Contributions
Abstract: P1053
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Comorbidity
Introduction: Smoking is associated with higher hyperintense white matter lesion load, increased brain volume loss and more pronounced disability even in early stages of multiple sclerosis (MS). Specific pathomechanisms for these relationships have not been identified so far.
Aim: We therefore investigated if smoking may have a specific impact on periventricular regions which have been associated with CSF mediated disease mechanisms both in terms of T2-lesion load (T2-LL) and microstructural changes of so-called 'normal appearing white matter' (NAWM).
Methods: We identified 157 patients with a clinically isolated syndrome (CIS, n=86) or relapsing remitting MS (n=71). Following a retrospective assessment, persons were classified into smokers if they had smoked more than 10 cigarettes per day for at least 6 months or into non-smokers, if otherwise. T2-hyperintense white matter lesions were segmented semi-automatically on fluid attenuated inversion recovery (FLAIR) images. The magnetisation transfer ratio (MTR) of the NAWM was measured stepwise centrifugally, creating a total of 10 bands of 1mm starting at the ventricle. Mean values for bands 1-5 and 6-10 were calculated.
Results: 62 (39.4%) patients were smokers. The mean age at disease onset (29.1 ± 9.2 years) and the median disease duration at baseline (11.0; IQR 2-81 months) did not differ between both groups. While the overall T2-lesion load was comparable (smokers: median 7.7ccm; IQR 2.9-20.4ccm versus non-smokers: 5,7ccm; IQR 3.1-12.7ccm), smokers had a higher percentage of periventricular lesions (PVL) (54.5% versus 43.6%, p=0.015). No effect of smoking could be shown on the MTR of the periventricular NAWM.
Conclusion: In this study, smoking was associated with a higher percentage of PVL, a result which might be explained by pro-inflammatory mechanisms triggered by tobacco ingredients. However, no effect could be shown on microstructural changes of the periventricular NAWM.
Disclosure: Alexander Pichler: nothing to disclose
Daniel Hochstrasser: nothing to disclose
Michael Khalil: Michael Khalil has received funding for travel and speaker honoraria from Bayer, Novartis, Merck, Biogen, Roche and Teva ratiopharm; serves on scientific advisory boards for Biogen and Roche and received a research grant from Teva ratiopharm.
Christian Langkammer: nothing to disclose
Lukas Pirpamer: nothing to disclose
Daniela Pinter: Daniela Pinter receives funding from the Austrian Science fund (T 690- B23) and has received funding for travel from Merck and funding from Genzyme/Sanofi-Aventis.
Stefan Ropele: nothing to disclose
Siegrid Fuchs: Siegrid Fuchs serves on scientific advisory boards and / or has received speaker honoraria from Biogen Idec, Merck, Novartis ; Roche, TEVA Pharmaceutical Industries and Sanofi-Aventis.
Christian Enzinger: Christian Enzinger received funding for traveling and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, Shire; received research support from Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries Ltd./sanofi-aventis; and serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, Genzyme, Roche, and Teva Pharmaceutical Industries Ltd./sanofi- Aventis
Franz Fazekas: Franz Fazekas serves on scientific advisory boards for Biogen-Idec, Genzyme-Sanofi, Merck, Novartis, and Teva Ratiopharm; serves on the editorial boards of the European Stroke Journal, Multiple Sclerosis Journal, Neurology, the Polish Journal of Neurology and Neurosurgery, and the Swiss Archives of Neurology and Psychiatry; provides consulting services for Actelion, Medday, Parexel and Teva Ratiopharm and has received speaker honoraria from Merck, Genzyme-Sanofi and Teva Ratiopharm
Abstract: P1053
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Comorbidity
Introduction: Smoking is associated with higher hyperintense white matter lesion load, increased brain volume loss and more pronounced disability even in early stages of multiple sclerosis (MS). Specific pathomechanisms for these relationships have not been identified so far.
Aim: We therefore investigated if smoking may have a specific impact on periventricular regions which have been associated with CSF mediated disease mechanisms both in terms of T2-lesion load (T2-LL) and microstructural changes of so-called 'normal appearing white matter' (NAWM).
Methods: We identified 157 patients with a clinically isolated syndrome (CIS, n=86) or relapsing remitting MS (n=71). Following a retrospective assessment, persons were classified into smokers if they had smoked more than 10 cigarettes per day for at least 6 months or into non-smokers, if otherwise. T2-hyperintense white matter lesions were segmented semi-automatically on fluid attenuated inversion recovery (FLAIR) images. The magnetisation transfer ratio (MTR) of the NAWM was measured stepwise centrifugally, creating a total of 10 bands of 1mm starting at the ventricle. Mean values for bands 1-5 and 6-10 were calculated.
Results: 62 (39.4%) patients were smokers. The mean age at disease onset (29.1 ± 9.2 years) and the median disease duration at baseline (11.0; IQR 2-81 months) did not differ between both groups. While the overall T2-lesion load was comparable (smokers: median 7.7ccm; IQR 2.9-20.4ccm versus non-smokers: 5,7ccm; IQR 3.1-12.7ccm), smokers had a higher percentage of periventricular lesions (PVL) (54.5% versus 43.6%, p=0.015). No effect of smoking could be shown on the MTR of the periventricular NAWM.
Conclusion: In this study, smoking was associated with a higher percentage of PVL, a result which might be explained by pro-inflammatory mechanisms triggered by tobacco ingredients. However, no effect could be shown on microstructural changes of the periventricular NAWM.
Disclosure: Alexander Pichler: nothing to disclose
Daniel Hochstrasser: nothing to disclose
Michael Khalil: Michael Khalil has received funding for travel and speaker honoraria from Bayer, Novartis, Merck, Biogen, Roche and Teva ratiopharm; serves on scientific advisory boards for Biogen and Roche and received a research grant from Teva ratiopharm.
Christian Langkammer: nothing to disclose
Lukas Pirpamer: nothing to disclose
Daniela Pinter: Daniela Pinter receives funding from the Austrian Science fund (T 690- B23) and has received funding for travel from Merck and funding from Genzyme/Sanofi-Aventis.
Stefan Ropele: nothing to disclose
Siegrid Fuchs: Siegrid Fuchs serves on scientific advisory boards and / or has received speaker honoraria from Biogen Idec, Merck, Novartis ; Roche, TEVA Pharmaceutical Industries and Sanofi-Aventis.
Christian Enzinger: Christian Enzinger received funding for traveling and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, Shire; received research support from Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries Ltd./sanofi-aventis; and serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, Genzyme, Roche, and Teva Pharmaceutical Industries Ltd./sanofi- Aventis
Franz Fazekas: Franz Fazekas serves on scientific advisory boards for Biogen-Idec, Genzyme-Sanofi, Merck, Novartis, and Teva Ratiopharm; serves on the editorial boards of the European Stroke Journal, Multiple Sclerosis Journal, Neurology, the Polish Journal of Neurology and Neurosurgery, and the Swiss Archives of Neurology and Psychiatry; provides consulting services for Actelion, Medday, Parexel and Teva Ratiopharm and has received speaker honoraria from Merck, Genzyme-Sanofi and Teva Ratiopharm