Serum cytokine and soluble cytokine receptor levels in patients with non‐alcoholic steatohepatitis

Abstract

This study shows that circulating TNF-alpha/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.

Relationship of serum bilirubin concentrations to kidney function and albuminuria in the United States adult population. Findings from the National Health and Nutrition Examination Survey 2001–2006

“…NAFLD can promote atherogenic dyslipidemia and contribute to CKD pathogenesis -as well as to accelerated atherogenesis -through the release of some pathogenetic mediators from the steatotic liver, including increased C-reactive protein and other inflammatory cytokines (26). Importantly, several studies have shown that these potential mediators of vascular and kidney damage are markedly higher in patients with NAFLD than in those without (26)(27)(28)(29)(30)(31), and are thought to be pathogenic factors for the development of CKD (32)(33)(34)(35). Consistent with the hypothesis that liver inflammation (or other liverderived factors) in NAFLD may play a role in kidney disease progression, it has been shown that type 2 diabetic subjects with chronic hepatitis B virus infection were more likely to develop end-stage renal disease compared with those not infected with hepatitis B virus (36).…”

“…In these analyses, we combined subjects with eGFR [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] The association between serum bilirubin and eGFR (included as continuous variable) was investigated using linear (unadjusted and fully adjusted) regression models in the whole group and in subgroups of participants stratified by diabetes status (Table 3). We excluded subjects who had a serum creatinine concentration )176.8 mmol/L ()2.0 mg/dL) or serum bilirubin concentrations )22.23 mmol/L ()1.3 mg/dL) (ns513).…”

Nonalcoholic fatty liver disease: a challenge for pediatricians

“…Reactive oxygen species: cytochrome P-450, 111 myeloperoxidase, nitric oxide synthase, lipid peroxidation products such as oxidized LDL, thiobarbituric acid-reacting substances 112 2. Inflammatory: TNFa, 113 adiponectine, 57,58,114,115 CRP, 48,83 visfatin, resistin, interleukin-6 and retinol binding protein-4 75,82 3. Apopetosis: cytokine-18 51,52 and fibrosis: hyaluronic acid 114 Table 2 represents the research results about the role of this group in predicting NASH.…”

“…111 Increased expression of proinflammatory cytokines such as TNFa and interleukin1b was may be responsible for observed decreases in respective P-450 activity. [113][114][115][116][117] Original European Liver Fibrosis study used age, tissue inhibitor of matrix metalloproteinase 1, hyaluronic acid, amino-terminal peptide of procollagen III for detection of fibrosis in fatty liver. In contrast, pathologists' agreement over histological scores ranged from very good to moderate (k ¼ 0.97-0.46).…”

Nonalcoholic Steatohepatitis in Children: The Modern Day Pediatric Epidemic

“…Some of these FFAs are stored as triglycerides that higher levels of proinflammatory cytokines [tumor necrosis factor-α and interleukin (IL)-6] when compared to SS patients. Unfortunately, we cannot use these cytokines as noninvasive markers for predicting the presence of NASH because the differences have not been significant enough [38,39] . Many potential biomarkers have been studied with conflicting results.…”