The diagnosis and treatment of Multiple Sclerosis (MS) have dramatically improved over recent decades due to scientific advancements, yet MS persists as one of the most disabling neurological disorders, having a significant impact on young adults - the age group most affected by the disease.
Continuing medical education provider, EXCEMED - Excellence in Medical Education, will draw leading international experts in MS to explore the roles of genetics and environment in MS pathology. The conference, "Multiple sclerosis: Improving patient outcomes through scientific and clinical advances" takes place in Dubai, United Arab Emirates, from 9 to 10 May 2014.
"This meeting will present the latest epidemiological and genetic knowledge about MS and link it to pathology and the practical management of therapy for people with MS" says Professor David Bates, Department of Neurology, Royal Victoria Infirmary, Newcastle upon Tyne, UK, and - scientific organizer of the event.
"We are proud to gather, year after year, an outstanding international panel of experts in neurology and MS research in order to contribute to the debate from the perspective of clinical practices. The goal is to identify the most appropriate treatments for this disease," says Professor Giancarlo Comi, President of the EXCEMED Scientific Committee and Professor in Neurology at University Vita-Salute San Raffaele, Milan, Italy.
The scientific programme of the event offers three sessions and six workshops: Session one will address basic research in MS pathogenesis including epidemiology, risk factors, genetics of MS and mechanism and prevention of neurodegeneration. Session two will address clinical approaches to MS and session three will deal with therapeutic management. The six workshops will be attended in rotation by each participant to allow for optimal exchange of opinions and a deeper understanding of the different MS related topics.
Source: Digital Journal copyright © 2014 digitaljournal.com (09/05/14)
Multiple sclerosis shows a "striking" association with obesity at age 20 years that strongly interacts with genetic susceptibility, according to an analysis of data from two case-control studies that examined environmental and genetic risk factors for MS.
This relationship between adolescent obesity and MS is of the same magnitude as the separate associations between MS and carriage of the high-risk HLA-DRB1*15 allele, absence of the protective HLA-A*02 allele, and smoking, said Dr. Anna Karin Hedström of the Institute of Environmental Medicine, Karolinska Institutet, Stockholm, and her associates.
"The biological explanations for these interactions are far from clear, but the data open [the way] for mechanistically oriented studies," they said.
Three previous studies have suggested that obesity in early life may be linked to increased risk of developing MS later. Dr. Hedström and her colleagues examined this association using data from a Swedish population-based, case-control study and from a separate American case-control study.
In the Swedish study, 1,510 adults with incident MS who were treated at 40 clinics across the country during a 7-year period and 2,017 control subjects completed detailed questionnaires concerning environmental exposures and other factors. The controls were matched for age, sex, and area of residence, and all the participants gave blood samples for HLA typing.
The American study involved 937 white adults with prevalent MS who were members of a single large health maintenance organization covering northern California and 609 white control subjects matched for age, sex, and area of residence. All the participants completed computer-assisted telephone interviews regarding environmental exposures and lifestyle factors.
All the subjects in both studies reported what their heights and weights had been at age 20 years, from which the investigators calculated body mass index (BMI).
In both studies, participants whose BMI at age 20 years was 27 kg/m2 or greater showed an increased risk of developing MS later in life, compared with those whose BMI was 18.5-21 kg/m2. The odds ratios (ORs) were 2.2 for subjects in the Swedish study and 1.8 for those in the American study, Dr. Hedström and her associates said (Neurology 2014 [doi:10.1212/WNL.0000000000000203]).
Similarly, participants with a slightly lower but still above-normal BMI of 25-27 kg/m2 showed a modestly increased risk of developing MS later in life: The ORs were 1.4 in the Swedish study and 1.3 in the American study.
These ORs were unchanged when a sensitivity analysis was performed, including only the study subjects who had been genotyped.
Participants who carried the high-risk HLA-DRB1*15 gene, did not carry the protective HLA-A*02 gene, and had a BMI of 27 kg/ m2 or greater at age 20 years had an OR of 16.2 for developing later MS, compared with those who had none of those risk factors. In contrast, subjects who had the same HLA profile but had not been obese at age 20 years had an OR of only 5.1.
The investigators proposed that the low-grade chronic inflammation associated with obesity, together with obesity’s adverse effects on autoimmunity, may raise the risk of HLA-related activation of T cells that attack the CNS.
Both the Swedish and the American study were limited in that they were retrospective and relied on participants’ self-reports. In addition, Dr. Hedström and her associates modified the usual definition of obesity for the purposes of their study. The typical standard for obesity is a BMI of greater than 30 kg/m2, not greater than 27 kg/m2. However, the number of subjects at this level of BMI was too small in the Swedish cohort to allow accurate analysis, so the researchers combined the top two categories of BMI into one designation of "obese."
This study was supported by several private nonprofit foundations, the Swedish Research Council for Health, Working Life and Welfare, and the U.S. National Institute of Neurological Disorders and Stroke. Dr. Hedström and five of the other seven authors reported no financial conflicts of interest. One coauthor reported ties to numerous industry sources and one reported receiving research support from Swedish government agencies.
Causality not yet established
This study and other research linking obesity early in life with the later development of MS are observational and cannot establish causality, so we don’t yet know whether decreasing obesity with diet and exercise will lead to a decrease in the incidence of MS.
Nevertheless, these findings are concerning. “It is time to begin developing a targeted approach to prevent MS by improving common health behaviors, including body weight and smoking,” Dr. Marrie and Dr. Beck said.
People who are at high genetic risk can be readily identified by focusing HLA genotyping on the first-degree relatives of known MS patients, they added.
Dr. Marrie is in the departments of internal medicine and community health sciences at the University of Manitoba, Winnipeg. She has received funding from Sanofi-Aventis and Canadian governmental agencies and nonprofit organizations, including the MS Society of Canada and the MS Scientific Foundation. Dr. Beck is in the department of biostatistics and computational biology at the University of Rochester (N.Y.) Medical Center. Dr. Beck has received support from a variety of healthcare companies as well the U.S. Food and Drug Administration and the U.S. National Institutes of Health.
These remarks were taken from their editorial accompanying Dr. Hedström’s report (Neurology 2014 [doi:10.1212/WNL.0000000000000195]).
Source: Clinical Endocrinology New Copyright © 2014 Frontline Medical Communications LLC (12/02/14)
Drinking alcohol appears to have a dose-dependent inverse (opposite) association with the risk of developing multiple sclerosis (MS) and researchers suggest their findings give no support to advising patients with MS to completely refrain from alcohol, according to a study by Anna Karin Hedstrom, M.D., of the Karolinska Institutet, Sweden, and colleagues.
The results of previous studies have been inconsistent about the impact of alcohol and the risk of developing MS.
Researchers investigated the association using two population studies in Sweden with participants between the ages of 16 and 70 years: 745 cases of MS plus 1,761 controls in the Epidemiological Investigation of Multiple Sclerosis (EIMS) study and 5,874 cases of MS with 5,246 controls in the Genes and Environment in Multiple Sclerosis (GEMS) study.
In EIMS, women who reported high alcohol consumption had an odds ratio (OR) of 0.6 of developing MS compared with nondrinking women, and men with high alcohol consumption had an OR of 0.5 compared with nondrinking men, according to the results. The corresponding OR comparison in GEMS was 0.7 for both women and men. Alcohol consumption also appeared to be associated with the attenuation (lessening) of the effect of smoking, the results also indicate.
"Although the effect of alcohol on already established MS has not been studied herein, the data may have relevance for clinical practice since they give no support for advising persons with MS to completely refrain from alcohol," the authors conclude.
Source: MedicalXpress © Medical Xpress 2011-2014 (07/01/14)
Exposure to cigarette smoke is emerging as an environmental risk factor for multiple sclerosis (MS).
We investigated the possible association between environmental tobacco smoke, its cumulative exposure, and MS risk.
We used data from the Iranian Multiple Sclerosis Registry to identify a case-control of 662 patients who had MS and a comparison group of 394 patients. Information regarding current smoking status, including the number of cigarettes smoked per day, duration, and smoking pack-years indicative of cumulative dose of tobacco smoked was obtained.
We analyzed the incidence of MS among ever-smokers who had been smokers during their disease course and prior to disease onset in comparison with never-smokers who had never been exposed by calculating the odds ratio (OR) with a 95% confidence interval (CI) employing logistic regression. Of the 662 MS patients, there were 523 women (79.0%) and 139 men (21.0%), with a mean age of 31±10.0years at disease onset.
The risk for MS was increased among ever-smokers (OR=1.78, 95% CI=1.22-2.59, p=0.03) compared to never-smokers. As compared with never smokers, the OR for patients with 6-10 pack years was 2.91 for men (95% CI=1.11-9.47, p=0.03) and 1.69 for women (95% CI=1.02-6.45, p=0.04).
Our results demonstrate that cigarette smoking is significantly associated with an increased risk for MS. The risk effects of smoking were more noticeable in male patients and at higher tobacco doses.
Asadollahi S, Fakhri M, Heidari K, Zandieh A, Vafaee R, Mansouri B.
School of Medicine, Shahid Beheshti University of Medical Science, Tehran, Iran.
Sources: J Clin Neurosci. 2013 Aug 20. pii: S0967-5868(13)00182-3. doi: 10.1016/j.jocn.2013.01.018. Copyright © 2013 Elsevier Ltd & Pubmed PMID: 23972559 (03/09/13)