Efficacy of Tumor Necrosis Factor and Interleukin-10 Analysis in the Follow-up of Nonalcoholic Fatty Liver Disease Progression

Tumor necrosis factor (TNF-α) is a cytokine involved in systemic inflammation during acute phase reactions. The current study was designed to investigate the levels of pro-inflammatory cytokine (TNF-α) along with the anti-inflammatory cytokine (IL-10) during progression of non-alcoholic fatty liver disease (NAFLD) from simple steatosis to non-alcoholic steatohepatitis (NASH) and fibrosis in diabetic patients, and correlate the levels of cytokines with the progression of NAFLD. Fifty-two diabetic patients compared to 18 healthy controls were participated in this study. Based on clinical diagnosis, patients were divided into three groups: simple steatosis, NASH and fibrosis. Serum liver function tests, fasting blood glucose, bilirubin, ALT, AST, TNF-α, IL-10 and lipid profile were measured. TNF-α levels were significantly higher in NAFLD patients compared to control subjects with a significant positive correlation with body mass index and fasting blood glucose (FBG) but with negative correlation with IL-10. Serum IL-10 levels were significantly lower in NAFLD patients compared with controls. A positive correlation between IL-10 and HDL-C with concomitant negative correlation between IL-10 and FBG and triacylglycerides was found. Cytokine analyses showed that there was a prominent imbalance between TNF-α and IL-10 in patients with NAFLD, and this imbalance increase by increasing the progression of NAFLD especially in obese diabetic patients. TNF-α and IL-10 could be used in diagnosis and follow-up of NAFLD stages in a way to avoid liver biopsies in greater proportion of patients.     

Association of Insulin Resistance with Adipocytokine Levels in Patients with Metabolic Syndrome

Metabolic syndrome (MetS) results from the derangement of adipocyte physiology and carbohydrate metabolism. Obesity and insulin resistance (IR) are integral features of MetS. The adipokine alterations in MetS often correlate with IR and body fat content. High adipose tissue content is associated with a decreased production of adiponectin and excessive production of tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), all of which induce IR. The present study evaluated the adipokine alterations in MetS and their association with IR. The findings of the current study indicate that MetS is associated with significant decrease in adiponectin and increase in TNF-α and IL-6. The present study also found that the adipocyte derived inflammatory adipokines, TNF-α and IL-6 correlate with IR while the anti-inflammatory adipokines, adiponectin does not correlate with the degree and severity of IR.     

Tumor Necrosis Factor-Α, Interleukin-6, C-Reactive Protein Levels and Insulin Resistance Associated with Type 2 Diabetes in Abdominal Obesity Women

We aim to investigate the association between elevated tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and high sensitivity-C-reactive protein (hs-CRP) with type 2 diabetes mellitus (T2DM) in abdominal obesity (AO) women subjects. A total of 428 AO subjects (age 48.4 ± 10.2 years), and 107 non-AO women subjects (age 48.8 ± 11.8 years) were enrolled for the all biochemistry testing, inflammatory cytokines, fasting insulin and Homeostasis Model Assessment of insulin resistance (HOMA-IR). Body mass index, waist circumference (WC), blood pressure (BP), plasma glucose (Glu), triglyceride (TG), insulin, HOMA-IR and inflammatory cytokines were significantly higher and lower total antioxidant capacity, HDL-C in AO subjects (p < 0.05). WC was significantly correlated with BP, Glu, TG, LDL-C, insulin, HOMA-IR, TNF-α, IL-6 and negative correlation with HDL-C in AO subjects. Elevation of TNF-α, IL-6, hs-CRP and insulin resistance were significantly associated with T2DM in AO subjects, after adjusting with insulin resistance, increased oxidative stress, elevated TG and reduced HDL-C by using multiple logistic regression analysis. In conclusions, elevation of inflammatory cytokines, oxidative stress and insulin resistance were associated with T2DM in AO women subjects. These inflammatory cytokines are positively associated with T2DM and may have a causal relation with an increased oxidative stress and insulin resistance in these AO women subjects.     

Clinicopathological spectrum of non-alcoholic fatty liver disease among patients in Kerala

Non-alcoholic fatty liver disease and its more aggressive form, non-alcoholic steatohepatitis are entities that are becoming more and more interesting to the medical community in general. A total of 93 Non-alcoholic fatty liver disease patients (64 male and 29 female) within the age range between 28 to 63 years were studied. All of them showed elevated alanine aminotransferase level (104.07 ± 56.04). Aspartate aminotransferase level (58.13 ± 31.96) was elevated more than its normal level in 82% cases and AST to ALT ratio was found 0.59 ± 0.26. Predisposing factors were diabetes mellitus (37%), obesity (13%) and hyperlipidemia (41%). In addition, 32% of the subjects were overweight.18% of the patients had elevated serum bilirubin. Our findings recommend a lower cutoff value than suggested by the World Health Organization for overweight and obesity among this racial-ethnic group.     

胰岛素样生长因子1与冠心病病变程度的关系

目的为了研究冠心病发病的机制. 方法测定了16例正常人血清胰岛素样生长因子1(IGF1)水平和40例冠心病患者血清IGF1水平,且把冠心病患者血清IGF1水平与冠脉造影的血管病变支数进行了比较分析. 结果冠心病患者外周血IGF1水平显著低于正常人(分别为27.23±15.48 μg/L和48.02±33.43 μg/L,P＜0.01);且在冠脉造影血管病变支数增加时其血清IGF1水平下降变得更加明显. 结论 IGF1可能参与了冠心病的病理生理过程.     

舟山渔民心脑血管病危险因素水平的变化趋势

为观察舟山渔民心脑血管病危险因素水平的变化趋势,对该地区的渔民在１９９４年和１９９８年前后二次进行了有关心脑血管病危险因素水平的抽样调查,测量了该人群的收缩压（ＳＢＰ）、舒张压（ＤＢＰ）、总胆固醇（ＴＣ）、高密度脂蛋白－胆固醇（ＨＤＬ－Ｃ）、空腹血糖（ＦＢＳ）,体重指数（ＢＭＩ）以及人群中高血清总胆固醇现患率,低ＨＤＬ－Ｃ现患率和高血压患病率及吸烟率的状况。比较结果显示：男性ＳＢＰ,ＤＢＰ,ＴＣ,     

Synergetic Interaction of HLA-DRB1*07 Allele and TNF-Alpha − 863 C/A Single Nucleotide Polymorphism in the Susceptibility to Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is an inflammatory autoimmune disease which is characterized by dysregulation of various cytokines propagating the inflammatory processes that is responsible for tissue damage. Tumor necrosis factor alpha (TNF-α) is one of the most important immunoregulatory cytokines that has been implicated in the different autoimmune diseases including SLE. Two hundred and two patients with SLE and 318 controls were included in the study. The TNF-α gene promoter region (from − 250 to − 1000 base pairs) was analyzed by direct Sanger’s DNA sequencing method to find promoter variants associated with South Indian SLE patients. We have analyzed six TNF-α genetic polymorphisms including, − 863C/A (rs1800630), − 857C/T (rs1799724), − 806C/T (rs4248158), − 646G/A (rs4248160), − 572A/C (rs4248161) and − 308G/A (rs1800629) in both SLE patients and controls. We did not find association of TNF-α gene promoter SNPs with SLE patients. However, the − 863A (rs1800630) allele showed association with lupus nephritis phenotype in patients with SLE (OR: 1.62, 95%CI 1.04–2.53, P = 0.034). We found serum TNF-α level was significantly elevated in SLE cases as compared to control and found no association with any of the polymorphisms. The haplotype analysis revealed a significant protective association between the wild TNF-α alleles at positions − 863C, − 857C, − 806C, − 646G, − 572A and − 308G (CCCGAG) haplotype with lupus nephritis phenotype (OR 0.53, 95% CI 0.35–0.82, P = 0.004). Additionally, the TNF-α − 863 C/A (rs1800630) polymorphism and HLA-DRB1*07 haplotype showed significant differences between SLE patients and controls (OR 4.79, 95% CI 1.73–13.29, P = 0.0009). In conclusion, TNF-α − 863A allele (rs1800630) polymorphism is associated with increased risk of nephritis in South Indian SLE patients. We also found an interaction between HLA-DRB1*07 allele with TNF-α − 863 C/A promoter polymorphism giving supportive evidence for the tight linkage disequilibrium between TNF-α promoter SNPs and MHC class II DRB1 alleles.