MRZR+ MS cases are different from others

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frodo
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MRZR+ MS cases are different from others

Post by frodo » Mon Aug 26, 2019 5:08 am

MRZR is a reaction about several viruses highly specific for MS, but little sensitive. This means that if you have MRZR is nearly sure that you have MS, but a lot of people with MS do not have MRZR.

This report has found that MRZR+ patients show at the same time other specific biomarkers like free kappa-light-chains, yielding two different subgroups of MS with different behaviours.

Source:
https://www.sciencedirect.com/science/a ... 8119320042


Highlights

• CSF kappa and Lambda free light chains are quantitative B-cell response markers.
• The MRZ reaction is the most specific neurochemical marker for multiple sclerosis.
• MRZ reaction is associated with kappa but not lambda free light chains.
• CSF kappa free light chains might be a helpful marker in multiple sclerosis.

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frodo
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MRZR separates MS from lupus-like with 97% confidence

Post by frodo » Fri Nov 29, 2019 5:59 am

Rheumatic diseases (lupus like diseases) and 60% of MS cases show antinuclear antibodies (ANA), leading to diagnosis confusion. MRZR can separate both conditions.

The MRZ-Reaction and Specific Autoantibody Detection for Differentiation of ANA-Positive Multiple Sclerosis From Rheumatic Diseases With Cerebral Involvement

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6433788/

Objective: Rheumatic diseases with involvement of the central nervous system (RDwCNS) may mimic multiple sclerosis (MS). Inversely, up to 60% of MS-patients have antinuclear autoantibodies (ANAs) and may be misdiagnosed as RDwCNS. The detection of antibodies against extractable nuclear antigens (ENA) and oligoclonal bands (OCB) are established valuable diagnostic tools in the differential diagnosis of RDwCNS and MS. The MRZ-reaction (MRZR) is defined by three antibody indices (AIs) against neurotropic viruses and is frequently positive in MS. To investigate the added value of MRZR combined with testing for antibodies against ENAs and OCB detection to distinguish RDwCNS from ANA positive MS.

Methods: MRZR was evaluated in RDwCNS (n = 40) and 68 ANA positive MS-patients. Two stringency levels, MRZR-1 and MRZR-2 (at least one respectively two of three AIs positive) were applied. Autoantibody testing included ANA plus ENA and anti-dsDNA antibodies, antiphospholipid antibodies, and anti-neutrophil cytoplasmic antibodies.

Results: Most of the RDwCNS patients (n = 32; 80%) suffered from systemic lupus erythematosus. Within the RDwCNS group 20% had a positive MRZR-1 and 8.5% a positive MRZR-2 compared to 80.9 and 60%, respectively within the MS-group (p < 0.0001 for both comparisons). Oligoclonal bands were found in 28.6% of the RDwCNS patients and 94.3% of the MS-patients (p < 0.0001). Conversely, autoantibodies to specific nuclear antigens or phospholipids were found more frequently in RDwCNS. A positive MRZR in conjunction with the absence of ENA autoantibodies distinguished MS from RDwCNS with high specificity (97.5%).

Conclusions: We suggest combining MRZR, OCBs, and specific autoantibody diagnostics to differentiate RDwCNS from MS.

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