Multiple Sclerosis: Soelberg Sørensen P

Elovaara I, Apostolski S, van Doorn P, Gilhus NE, Hietaharju A, Honkaniemi J, van Schaik IN, Scolding N, Soelberg Sørensen P, Udd B, Anonymous00010. · Department of Neurology and Rehabilitation, Tampere University Hospital and Medical School, University of Tampere, Tampere, Finland. · Eur J Neurol. · Pubmed #18796075 No free full text.

Abstract: Despite high-dose intravenous immunoglobulin (IVIG) is widely used in treatment of a number of immune-mediated neurological diseases, the consensus on its optimal use is insufficient. To define the evidence-based optimal use of IVIG in neurology, the recent papers of high relevance were reviewed and consensus recommendations are given according to EFNS guidance regulations. The efficacy of IVIG has been proven in Guillain-Barré syndrome (level A), chronic inflammatory demyelinating polyradiculoneuropathy (level A), multifocal mononeuropathy (level A), acute exacerbations of myasthenia gravis (MG) and short-term treatment of severe MG (level A recommendation), and some paraneoplastic neuropathies (level B). IVIG is recommended as a second-line treatment in combination with prednisone in dermatomyositis (level B) and treatment option in polymyositis (level C). IVIG should be considered as a second or third-line therapy in relapsing-remitting multiple sclerosis, if conventional immunomodulatory therapies are not tolerated (level B), and in relapses during pregnancy or post-partum period (good clinical practice point). IVIG seems to have a favourable effect also in paraneoplastic neurological diseases (good practice point) [corrected],stiff-person syndrome (level A), some acute-demyelinating diseases and childhood refractory epilepsy (good practice point).

Hillert J, Soelberg Sørensen P. · No affiliation provided · J Neurol. · Pubmed #18317670 No free full text.

This publication has no abstract.

Sellebjerg F, Datta P, Larsen J, Rieneck K, Alsing I, Oturai A, Svejgaard A, Soelberg Sørensen P, Ryder LP. · Department of Neurology, Danish Multiple Sclerosis Research Center, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark. · Mult Scler. · Pubmed #18408020 No free full text.

Abstract: Treatment with interferon-beta (IFN-beta) induces the expression of hundreds of genes in blood mononuclear cells, and the expression of several genes has been proposed as a marker of the effect of treatment with IFN-beta. However, to date no molecules have been identified that are stably induced by treatment with IFN-beta. We use DNA microarrays to study gene expression in 10 multiple sclerosis (MS) patients who began de novo treatment with IFN-beta. After the first injection of IFN-beta, the expression of 74 out of 3428 genes changed at least two-fold and statistically significantly (after Bonferroni correction). In contrast, we observed no persisting effects of IFN-beta on gene expression. Among the most strongly induced genes was MXA, which has been used in previous biomarker studies in MS. In addition, the study identified the induction of LGALS9 and TCIR1G, involved in negative regulation of T helper type I immunity and T-cell activation, as novel effects of IFN-beta therapy in MS.

Andersen O, Elovaara I, Färkkilä M, Hansen HJ, Mellgren SI, Myhr KM, Sandberg-Wollheim M, Soelberg Sørensen P. · Institute of Clinical Neuroscience, Sahlgrenska University Hospital, University of Göteborg, Göteborg, Sweden. · J Neurol Neurosurg Psychiatry. · Pubmed #15090564 links to  free full text

Abstract: OBJECTIVE: Interferon (IFN) beta has repeatedly shown benefit in multiple sclerosis (MS) in reducing the rate of relapse, the disease activity as shown with magnetic resonance imaging and, to some degree, the progression of disability; however, it is unknown how much the therapeutic response depends on the dose, the subgroup involved, and the disease stage. This multicentre, double blind, placebo controlled study explored the dose-response curve by examining the clinical benefit of low dose IFN beta-1a (Rebif), 22 micro g subcutaneously once weekly, in patients with secondary progressive MS. METHODS: A total of 371 patients with clinically definite SPMS were randomised to receive either placebo or subcutaneous IFN beta-1a, 22 micro g once weekly, for 3 years. Clinical assessments were performed every 6 months. The primary outcome was time to sustained disability, as defined by time to first confirmed 1.0 point increase on the Expanded Disability Status Scale (EDSS). Secondary outcomes included a sensitive disability measure and relapse rate. RESULTS: Treatment had no beneficial effect on time to confirmed progression on either the EDSS (hazard ratio (HR) = 1.13; 95% confidence interval (CI) 0.82 to 1.57; p = 0.45 for 22 micro g v placebo) or the Regional Functional Status Scale (HR = 0.93; 95% CI 0.68 to 1.28; p = 0.67). Other disability measures were also not significantly affected by treatment. Annual relapse rate was 0.27 with placebo and 0.25 with IFN (rate ratio = 0.90; 95% CI 0.64 to 1.27; p = 0.55). The drug was well tolerated with no new safety concerns identified. No significant gender differences were noted. CONCLUSIONS: This patient population was less clinically active than SPMS populations studied in other trials. Treatment with low dose, IFN beta-1a (Rebif) once weekly did not show any benefit in this study for either disability or relapse outcomes, including a subgroup with preceding relapses. These results add a point at one extreme of the dose-response spectrum of IFN beta therapy in MS, indicating that relapses in this phase may need treatment with higher doses than in the initial phases.

Jønsson A, Andresen J, Storr L, Tscherning T, Soelberg Sørensen P, Ravnborg M. · Department of Neurology, Section 6131, Danish Multiple Sclerosis Centre, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen, Denmark. · J Neurol Sci. · Pubmed #16647089 No free full text.

Abstract: Cognitive impairment occurs in early multiple sclerosis (MS), may decline over time, and has major impact on social functioning. The objectives of this study were to examine cognitive functioning in newly diagnosed MS, and to follow up over a period of 5 years. The results of the first three yearly re-examinations are reported. Eighty newly diagnosed (<1 year) MS patients participated (male/female: 19:61, mean age: 35 years, mean EDSS 2.7, course: 75 relapsing-remitting, 3 primary progressive, 2 secondary progressive). Seventy-five healthy persons served as controls. The neuropsychological (NP) test battery comprised 30 test measures and was grouped into seven cognitive domains. A residual score of -1.5 SD as cut-off point was used to diagnose cognitive impairment. At the first examination, 44-48% had cognitive impairment. None of the patients were clinically depressed, 51% had no signs of depression on Beck Depression Inventory (BDI), and none had severe signs. Sixty-four patients completed four examinations, and a significant linear improvement over time was seen in three cognitive domains, no change in two domains, and deterioration in one domain. At the time of the fourth examination, 4.3 years since diagnosis, 33-34% of the patients had cognitive impairment. Thirty percent of the patients were on disablement pension, 34% received social services in relation to work and 13% had home care. Methodological problems are discussed, especially the practice effect and the importance of identifying sensitive and stable test measures.