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- Figure 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy
Patient 1 improved dramatically after rituximab treatment in both Rasch-built Overall Disability Scale (R-ODS) and Overall Neuropathy Limitations Scale (ONLS) scores, reaching full recovery at 12 months (A). Anti–contactin-1 (CNTN1) antibody titers decreased rapidly and were undetectable as early as 6 months after treatment, whereas anti–tetanic toxoid (TT) antibodies remained stable after treatment (B). Patient 2 had marked improvement after rituximab treatment in both R-ODS and ONLS scores, although mild leg distal weakness persisted (C). Anti–neurofascin-155 (NF155) antibody titers decreased rapidly and remained low 18 months after treatment. Anti-TT antibodies, however, decreased immediately after treatment and stabilized thereafter (D). Patient 3 improved slightly after rituximab treatment in both R-ODS and ONLS scores, although marked disability persisted (E). This patient had a significantly longer disease duration (more than 15 years) and secondary axonal damage. Nevertheless, anti-NF155 antibody titers decreased rapidly after treatment and stabilized at a titer of 1/900. An additional rituximab course further decreased anti-NF155 antibody titers. Anti-TT antibodies remained stable after treatment (F). Arrows represent additional rituximab courses.
- Figure 2 Clinical and autoantibody status of 2 CNTN1 or NF155+ patients not receiving rituximab
Despite corticosteroids and methotrexate treatment, patient 5 remained significantly disabled but declined to be treated with rituximab and his clinical status and autoantibody levels remained stable (A). Patient 7 is the only patient from our cohort fully responding to corticosteroids. Clinical scales improved clearly and anti–contactin-1 (CNTN1) antibodies disappeared (B). NF155 = neurofascin-155; R-ODS = Rasch-built Overall Disability Scale.
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