The picture of demyelinating diseases gets more complicated

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frodo
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The picture of demyelinating diseases gets more complicated

Post by frodo »

This is the current picture as far as the current knowledge suggest. The picture is more complex than previously thought, even if anti-neurofascin diseases are not represented:

Image

There is a big overlapping of anti-AQP4 with NMOSD (neuromyelitis-like) and also of anti-MOG with ADEM and Marburg. The rest of the diseases/varieties can still be considered idiopatic.

PS: Taken from here:
Neuromyelitis optica spectrum and myelin oligodendrocyte glycoprotein antibody‐related disseminated encephalomyelitis
https://onlinelibrary.wiley.com/doi/ful ... cen3.12491

PS2: This is the picture including neurofascins

Image

taken from here: https://ars.els-cdn.com/content/image/1 ... 39-gr1.jpg
Last edited by frodo on Mon Jul 13, 2020 8:55 am, edited 1 time in total.
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frodo
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News about NFs: Plasma exchange for Immune-Mediated Neuropathies

Post by frodo »

Immunoadsorption and Plasma Exchange in Seropositive and Seronegative Immune-Mediated Neuropathies

Abstract

The inflammatory neuropathies are disabling conditions with diverse immunological mechanisms. In some, a pathogenic role for immunoglobulin G (IgG)-class autoantibodies is increasingly appreciated, and immunoadsorption (IA) may therefore be a useful therapeutic option.

We reviewed the use of and response to IA or plasma exchange (PLEx) in a cohort of 41 patients with nodal/paranodal antibodies identified from a total of 573 individuals with suspected inflammatory neuropathies during the course of routine diagnostic testing (PNAb cohort). 20 patients had been treated with PLEx and 4 with IA.

Following a global but subjective evaluation by their treating clinicians, none of these patients were judged to have had a good response to either of these treatment modalities. Sequential serology of one PNAb+ case suggests prolonged suppression of antibody levels with frequent apheresis cycles or adjuvant therapies, may be required for effective treatment.

We further retrospectively evaluated the serological status of 40 patients with either Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP), and a control group of 20 patients with clinically-isolated syndrome/multiple sclerosis (CIS/MS), who had all been treated with IgG-depleting IA (IA cohort).

32 of these patients (8/20 with CIDP, 13/20 with GBS, 11/20 with MS) were judged responsive to apheresis despite none of the serum samples from this cohort testing positive for IgG antibodies against glycolipids or nodal/paranodal cell-adhesion molecules. Although negative on antigen specific assays, three patients’ pre-treatment sera and eluates were reactive against different components of myelinating co-cultures.

In summary, preliminary evidence suggests that GBS/CIDP patients without detectable IgG antibodies on routine diagnostic tests may nevertheless benefit from IA, and that an unbiased screening approach using myelinating co-cultures may assist in the detection of further autoantibodies which remain to be identified in such patients.

Figure: Some proteins attacked during inflammatory neuropathies.
Image
Source: https://www.nature.com/articles/s41582-020-0375-x
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