Presentation is loading. Please wait.

Presentation is loading. Please wait.

Figure 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy.

Published byLukas Sachs Modified over 5 years ago

Similar presentations

Presentation on theme: "Figure 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy."— Presentation transcript:

1 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). 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. Luis Querol et al. Neurol Neuroimmunol Neuroinflamm 2015;2:e149 © 2015 American Academy of Neurology

Download ppt "Figure 1 Clinical status and autoantibody titers in rituximab-treated patients with anti-CNTN1/NF155 chronic inflammatory demyelinating polyneuropathy."

Similar presentations

Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the disease  C Bjartmar, J.R Wujek, B.D Trapp  Journal of.

Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the disease  C Bjartmar, J.R Wujek, B.D Trapp  Journal of.
Figure EDSS, FS scores, and Modified MSFC scores

Figure EDSS, FS scores, and Modified MSFC scores
Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)

Figure 2 ALSFRS-R changes (A) Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised (ALSFRS-R) slope after 6 months of treatment without (left)
Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)

Figure 1. Absence of anti–neurofascin-155 (NF155) antibodies in combined central and peripheral demyelination (CCPD)‏ Absence of anti–neurofascin-155 (NF155)
Figure 2. Infliximab treatment effect

Figure 2. Infliximab treatment effect
Figure 2. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.

Figure 2. Change in total PSPRS score from baseline to each study visit for all participants Change in total PSPRS score from baseline to each study visit.
Figure 1 Percent positivity by clinical feature Overall, 6

Figure 1 Percent positivity by clinical feature Overall, 6
Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.

Figure 3 Classical complement pathway activity and disease severity (A) Association between high innate classical pathway (CP) activity and degree of muscle.
Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.

Figure Brain MRI of the patient throughout the disease course(A) Brain MRI at the time of cerebral toxoplasmosis diagnosis (a) and after 1 month of toxoplasmosis.
Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.

Figure Clinical course of acute neuritis and NMDA receptor (NMDAR) encephalitis, sural nerve biopsy, and detection of NMDAR antibodies(A) Approximately.
Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.

Figure 3 Immune response to neoantigen: Geometric mean titers of antirabies antibody levels over timeAt days 31 and 38, all subjects achieved antibody.
Figure 3 Example of venous narrowing

Figure 3 Example of venous narrowing
Figure 3 JCV index changes in JCV+ patients

Figure 3 JCV index changes in JCV+ patients
Nat. Rev. Neurol. doi: /nrneurol

Nat. Rev. Neurol. doi: /nrneurol
Figure 1. Brain MRI follow-up of Sjögren syndrome–associated type II mixed cryoglobulinemic cerebral vasculitis treated with rituximab Brain MRI follow-up.

Figure 1. Brain MRI follow-up of Sjögren syndrome–associated type II mixed cryoglobulinemic cerebral vasculitis treated with rituximab Brain MRI follow-up.
Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.

Figure 1 Flow diagram of the assays and the samples that were evaluatedA total of 1,109 samples were initially screened at a serum dilution of 1:20 for.
Figure 2 Clinical course and response to therapy in 6 Australian patients with HMGCR antibodies The clinical course, creatine kinase (CK) levels, Medical.

Figure 2 Clinical course and response to therapy in 6 Australian patients with HMGCR antibodies The clinical course, creatine kinase (CK) levels, Medical.
Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.

Figure 2 Brain biopsy Brain biopsy (A) Double staining with anti-aquaporin-4 (AQP4) antibody (dark green) and Luxol fast blue (blue) is shown. Loss of.
Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.

Figure 1 MOR103 sequential-dose trial flowchart of study population with multiple sclerosis aPatients received 2 doses of study drug before trial withdrawal.
Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Figure 2 Correlation between total IgG levels and anti-AQP4 IgG titer

Similar presentations

Ads by Google