Serum gelatinase B/MMP-9 in primary progressive multiple sclerosis patients treated with interferon-beta-1a

2003 ◽  
Vol 250 (9) ◽  
pp. 1037-1043 ◽  
Author(s):  
Bénédicte Dubois ◽  
Siobhan M. Leary ◽  
Inge Nelissen ◽  
Ghislain Opdenakker ◽  
Gavin Giovannoni ◽  
...  
2004 ◽  
Vol 251 (12) ◽  
pp. 1498-1501 ◽  
Author(s):  
Andreas Bitsch ◽  
Alexander Dressel ◽  
Kathrin Meier ◽  
Timon Bogumil ◽  
Florian Deisenhammer ◽  
...  

2017 ◽  
Vol 653 ◽  
pp. 159-162 ◽  
Author(s):  
Sabrina Giacoppo ◽  
Oxana Bereshchenko ◽  
Stefano Bruscoli ◽  
Carlo Riccardi ◽  
Placido Bramanti ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mario Amatruda ◽  
Maria Petracca ◽  
Maureen Wentling ◽  
Benjamin Inbar ◽  
Kamilah Castro ◽  
...  

Abstract The disease course of patients with a confirmed diagnosis of primary progressive multiple sclerosis (PPMS) is uncertain. In an attempt to identify potential signaling pathways involved in the evolution of the disease, we conducted an exploratory unbiased lipidomic analysis of plasma from non-diseased controls (n = 8) and patients with primary progressive MS (PPMS, n = 19) and either a rapid (PPMS-P, n = 9) or slow (PPMS-NP, n = 10) disease course based on worsening disability and/or MRI-visible appearance of new T2 lesions over a one-year-assessment. Partial least squares-discriminant analysis of the MS/MSALL lipidomic dataset, identified lipids driving the clustering of the groups. Among these lipids, sphingomyelin-d18:1/14:0 and mono-hexosylceramide-d18:1/20:0 were differentially abundant in the plasma of PPMS patients compared to controls and their levels correlated with MRI signs of disease progression. Lyso-phosphatidic acid-18:2 (LPA-18:2) was the only lipid with significantly lower abundance in PPMS patients with a rapidly deteriorating disease course, and its levels inversely correlated with the severity of the neurological deficit. Decreased levels of LPA-18:2 were detected in patients with more rapid disease progression, regardless of therapy and these findings were validated in an independent cohort of secondary progressive (SPMS) patients, but not in a third cohorts of relapsing–remitting (RRMS) patients. Collectively, our analysis suggests that sphingomyelin-d18:1/14:0, mono-hexosylceramide-d18:1/20:0, and LPA-18:2 may represent important targets for future studies aimed at understanding disease progression in MS.


2010 ◽  
Vol 16 (5) ◽  
pp. 597-603 ◽  
Author(s):  
Claudia Cristina Ferreira Vasconcelos ◽  
Luiz Claudio Santos Thuler ◽  
Gutemberg Augusto Cruz dos Santos ◽  
Marcos Papais Alvarenga ◽  
Marina Papais Alvarenga ◽  
...  

Recent studies have suggested faster clinical progression and greater disability in multiple sclerosis patients of African descent. This study analysed the effect of ethnicity on progression and disability. Sixty-five patients with primary progressive multiple sclerosis were selected and classified as being of African descent or white. Time from onset of the disease until reaching Expanded Disability Status Scale grades 3, 6, and 8 was assessed, as well as irreversible disability (Expanded Disability Status Scale grade maintained for ≥6 months). In the African descent group, the median time to reach Expanded Disability Status Scale 3 was 1 year shorter (1 year vs 2 years, p= 0.02), and to reach Expanded Disability Status Scale 6 was 2 years shorter (3 years vs 5 years, p= 0.01) than in the group of white patients. According to the Kaplan—Meier survival curves, patients of African descent reached every disability stage faster than white patients ( p= 0.03, p = 0.04, and p = 0.03, respectively, for Expanded Disability Status Scale grades 3, 6, and 8). As in United States and European patients of African descent, the more severe and faster progression of multiple sclerosis seen in Brazilian primary progressive multiple sclerosis patients of African descent suggests a possibly greater effect of ethnicity rather than environment on the progression of multiple sclerosis.


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