Multiple Sclerosis: Jensen D

Midgard R, Beiske AG, Celius EG, Jensen D, Hovdal H, Mellgren SI, Myhr KM. · Molde sjukehus/Haukeland Universitetssykehus 6407 Molde. · Tidsskr Nor Laegeforen. · Pubmed #12806674 No free full text.

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Jensen D. · Nevrologisk avdeling Rikshospitalet, Oslo. · Tidsskr Nor Laegeforen. · Pubmed #10522481 No free full text.

Abstract: The use of beta-interferon in the relapsing-remitting phase of multiple sclerosis is a new though fairly established therapy. The beneficial effect of this treatment is thought to be due to immune modulation, with inhibitory action on proliferation of leukocytes and antigen presentation, an increased amount of interleukins, but no change in the proinflammatory cytokine interferon-gamma. In Norway, one interferon-beta 1b and two interferon-beta 1a products have recently been introduced for administration by either subcutaneous or intramuscular injection. Approximately 30% reduction in the relapse rate is reported for both products,but differences appear in the effect on the disability progression, and also with regard to adverse reactions. Patients less strongly affected by the illness seem to have the best outcome. Neutralizing antibodies are often produced during this treatment, but the significance of this is still unclear. Results from international studies on interferon therapy of multiple sclerosis are discussed. Initial results from studies on interferon treatment of secondary progressive multiple sclerosis are now available. A further expansion, also in Norway, of the indications for beta-interferon therapy of multiple sclerosis is expected in the near future.

Wergeland S, Beiske A, Nyland H, Hovdal H, Jensen D, Larsen JP, Marøy TH, Smievoll AI, Vedeler CA, Myhr KM. · The Multiple Sclerosis National Competence Centre, Department of Neurology, Haukeland University Hospital, Bergen, Norway. · Eur J Neurol. · Pubmed #15693804 No free full text.

Abstract: The level of interleukin-10 (IL-10) expression is related to polymorphisms -1082 (G/A), -819 (T/C) and -592 (A/C) in the promoter region of the IL-10 gene, which constitute three haplotypes, GCC, ATA, and ACC. The ATA (a non-GCC) haplotype, which is associated with low IL-10 expression, has been shown to improve interferon (IFN) treatment response in hepatitis C. We analysed the distribution of IL-10 promoter haplotype combinations to determine whether they could influence initial IFN treatment response in 63 patients with relapsing-remitting multiple sclerosis (MS). The patients were grouped into non-GCC or GCC haplotypes, and the clinical and magnetic resonance imaging (MRI) disease activity was compared in the two groups. During the first 6 months of treatment, MS patients with non-GCC haplotypes experienced fewer new MRI T1-contrast enhancing lesions [0.77+/-0.36 (SEM)] than patients with the GCC haplotype (2.45+/-0.57) (P=0.05, Mann-Whitney U test). No differences were detected on clinical disease activity. The results suggest an influence of IL-10 promoter polymorphisms on IFN treatment response in MS.

Myhr KM, Riise T, Green Lilleås FE, Beiske TG, Celius EG, Edland A, Jensen D, Larsen JP, Nilsen R, Nortvedt MW, Smievoll AI, Vedeler C, Nyland HI. · Department of Neurology, Haukeland University Hospital, University of Bergen, Norway. · Neurology. · Pubmed #10102427 No free full text.

Abstract: OBJECTIVE: To evaluate the efficacy and safety of interferon-alpha2a (IFN-alpha2a) in relapsing-remitting MS (RRMS). BACKGROUND: Several immune-modulating therapy regimens of IFN-alpha have shown varying results in MS. A recent pilot study suggested benefits from IFN-alpha2a. METHODS: Ninety-seven patients were randomized to receive subcutaneous injections of placebo (33 patients) or 4.5 million international units (mIU) (32 patients) or 9.0 mIU (32 patients) of IFN-alpha2a three times weekly for 6 months, with a further 6 months of follow-up. Monthly gadodiamide-enhanced MRI was the primary method of evaluating efficacy. RESULTS: IFN-alpha2a treatment resulted in fewer new MRI lesions during the treatment period (p < 0.003). The probability of no new lesions during treatment was >2.5 times higher with 9.0 mIU IFN-alpha2a than with placebo (p < 0.005). The median number of lesions at the end of treatment was lower with IFN-alpha2a treatment than with placebo (p = 0.0004), but the difference disappeared during follow-up. The total number of lesions (mean) increased by 4.78 with placebo, 0.86 with 4.5 mIU IFN-alpha2a, and 0.28 with 9.0 mIU IFN-alpha2a during treatment (p = 0.030). No treatment effect on exacerbation rate, progression of disability, or quality of life was detected. Nine patients discontinued treatment, five because of adverse events. CONCLUSIONS: IFN-alpha2a treatment significantly reduced disease activity as measured by MRI, but the efficacy disappeared within 6 months after discontinuation of treatment. A long-term study of more patients using disability as a primary outcome measure is needed to evaluate the clinical impact.

Reichelt KL, Jensen D. · Institute of Pediatric Research, University of Oslo, Oslo, Norway. · Acta Neurol Scand. · Pubmed #15355487 No free full text.

Abstract: BACKGROUND: Multiple changes in antibodies against various antigens are found in multiple sclerosis (MS). OBJECTIVE: We wanted to measure immunoglobulin A (IgA) antibodies to some common food antigens in MS and also IgG against gliadin and gluten. METHODS: The IgA antibodies were measured in serum against gluten, gliadin, lactoglobulin, lactalbumin, casein and ovalbumin in patients with MS and controls using ELISA technique. IgG was likewise measured for gluten and gliadin. RESULTS: Highly significant increases compared with controls were found for IgA and IgG antibodies against gliadin and gluten. IgA antibodies against casein were significantly increased. Anti-endomycium and anti-transglutaminase antibodies were negative. CONCLUSIONS: The data presented indicate that there may be a possible moderately increased uptake of some specific proteins from the gut in MS compared with controls.

Midgard R, Seland JH, Hovdal H, Celius EG, Eriksen K, Jensen D, Heger H, Mellgren SI, Wexler A, Beiske AG, Myhr KM. · Nevrologisk avdeling, Molde sjukehus, 6407 Molde. · Tidsskr Nor Laegeforen. · Pubmed #15742012 links to  free full text

Abstract: A national group of neurologists and ophthalmologists have evaluated guidelines and recommendations for diagnosis, treatment and follow up of optic neuritis based on clinical experience and a review of relevant literature. Optic neuritis is a common, well characterised condition that appears as an isolated syndrome or as a manifestation of multiple sclerosis. Several other diseases must be considered for a differential diagnosis. Corticosteroid treatment of optic neuritis has been investigated in a number of trials, which show that corticosteroid treatment speeds up the recovery of vision without affecting the final visual outcome. The diagnostic procedure and the treatment options have changed over the last few years. Some aspects of investigation, treatment and follow up are still controversial.