Not being treated is a risk factor for secondary progressive MS


Transition to secondary progression in relapsing-onset multiple sclerosis: Definitions and risk factors.Iaffaldano P, Lucisano G, Patti F, Brescia Morra V, De Luca G, Lugaresi A, Zaffaroni M, Inglese M, Salemi G, Cocco E, Conte A, Ferraro D, Galgani S, Bergamaschi R, Pozzilli C, Salvetti M, Lus G, Rovaris M, Maniscalco GT, Logullo FO, Paolicelli D, Achille M, Marrazzo G, Lovato V, Comi G, Filippi M, Amato MP, Trojano M; Italian MS Register.Mult Scler. 2020 Nov 19:1352458520974366. doi: 10.1177/1352458520974366. Online ahead of print.PMID: 33210986

Background: No uniform criteria for a sensitive identification of the transition from relapsing-remitting multiple sclerosis (MS) to secondary-progressive multiple sclerosis (SPMS) are available.

Objective: To compare risk factors of SPMS using two definitions: one based on the neurologist judgment (ND) and an objective data-driven algorithm (DDA).

Methods: Relapsing-onset MS patients (n = 19,318) were extracted from the Italian MS Registry. Risk factors for SPMS and for reaching irreversible Expanded Disability Status Scale (EDSS) 6.0, after SP transition, were estimated using multivariable Cox regression models.

Results: SPMS identified by the DDA (n = 2343, 12.1%) were older, more disabled and with a faster progression to severe disability (p < 0.0001), than those identified by the ND (n = 3868, 20.0%). In both groups, the most consistent risk factors (p < 0.05) for SPMS were a multifocal onset, an age at onset >40 years, higher baseline EDSS score and a higher number of relapses; the most consistent protective factor was the disease-modifying therapy (DMT) exposure. DMT exposure during SP did not impact the risk of reaching irreversible EDSS 6.0.

Conclusion: A DDA definition of SPMS identifies more aggressive progressive patients. DMT exposure reduces the risk of SPMS conversion, but it does not prevent the disability accumulation after the SP transition.

So yet again DMT use is shown to be advantageous however those drugs were injectables (86.8%), azathioprine (8.2%), mitoxantrone (2.4%), new oral DMTs (1.6%), or natalizumab (1.1%). Therefore you can’t say much, until the treatments are high efficacy DMT the information will continue to be of limited value. Also the accumulation of lesions (Below) is not good for you.

Expansion of chronic lesions is linked to disease progression in relapsing-remitting multiple sclerosis patients.Klistorner S, Barnett MH, Yiannikas C, Barton J, Parratt J, You Y, Graham SL, Klistorner A.Mult Scler. 2020 Nov 20:1352458520974357. doi: 10.1177/1352458520974357.

Background: Slow-burning inflammation is putatively associated with lesion expansion and leads to progressive loss of axons and disability worsening.

Objective: To investigate the incidence and extent of chronic white matter lesion expansion in relapsing-remitting multiple sclerosis (RRMS) patients and to evaluate its relationship with biomarkers of disease progression.

Methods: Pre- and post-gadolinium T1, fluid-attenuated inversion recovery (FLAIR) and diffusion tensor images were acquired from 33 patients. Lesional activity were analysed between baseline and 48 months using custom-designed software.

Results: A total of 569 lesions were identified as chronic at baseline, of which 261 were expanding, 236 were stable and 72 were shrinking. In addition, 139 new lesions (both confluent and free-standing) were observed. Chronic lesion expansion was associated with patient’s age and accounted for the bulk (67.3%) of total brain lesion volume increase, while only 32.7% was attributable to new lesion formation. Change in chronic lesion volume correlated with the rate of brain atrophy (r = -0.57, p = 0.001), change of Expanded Disability Status Scale (EDSS; r = 0.38, p = 0.03) and an increase of isotropic diffusivity inside the lesions (r = 0.75, p < 0.001).

Conclusion: Expansion of chronic lesions in RRMS patients is the primary determinant of increased T2 total lesion load. It significantly contributes to disease progression and partially driving axonal loss inside the lesions and brain damage outside of lesional tissue.

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