MS signature in plasma and CSF

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frodo
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MS signature in plasma and CSF

Post by frodo » Thu Oct 31, 2019 11:53 am

Multiple sclerosis has a distinct lipid signature in plasma and cerebrospinal fluid

http://www.scielo.br/scielo.php?pid=S00 ... ci_arttext

ABSTRACT

The diagnosis of multiple sclerosis (MS) has changed over the last decade, but remains a composite of clinical assessment and magnetic resonance imaging to prove dissemination of lesions in time and space. The intrathecal synthesis of immunoglobulin may be a nonspecific marker and there are no plasma biomarkers that are useful in the diagnosis of MS, presenting additional challenges to their early detection.

Methods

We performed a preliminary untargeted qualitative lipidomics mass spectrometry analysis, comparing cerebrospinal fluid (CSF) and plasma samples from patients with MS, other inflammatory neurological diseases and idiopathic intracranial hypertension.

Results

Lipid identification revealed that fatty acids and sphingolipids were the most abundant classes of lipids in the CSF and that glycerolipids and fatty acids were the main class of lipids in the plasma of patients with MS. The area under the curve was 0.995 (0.912–1) and 0.78 (0.583–0.917), respectively. The permutation test indicated that this ion combination was useful for distinguishing MS from other inflammatory diseases (p < 0.001 and 0.055, respectively).

Conclusion

This study concluded that the CSF and plasma from patients with MS bear a unique lipid signature that can be useful as a diagnostic biomarker.

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Petr75
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Re: MS signature in plasma and CSF

Post by Petr75 » Thu Nov 21, 2019 10:29 pm

2019 Oct 14
Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel
HDL-cholesterol elevation associated with fingolimod and dimethyl fumarate therapies in multiple sclerosis.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6794658/

Abstract
Background:
Patients with Multiple Sclerosis (PwMS) display altered lipoproteins levels and function, which seem to affect disease risk and progress. Whether disease-modifying therapies affect the lipoprotein profile in PwMS has scarcely been studied.
Objective:
The study aims to assess whether fingolimod and dimethyl fumarate (DMF) affect lipoproteins in PwMS.
Methods:
We compared retrospectively the blood lipoprotein levels of 29 fingolimod-treated and 41 DMF-treated patients before and after 3 and 12 months of therapy. Patients treated with cholesterol-reducing medications were not included. Data on weight change and disease activity during 1-year follow-up were obtained.
Results:
HDL level, HDL/LDL ratio and HDL/total cholesterol ratio were increased in both treatment groups after 3 months' therapy and sustained, with no change in LDL or triglycerides. While at baseline only 26% of patients met the recommended minimum of HDL 60 mg/dl, after 3 months' therapy, 43% of fingolimod-treated and 47% of DMF-treated patients reached the recommended level. The majority of patients had no weight reduction.
Conclusions:
Fingolimod and DMF therapies are associated with a specific increase in HDL in PwMS. Further studies are required to validate these findings and their potential implication as biomarker of reduced inflammatory state and/or reduced risk of neurodegeneration or cardiovascular comorbidity.

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