Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis

Nobuyuki Fujita, Naobumi Hosogane, Tomohiro Hikata, Akio Iwanami, Kota Watanabe, Yuta Shiono, Eijiro Okada, Masayuki Ishikawa, Takashi Tsuji, Masayuki Shimoda, Keisuke Horiuchi, Masaya Nakamura, Morio Matsumoto, Ken Ishii

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Study Design. Multicenter case-control study. Objective. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). Summary of Background Data. SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Methods. 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-a (TNF-a), interleukin (IL)-1b, IL-6, and IL-8. Results. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m2, 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 mm2, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-a and IL-1b 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]. Conclusion. 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.

Original languageEnglish
Pages (from-to)E1402-E1407
JournalSpine
Volume41
Issue number23
DOIs
Publication statusPublished - 01-01-2016
Externally publishedYes

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Lipomatosis
Obesity
Inflammation
Fats
Body Mass Index
Interleukins
Decompression
Adipocytes
Tumor Necrosis Factor-alpha
Adiponectin
Leptin
Interleukin-8
Case-Control Studies
Interleukin-6
Histology
Pathologic Constriction
History
Steroids
Cytokines
Control Groups

All Science Journal Classification (ASJC) codes

  • Orthopedics and Sports Medicine
  • Clinical Neurology

Cite this

Fujita, N., Hosogane, N., Hikata, T., Iwanami, A., Watanabe, K., Shiono, Y., ... Ishii, K. (2016). Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis. Spine, 41(23), E1402-E1407. https://doi.org/10.1097/BRS.0000000000001646
Fujita, Nobuyuki ; Hosogane, Naobumi ; Hikata, Tomohiro ; Iwanami, Akio ; Watanabe, Kota ; Shiono, Yuta ; Okada, Eijiro ; Ishikawa, Masayuki ; Tsuji, Takashi ; Shimoda, Masayuki ; Horiuchi, Keisuke ; Nakamura, Masaya ; Matsumoto, Morio ; Ishii, Ken. / Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis. In: Spine. 2016 ; Vol. 41, No. 23. pp. E1402-E1407.
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abstract = "Study Design. Multicenter case-control study. Objective. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). Summary of Background Data. SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Methods. 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-a (TNF-a), interleukin (IL)-1b, IL-6, and IL-8. Results. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m2, 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 mm2, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-a and IL-1b 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]. Conclusion. 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.",
author = "Nobuyuki Fujita and Naobumi Hosogane and Tomohiro Hikata and Akio Iwanami and Kota Watanabe and Yuta Shiono and Eijiro Okada and Masayuki Ishikawa and Takashi Tsuji and Masayuki Shimoda and Keisuke Horiuchi and Masaya Nakamura and Morio Matsumoto and Ken Ishii",
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Fujita, N, Hosogane, N, Hikata, T, Iwanami, A, Watanabe, K, Shiono, Y, Okada, E, Ishikawa, M, Tsuji, T, Shimoda, M, Horiuchi, K, Nakamura, M, Matsumoto, M & Ishii, K 2016, 'Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis', Spine, vol. 41, no. 23, pp. E1402-E1407. https://doi.org/10.1097/BRS.0000000000001646

Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis. / Fujita, Nobuyuki; Hosogane, Naobumi; Hikata, Tomohiro; Iwanami, Akio; Watanabe, Kota; Shiono, Yuta; Okada, Eijiro; Ishikawa, Masayuki; Tsuji, Takashi; Shimoda, Masayuki; Horiuchi, Keisuke; Nakamura, Masaya; Matsumoto, Morio; Ishii, Ken.

In: Spine, Vol. 41, No. 23, 01.01.2016, p. E1402-E1407.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Potential involvement of obesity-associated chronic inflammation in the pathogenesis of idiopathic spinal epidural lipomatosis

AU - Fujita, Nobuyuki

AU - Hosogane, Naobumi

AU - Hikata, Tomohiro

AU - Iwanami, Akio

AU - Watanabe, Kota

AU - Shiono, Yuta

AU - Okada, Eijiro

AU - Ishikawa, Masayuki

AU - Tsuji, Takashi

AU - Shimoda, Masayuki

AU - Horiuchi, Keisuke

AU - Nakamura, Masaya

AU - Matsumoto, Morio

AU - Ishii, Ken

PY - 2016/1/1

Y1 - 2016/1/1

N2 - Study Design. Multicenter case-control study. Objective. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). Summary of Background Data. SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Methods. 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-a (TNF-a), interleukin (IL)-1b, IL-6, and IL-8. Results. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m2, 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 mm2, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-a and IL-1b 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]. Conclusion. 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.

AB - Study Design. Multicenter case-control study. Objective. To characterize the pathogenesis of idiopathic spinal epidural lipomatosis (SEL). Summary of Background Data. SEL is often associated with the history of steroid use or endocrine disorders; however, the pathogenesis of idiopathic SEL remains poorly understood. Methods. 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-a (TNF-a), interleukin (IL)-1b, IL-6, and IL-8. Results. The mean BMI of the L group was significantly higher than that of the C group (29.1 vs. 25.2 kg/m2, 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 mm2, P = 0.017). Furthermore, the expression levels of the transcripts for TNF-a and IL-1b 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]. Conclusion. 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.

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