Dataset Information

Lipids, apolipoproteins, and prognosis of amyotrophic lateral sclerosis.

ABSTRACT:

Objective

To determine whether lipids and apolipoproteins predict prognosis of patients with amyotrophic lateral sclerosis in a cohort study of 99 patients with amyotrophic lateral sclerosis who were diagnosed during 2015 to 2018 and followed up until October 31, 2018, at the Neurology Clinic in Karolinska University Hospital in Stockholm, Sweden.

Methods

Total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, apolipoprotein AI, apolipoprotein B, and lipid ratios were measured at the time of amyotrophic lateral sclerosis diagnosis or shortly thereafter. Death after amyotrophic lateral sclerosis diagnosis was used as the main outcome. The Cox model was used to estimate hazard ratios with 95% confidence intervals of death after amyotrophic lateral sclerosis diagnosis, after controlling for sex, age at diagnosis, site of symptom onset, diagnostic delay, body mass index, Amyotrophic Lateral Sclerosis Functional Rating Scale-Revised score, and progression rate.

Results

A 1-SD increase of total cholesterol (hazard ratio 0.60, 95% confidence interval 0.41-0.89, p = 0.01), low-density lipoprotein cholesterol (hazard ratio 0.64, 95% confidence interval 0.44-0.92, p = 0.02), low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio (hazard ratio 0.65, 95% confidence interval 0.46-0.92, p = 0.02), apolipoprotein B (hazard ratio 0.62, 95% confidence interval 0.44-0.88, p = 0.01), or apolipoprotein B/apolipoprotein AI ratio (hazard ratio 0.61, 95% confidence interval 0.43-0.86, p < 0.01) was associated with a lower risk of death after amyotrophic lateral sclerosis diagnosis. A dose-response relationship was also noted when these biomarkers were analyzed as categorical variables.

Conclusions

Lipids and apolipoproteins are important prognostic indicators for amyotrophic lateral sclerosis and should be monitored at the diagnosis of amyotrophic lateral sclerosis.

SUBMITTER: Ingre C

PROVIDER: S-EPMC7274849 | biostudies-literature |

REPOSITORIES: biostudies-literature

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