Contributions
Abstract: P389
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Inflammation and tissue damage
Background: The relationship between prolactin (PRL) serum levels and white matter volume in patients with multiple sclerosis (MS) supports a role of PRL in promoting myelin repair. In experimental models, PRL shows beneficial effects on clinical signs of disease when administered in combination with Interferon beta (IFN beta). Here, we test the hypothesis that PRL serum levels predict the development of inflammatory damage during the treatment with IFN beta.
Methods: Blood samples for the assessment of PRL serum level were obtained in relapsing-remitting MS (RRMS) patients who were randomly assigned in a 1:1:1 ratio to receive subcutaneous IFN beta only or IFN beta in association with two different doses of estroprogestins. Patients underwent brain MRI scan and clinical evaluation at baseline and after 1 and 2 years of treatment. We quantified white matter hyperintense lesion volume on T2-weighted images (T2LL) and hypointense lesion volume on T1-weighted pre- and post-contrast images (T1LL and Gd+LL). We also calculated the number of combined unique active (CUA) lesions, defined as new T2 lesions or gadolinium enhancing (Gd+) lesions without double counting. Baseline predictors of CUA number during IFN beta treatment were assessed with a Poisson regression model.
Results: We included 99 women with MS with a mean (SD) age of 30 (7) years, mean MS duration of 3.5 (3.8) years, median EDSS of 1.5 (range 0-4.5); mean PRL level was 13.8 (7.7) ng/ml. No correlation was found between PRL levels and demographic or clinical baseline data. PRL level showed a negative correlation with baseline T2LL and T1LL (rho=-0.245, p=0.014 and rho=-0.236 p=0.018, respectively), but not with Gd+LL. Mean number of CUA was 1.9 (2.6) at year 1 and 1.4 (3.17) at year 2. We found a negative correlation between CUA number at 2 year and baseline PRL level (rho=-0.221, p=0.02). Lower CUA number at year 2 was predicted by higher EDSS score (HR 0.373, 95%CI 0.282-0.494, p< 0.001), higher PRL levels (HR 0.557, 95% CI 0.435-0.713 p>0.001) and the absence of Gd+ lesions (HR 3.506, 95%CI 2.318-5.304, p< 0,001) at baseline.
Conclusion: The association between higher baseline levels of PRL and lower inflammatory damage at follow-up suggests that PRL is an independent predictor of tissue damage development during treatment with IFN beta.
Disclosure:
LDG has nothing to disclose
FM has nothing to disclose
VTB has nothing to disclose
LP has received consulting and/or lecture fees and travel grant from Bayer Schering, Biogen Idec, Genzyme, Biogen Idec, Novartis and Teva
FG has nothing to disclose
VT has nothing to disclose
PP has received founding for travel from Novartis, Genzyme and Bracco and speaker honoraria from Byogen
CP has received consulting and lecture fees from Bayer Schering, Biogen, Merck-Serono, Novartis, and Sanofi-Aventis; has received research funding from Bayer Schering, Merck Serono, Novartis, and Sanofi-Aventis.
Abstract: P389
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Inflammation and tissue damage
Background: The relationship between prolactin (PRL) serum levels and white matter volume in patients with multiple sclerosis (MS) supports a role of PRL in promoting myelin repair. In experimental models, PRL shows beneficial effects on clinical signs of disease when administered in combination with Interferon beta (IFN beta). Here, we test the hypothesis that PRL serum levels predict the development of inflammatory damage during the treatment with IFN beta.
Methods: Blood samples for the assessment of PRL serum level were obtained in relapsing-remitting MS (RRMS) patients who were randomly assigned in a 1:1:1 ratio to receive subcutaneous IFN beta only or IFN beta in association with two different doses of estroprogestins. Patients underwent brain MRI scan and clinical evaluation at baseline and after 1 and 2 years of treatment. We quantified white matter hyperintense lesion volume on T2-weighted images (T2LL) and hypointense lesion volume on T1-weighted pre- and post-contrast images (T1LL and Gd+LL). We also calculated the number of combined unique active (CUA) lesions, defined as new T2 lesions or gadolinium enhancing (Gd+) lesions without double counting. Baseline predictors of CUA number during IFN beta treatment were assessed with a Poisson regression model.
Results: We included 99 women with MS with a mean (SD) age of 30 (7) years, mean MS duration of 3.5 (3.8) years, median EDSS of 1.5 (range 0-4.5); mean PRL level was 13.8 (7.7) ng/ml. No correlation was found between PRL levels and demographic or clinical baseline data. PRL level showed a negative correlation with baseline T2LL and T1LL (rho=-0.245, p=0.014 and rho=-0.236 p=0.018, respectively), but not with Gd+LL. Mean number of CUA was 1.9 (2.6) at year 1 and 1.4 (3.17) at year 2. We found a negative correlation between CUA number at 2 year and baseline PRL level (rho=-0.221, p=0.02). Lower CUA number at year 2 was predicted by higher EDSS score (HR 0.373, 95%CI 0.282-0.494, p< 0.001), higher PRL levels (HR 0.557, 95% CI 0.435-0.713 p>0.001) and the absence of Gd+ lesions (HR 3.506, 95%CI 2.318-5.304, p< 0,001) at baseline.
Conclusion: The association between higher baseline levels of PRL and lower inflammatory damage at follow-up suggests that PRL is an independent predictor of tissue damage development during treatment with IFN beta.
Disclosure:
LDG has nothing to disclose
FM has nothing to disclose
VTB has nothing to disclose
LP has received consulting and/or lecture fees and travel grant from Bayer Schering, Biogen Idec, Genzyme, Biogen Idec, Novartis and Teva
FG has nothing to disclose
VT has nothing to disclose
PP has received founding for travel from Novartis, Genzyme and Bracco and speaker honoraria from Byogen
CP has received consulting and lecture fees from Bayer Schering, Biogen, Merck-Serono, Novartis, and Sanofi-Aventis; has received research funding from Bayer Schering, Merck Serono, Novartis, and Sanofi-Aventis.