MémoireVitamine D et sclérose en plaques. Étude prospective d’une cohorte de patients de la région Poitou-CharentesVitamin D and multiple sclerosis. A prospective survey of patients of Poitou-Charentes area
Section snippets
Patients et méthodes
Les patients porteurs d’une sclérose en plaques définie selon les critères révisés de McDonald (Polman et al., 2005) admis en consultation dans trois cabinets libéraux de la région Poitou-Charentes (Vienne, Deux Sèvres et Charente) et dans la consultation SEP du CHU de Poitiers (Vienne) ont été inclus dans cette étude. Tous les patients SEP ont été recrutés dans le premier trimestre 2010.
Les critères d’inclusion étaient un âge supérieur à 18 ans, une SEP définie selon les critères révisés de
Résultats
Du premier janvier au 31 mars 2010, 170 patients SEP ont été inclus dans cette étude. Aucun patient n’a refusé la participation à cette étude. L’âge moyen était de 46 ans ± 11,3 ans, avec des extrêmes de 20 à 75 ans. Le sexe ratio était de trois femmes pour un homme.
Les formes SEP-RR (n = 102) représentaient 62,9 % de la population totale, les formes RR-SP (n = 48), 29,7 % et les formes PP (n = 12), 7,4 % de SEP.
L’ancienneté de la maladie était de 139,6 ± 92,8 mois et 50 % environ des patients avaient
Discussion
S’il est connu depuis près d’un siècle que la vitamine D intervient dans l’absorption du calcium et du phosphore et joue un rôle essentiel dans la minéralisation des os, son action potentielle apparaît à l’heure actuelle plus diversifiée, comportant un rôle anti-inflammatoire, anti-infectieux, antiprolifératif et immunomodulateur.
Ainsi, des données récentes suggèrent une carence de la vitamine D dans la genèse de certains cancers, notamment de la prostate (Barnett et al., 2010) ou du pancréas (
Conclusion
La réalisation d’un dosage plasmatique de 25-OH vit D doit être systématiquement réalisé chez les patients SEP. Compte tenu de l’absence de toxicité (Kimball et al., 2007) d’un traitement supplétif par la vitamine D en l’absence d’hypercalcémie (Wingerchuk et al., 2005), et de son efficacité avec une élévation rapide du taux plasmatique de 25-OH vit D (Wingerchuk et al., 2005), un traitement substitutif par une ampoule buvable mensuelle de 100 000 UI de colécalciférol devrait être proposée chez
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2018, Revue NeurologiqueCitation Excerpt :In contrast, other studies have found associations between DSL and each of the three above-mentioned outcomes. Most have looked at disability and showed that lower DSLs were correlated with increased EDSS scores [33,36,49,50]. Regarding MS type, two studies have noted that DSL was significantly lower in progressive forms (SPMS and PPMS) compared with the relapsing-remitting (RRMS) form [36,50].
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2016, Revue NeurologiqueCitation Excerpt :Several studies have attempted to define the vitamin D status of MS patients and/or evaluate the impact of vitamin D status on MS progression. Soilu-Hänninen et al. [49] used data from the PRIMS study (concerning patients randomized for interferon (INF)β-1a, 22, 44 μg versus placebo) and found an inverse relationship between the serum level of 25(OH)D and clinical activity of MS. Neau et al. [50] found a significantly lower level of 25(OH)D in patients with secondary progressive (SP) or primary progressive (PP) MS versus relapsing-remitting (RR) MS. In addition, they noted that the serum levels of 25(OH)D were inversely correlated with disability measured by the Expanded disability status scale (EDSS). Nevertheless, there was no correlation for the annualized rate of exacerbations, or for the presence of active lesions on the MRI in patients with RR-MS. Similar results were reported by other authors [51,52].
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2013, Multiple Sclerosis and Related DisordersCitation Excerpt :The most widely used model of disease causality is based on the Bradford-Hill criteria (Hill, 1965), which include strength and consistency of correlation, specificity, temporality, biological gradient or dose-response, biological plausibility, coherence, experimental evidence, and reasoning by analogy. The evidence from cross-sectional (van der Mei et al., 2007; Demirkaya et al., 2009; Weinstock-Guttman et al., 2011; Pakdaman et al., 2012; Shahbeigi et al., 2012; Rose et al., 2012) and longitudinal retrospective (Smolders et al., 2008; Mowry et al., 2010; Neau et al., 2011; Scott et al., 2012) and prospective (Soilu-Hanninen et al., 2005, 2008; Simpson et al., 2010; Runia et al., 2012; Mowry et al., 2012, Stewart et al., 2012; Loken-Amsrud et al., 2012) studies demonstrates a strong and consistent correlation between vitamin D deficiency and incidence of subsequent relapse and/or disability in MS. In addition, the apparent regulatory effect of vitamin D levels on the IgG index, T-cells, and dendritic cells demonstrated by several cross-sectional studies (Correale et al., 2009, 2011; Royal et al., 2009; Smolders et al., 2009; Lysandropoulos et al., 2011; Bartosik-Psujek et al., 2010; Vogt et al., 2010), help advance a plausible model for vitamin D immunomodulation in MS that is coherent with the conception of MS as an autoimmune disease, and complemented by the analogous evidence of vitamin D levels correlating with the development of MS. This is further supported by interventional studies of vitamin D supplementation (Mahon et al., 2003; Vojinovic et al., 2005; Kimball et al., 2011a) which suggest that vitamin D plays an immunomodulatory role in MS, modifying serum cytokines to a more anti-inflammatory profile. Although there is some preliminary evidence for a temporal association between vitamin D levels and MS activity, additional cohort studies are needed to definitively demonstrate this relationship.
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