Potential Involvement of Obesity-Associated Chronic Inflammation in the Pathogenesis of Idiopathic Spinal Epidural Lipomatosis.

Abstract

Multicenter case-control study. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Sixteen patients who underwent lumbar decompression surgery due to severe idiopathic SEL were included in the study (L group, 15 men and 1 woman; mean age, 71.5 yrs). Fifteen patients without SEL, who underwent decompression surgery for lumbar canal stenosis, were selected as controls (C group, 14 men and 1 woman; mean age, 70.3 yrs). The following parameters were analyzed in these two groups: body mass index (BMI), medical history, histology, the size of adipocytes in the epidural fat (EF) tissues, and the expression level of the transcripts for adiponectin, leptin, tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, and IL-8. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m, P = 0.006), and there was a significant correlation between BMI and the width of EF in both groups. The average adipocyte size in the EF was significantly larger in the L group than in the C group (2846.8 vs. 1699.0 μm, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-α and IL-1β in the L group were significantly higher than those in the C group [2.59-fold increase (P = 0.023) and 2.60-fold increase (P = 0.015), respectively]. Our data suggest that the pathogenesis of idiopathic SEL is associated with obesity. In addition, the increased expression of two major inflammatory cytokines in the EF in the L group may indicate that SEL is causally related to chronic inflammation. 3.