Serum Lipid Profiles Are Associated With Disability and MRI Outcomes in Multiple Sclerosis

Bianca Weinstock-Guttman; Robert Zivadinov; Naeem Mahfooz; Ellen Carl; Allison Drake; Jaclyn Schneider; Barbara Teter; Sara Hussein; Bijal Mehta; Marc Weiskopf; Jacqueline Durfee; Niels Bergsland; Murali Ramanathan

Disclosures

J Neuroinflammation. 2011;8(127) 

In This Article

Results

Demographic and Clinical Characteristics

The clinical, demographic and MRI features of the cohort are summarized in Table 1. The frequency of Caucasian-Americans was 422 (85.8%), African-Americans was 28 (5.7%), Hispanics was 5 (1%), Native American 1 (0.2%), and the racial information for 34 (6.9%) patients was missing.

The median absolute time difference between lipid profile and baseline EDSS assessment was 25 days (Inter-quartile range: 51 days). The median absolute time difference between MRI and lipid profile assessments was 30 days (Inter-quartile range: 46 days). The median time between baseline EDSS and follow-up EDSS was 1.88 years (Inter-quartile range: 1.62 years).

The majority of patients were on disease-modifying therapies: 45% were on interferon-beta-1a monotherapy, 0.8% were on interferon-beta-1b monotherapy, 14% were on glatiramer acetate, 20% were on natalizumab, 8% were on no therapy and the remainder were on combination therapies or chemotherapies.

MRI data were available for 210 patients. There was no evidence for lipid profile differences between the groups with and without MRI available (See Additional File 1, Table S1). The group with MRI differed from the group without MRI in the higher frequency of progressive forms of MS and a modestly shorter time between baseline EDSS and follow up EDSS (See Additional File 1, Table S1).

The frequency of statin usage was 109/491 patients (22.2%). There was no evidence for differences in the groups with and without statin treatment in the lipid profile variables including HDL, LDL, triglycerides, total cholesterol and cholesterol to HDL. Not surprisingly, the group on statin treatment had a higher proportion of males, greater mean age, disease duration, BMI and baseline EDSS than the group not on statin treatment (Table 2).

The frequency of disease-modifying therapy usage in the group on statin treatment (51% interferon-beta 1a, 7% glatiramer acetate, 20% natalizumab, 9% no current disease-modifying therapy, with the remainder on combination therapies or chemotherapies) was similar to the group not receiving statins (43% interferon-beta 1a, 16% glatiramer acetate, 20% natalizumab, 8% no therapy, with the remainder on combination therapies or chemotherapies). There was no evidence for significant differences in the lipid profile variables among the interferon-beta, glatiramer acetate, natalizumab, combination therapy or chemotherapies and no current disease-modifying therapy groups (one-way ANOVA).

Associations With Disability and Disability Changes

Higher total cholesterol to HDL ratio showed an association trend with baseline MSSS (Slope = 0.161 ± 0.092, Partial correlation coefficient rp = 0.080, p = 0.080) and with higher probability of occurrence of baseline EDSS ≥ 4.0 (p = 0.082, OR = 1.17). There was no evidence for associations for the other lipid profile variables or BMI. In the subset without statin treatment, the probability of occurrence of baseline EDSS ≥ 4.0 exhibited increasing trends with higher total cholesterol (p = 0.040) and cholesterol to HDL ratio (p = 0.017). There was no evidence for an association with HDL. Baseline MSSS trended higher with higher total cholesterol to HDL ratio (Slope = 0.23 ± 0.11, rp = 0.11, p = 0.038).

The associations of lipid profile variables with EDSS and MSSS changes are summarized in Table 3. Worsening EDSS changes were associated with higher LDL (p = 0.006), triglycerides (p = 0.025), total cholesterol (p = 0.001) and exhibited a trend with total cholesterol to HDL ratio (p = 0.047) levels. The EDSS change was not associated with higher HDL (p = 0.79). Similarly, worsening MSSS changes were associated with higher total cholesterol levels (p = 0.008); trends were also found with higher LDL (p = 0.012) and triglyceride (p = 0.037) levels. BMI was not associated with disability changes on either the EDSS or MSSS (results not shown). Qualitatively, similar results were obtained in the subset of patients who were not on statin treatment (results not shown).

These results indicate that LDL, triglyceride and total cholesterol lipid profile variables are associated with disability changes in MS patients.

Associations With MRI

Higher HDL levels were associated with a lower probability for the presence of CEL (p = 0.01) and lower CE-LV (p < 0.001). A qualitatively similar pattern of protective associations for higher HDL was found in the group not receiving statin treatment for the presence of CEL (p = 0.029, a trend) and for CE-LV (p < 0.001).

In contrast, higher triglyceride levels were associated with trends for a higher probability for the presence of CEL (p = 0.038) and with higher CE-LV (p = 0.023). There were similar trends for triglyceride levels with the presence of CEL (p = 0.060) in the group not receiving statins.

There was no evidence for associations between the presence of CEL and LDL (p = 0.80) or total cholesterol (p = 0.44) levels. There was also no evidence for associations between CE-LV with total cholesterol levels (p = 0.20). Greater levels of total cholesterol were associated as a trend with lower CEL number (p = 0.046) in part as a consequence of the HDL associations with CEL number. Lower CE-LV was also associated as a trend with lower levels of cholesterol to HDL ratio (p = 0.025). There was no evidence for associations of LDL with CEL number (p = 0.44) or CE-LV (p = 0.89) in patients not on statins.

There were no significant associations of T2-LV and T1-LV with any of the lipid profile variables (HDL, LDL, Triglycerides, total cholesterol and cholesterol to HDL ratio) or BMI. However, lower BPF values were associated with high total cholesterol levels (rp = -0.16, p = 0.033). There was also a trend toward an association between lower BPF values with higher total cholesterol in the sub-group that was not on statin treatment (rp = -0.16, p = 0.054).

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