Oligoclonal Immunoglobulin Gamma Bands in the Cerebrospinal Fluid and Risk of Conversion to Secondary Progress in Multiple Sclerosis (P1.370)

Abstract

Objective: To determine whether the cerebrospinal fluid (CSF) oligoclonal bands (OCB) status in multiple sclerosis (MS) patients is predictive of conversion to secondary progressive MS (SPMS). Background: MS patients without the MS typical OCB distribution of immunoglobulin gamma (IgG) (OCB negative; OCB-) in the CSF have a different genetic background than MS patients with an OCB+ pattern. OCB- patients as a group are significantly different than OCB+ patients in terms of brain lesion distribution and signs of global and regional atrophy. A difference in long-term clinical outcome would be a strong argument for OCB- MS to qualify as a clinically and pathogenically distinct disease entity. Methods: We used data from clinically definite MS patients with known OCB status in the Swedish MS register. Date of birth, MS onset and conversion to SPMS, sex, and duration of exposure to first- and second-line Immunomodulatory treatments (IMTs) was collected. Multivariate Poisson regression models were used to investigate the influence of OCB-status on the risk of conversion to SPMS. Results: 4,728 relapsing-remitting MS (RRMS) patients were included. Overall, 475 (10[percnt]) were OCB- . The proportion of OCB- patients was significantly higher in those who had converted to SPMS than RRMS (11.4[percnt] vs. 9.4[percnt], P=0.02). Median age at conversion was 54.2 years (95[percnt] Confidence Intervals (CI): 53.6 to 55.5) and was not different between the OCB+ and OCB- groups (P= 0.3). While controlling for confounders, only OCB+ males showed higher risk of conversion to SPMS compared with OCB- females (relative risk-ratio: 1.5, 95[percnt] CI: 1.18 to 1.90, P=0.001). Conclusions: OCB- MS patients are just as prone to convert to SPMS as OCB+ MS patients. This indicates that possibly different in physiopathology, OCB- MS is unlikely to mimic other neuroinflammatory MS-like disorders. Our findings emphasize clinical phenotype similarities rather than differences between OCB+ and OCB- MS.

Disclosure: Dr. Karrenbauer has received research support from Novartis and Biogen. Dr. Hillert has received personal compensation for activities with BiogenIdec and Genzyme as an advisory board member, with Merck-Serono as a consultant, and with BiogenIdec, Merck-Serono, Novartis and Teva as a speaker. Dr. Manouchehrinia has nothing to disclose.