Premium
Serum cytokine and soluble cytokine receptor levels in patients with non‐alcoholic steatohepatitis
Author(s) -
Abiru Seigo,
Migita Kiyoshi,
Maeda Yumi,
Daikoku Manabu,
Ito Masahiro,
Ohata Kazuyuki,
Nagaoka Shinya,
Matsumoto Takehiro,
Takii Yasushi,
Kusumoto Koichiro,
Nakamura Minoru,
Komori Atsumasa,
Yano Koji,
Yatsuhashi Hiroshi,
Eguchi Katsumi,
Ishibashi Hiromi
Publication year - 2006
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2005.01191.x
Subject(s) - steatohepatitis , proinflammatory cytokine , steatosis , cytokine , pathogenesis , medicine , receptor , cytokine receptor , tumor necrosis factor alpha , endocrinology , fatty liver , immunology , inflammation , disease
Background: Although the pathogenesis of non‐alcoholic steatohepatitis (NASH) remains poorly understood, proinflammatory cytokines seem to play an important role in the process of NASH. We have undertaken this study in order to elucidate the role of proinflammatory cytokines and their soluble receptors in NASH patients. Methods: Serum cytokines and soluble cytokine receptors levels were determined using an enzyme‐linked immunosorbent assay kit in 23 patients with NASH, 21 patients with simple steatosis, and 18 healthy volunteers. Results: Patients with NASH had significantly higher serum tumor necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) levels than did the simple steatosis patients. Similarly, when compared with simple steatosis, NASH was associated with higher soluble TNF receptor 1 (sTNFR1) and soluble IL‐6 receptor (sIL‐6R) levels, and a significant positive correlation was seen between the levels of sTNFR1 and aminotranferases in NASH patients. Conclusions: This study shows that circulating TNF‐α/sTNFR1 and IL‐6/sIL‐6R levels are significantly increased in NASH patients as compared with simple steatosis patients and healthy volunteers, and that these increased levels may be implicated in the pathogenesis of NASH.