Frequent hepatic steatosis in ALS: implication for systemic involvement (P6.098)

Abstract

OBJECTIVE:To study whether evidence of dysmetabolism of patients with amyotrophic lateral sclerosis (ALS) can be detected non-invasively by imaging study, such as liver sonography. BACKGROUND:Abnormal energy metabolism has been reported in ALS that broadens the concept of ALS as a systemic disease. Dyslipidemia is likely to reflect clinical outcome in ALS. A recent animal study suggested that the liver is a target organ in ALS. DESIGN/METHODS:Abdominal sonography, lipid profiles, and liver enzymes were obtained in three groups of individuals: (1) the patients with ALS (N=54), (2) other neurodegenerative diseases (N=37), and (3) asymptomatic dyslipidemic persons (N=32). The sonographic steatosis grade was determined by a blinded technician. Statistical tests including one-way ANOVA with post-hoc test and multiple linear regression were performed. RESULTS:The lipid profiles and liver enzymes were similar between the ALS and dyslipidemic groups. The disease control group had lower LDL, LDL/HDL ratio, and triglyceride than other groups. Hepatic steatosis was present in 76[percnt] in ALS, 19[percnt] in the disease control, and 38[percnt] in the dyslipidemic group (P < 0.001: vs. ALS). To assess a possible cofounding factor among the groups, multiple linear regression analysis was performed. Only the patient group was significantly correlated with the sonographic grade for steatosis, which argues against a possible confounding factor to explain the different distribution of the sonographic grades among the three groups. CONCLUSIONS:In ALS, sonographic evidence of steatosis is frequent and could reflect a more sensitive measure of dysmetabolic state than blood lipid profiles. Given the more frequent sonographic abnormality and similar degrees of dyslipidemia in comparison with dyslipidemic controls, steatosis in ALS is unlikely to be only direct consequence of dyslipidemia, but could be extra-neuronal involvement of ALS. Sonography can be used as a disease marker for ALS.

Disclosure: Dr. Izumi has nothing to disclose. Dr. Takamatsu has nothing to disclose. Dr. Muguruma has nothing to disclose. Dr. Ukimoto has nothing to disclose. Dr. Nishio has nothing to disclose. Dr. Oda has nothing to disclose. Dr. Nodera has nothing to disclose. Dr. Kaji has received research support from GlaxoSmithKline and Eisai Inc.