Abstract
BackgroundSmoking, cardiovascular risk factors, and genetic factors can have adverse effects in MS. ObjectiveTo determine if smoking after disease onset, cardiovascular risk factors, and genetic variants influence primary progressive MS (PPMS). MethodIn this cross-sectional study, smoking habits, Framingham Risk Score (FRS), genetic variants, including the low-density lipoprotein receptor-related protein 2 (LRP2) SNP rs12988804 and MRI were collected in 60 PPMS trial participants. Disability and cognition were assessed with the Age-Related Multiple Sclerosis Severity (ARMSS) score, the Progressive-Onset MS Multiple Sclerosis Severity Score, and the Brief International Cognitive Assessment for MS. ResultsSmoking after PPMS onset was significantly associated with higher ARMSS (95% CI 0.8–2.4, p = 0.00016) statistically significant after Bonferroni correction. Lower magnetization transfer ratio in lesions was also significantly associated with smoking after onset of PPMS after correction (95% CI -0.9–-4.4, p = 0.0035). Pack-years in people who smoked after onset was likewise significantly associated with higher ARMSS score (b = 0.06 95% CI 0.02–0.09, p = 0.0021) as well as lower Symbol Digit Modalities Test scores (b = -0.40; 95% CI -0.66–-0.13, p = 0.0037), both statistically significant after Bonferroni correction. The LRP2 risk allele was associated with decreased performance on the California Verbal Learning Test 2 after correction (CC vs. CT+TT 95% CI -14.2–-3.4, p = 0.0018). ConclusionIf validated, these findings suggest that intervention regarding smoking may be beneficial in PPMS. If confirmed, assessment of the LRP2 gene variant may aid in the understanding of underlying pathological mechanisms in PPMS.
Highlights
Primary progressive multiple sclerosis (PPMS) represents approxi mately 10–15% of the MS population (Miller and Leary, 2007)
This study shows a significant association between continued smoking after disease onset and more severe disability with a 1.6-point higher Age-Related Multiple Sclerosis Severity (ARMSS) score in the group that continued smoking after disease onset
A division regarding smoking habits can be influenced by recall bias, but because the participants who continued smoking after primary progressive MS (PPMS) onset did so with a median duration of 4.5 years, we believe this way of grouping is reliable
Summary
Primary progressive multiple sclerosis (PPMS) represents approxi mately 10–15% of the MS population (Miller and Leary, 2007). The Framingham Risk Score was developed to estimate the 10-year likelihood of a cardiovascular event It combines individual cardiovas cular risk factors into one outcome measure that has been associated with MS disability, relapse rate, severity, course, and risk of escalation of disease-modifying treatment (D’Agostino et al, 2008; Moccia et al, 2015; Petruzzo et al, 2020). Objective: To determine if smoking after disease onset, cardiovascular risk factors, and genetic variants influence primary progressive MS (PPMS). Pack-years in people who smoked after onset was likewise significantly associated with higher ARMSS score (b = 0.06 95% CI 0.02–0.09, p = 0.0021) as well as lower Symbol Digit Modalities Test scores (b = -0.40; 95% CI -0.66–-0.13, p = 0.0037), both statistically significant after Bonferroni correction. Assessment of the LRP2 gene variant may aid in the understanding of underlying pathological mechanisms in PPMS
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