Transcript
Emerging biomarkers in CIDP
Claudia Sommer, MD
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When we think of biomarkers, it's not only the blood biomarkers, imaging is also a biomarker and we can use MRI or ultrasound of the nerves, which now are beautifully available to monitor our patients with CIDP. Cytokines, interleukins complement have been used in several studies and we will have a look at these data. And then there are the biomarkers of axonal or myelin damage like neurofilament light, like peripherin or sphingomyelin, which comes out of the myelin teeth. On the left you see some beautiful ultrasound images. They are, can show that nerves are enlarged in CIDP and sometimes people have been successful in showing the change after treatment so that these diameters, I don't know if you can read it, but this one, this median nerve at the forearm is 13 millimetres and then it's nine millimetres after treatment. And this median nerve at the upper arm also became smaller after treatment. On the right you see a nice example of MRI imaging. For example, imaging the plexus and DRG or in the middle showing the sciatic nerve with quite remarkable enlargement and hyperintensity of the fascicules.
This was 2016 and then when the patient was seen much later under treatment you see on the right in 2022 these hyperintensities are gone. Most of these are small case series and sometimes case reports, so it's difficult to say how good a biomarker would this be in my individual patient. But for sure these are, there's a lot of data out there and more coming. Okay, let's look at the fluid biomarkers. On the left you see the terminal complement. This is serum C5A and in the lower panel CSFC5A. People with CIDP compared to controls and for the serum there is a a very nice differentiation. So this is what you would like a biomarker to look like. No overlap between your populations. IL-8 as an example of a cytokine. There's also an increase in the CIDP patients, but there is some overlap. And on the right you see calprotectin also with differences, but big overlaps to the other groups. Sphingomyelin is interesting because it's a biomarker that would identify and monitor myelin damage. And you can see here on the left, it's considerably higher in active CIDP, then in stable CIDP or other neurological diseases.
And in the middle you see it's a little higher in typical CIDP than in the atypical ones. And on the right you show it's remarkably increased in active CIDP compared to axonal neuropathies, which you would expect because it's the myelin molecule, but this is nice to see. So peripherin has been put forward. You see on the left that this seems to recognise GBS more than CIDP and neurofilament light. Of course in the acute phase of GBS, as you would expect, it is also higher, but here also CIDP picks it up. So, what are future directions for these biomarkers? Given the heterogeneity of CIDP and that this might require individualised monitoring and treatment, we would very much like to have reliable biomarkers. They could improve diagnostic accuracy and they might guide treatment decisions. We may not be entirely there yet, but as you have seen on this Congress, the field is very active and a lot of data are coming up right now. At the moment, we can distinguish diagnostic biomarkers like the auto antibodies, the electrophysiology, the imaging, maybe imaging is also a biomarker for treatment response. And then biomarkers for treatment response, NfL, which is elevated in many disorders that entail axonal damage. But it will show us if our patient is in the active phase or responding to treatment and maybe the cytokines and some others that you see here on the right.
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