, particularly with rituximab, IV immunoglobulin, and steroids.

Main Results:

  • Patients presented with progressive, symmetric sensorimotor weakness, tremor, and ataxia.
  • Rituximab showed a high response rate (77.3%), unlike IV immunoglobulin or steroids.
  • Anti-NF155 antibody titers correlated with mRS, and serum NfL levels correlated with disease severity and antibody titers.

Conclusions:

  • Anti-NF155 AN exhibits a unique clinical phenotype with a favorable response to rituximab.
  • Autoantibody titers and serum NfL levels serve as valuable biomarkers for monitoring disease activity.
  • Utilizing untagged-NF155 plasmids is crucial for accurate diagnosis by minimizing false positives.