ABSTRACT
BACKGROUND AND AIMS: Pancreatic cancer (PC) is the fourth most common cause of death from cancer in Egypt. Few studies have been conducted to assess the relationship between vitamin D serum level and vitamin D receptor (VDR) polymorphisms with the survival of PC patients. This is the first study in Egypt to investigate the association of the status of vitamin D serum level and genotypic distribution of single nucleotide polymorphisms (SNP) Fok1 with the risk of developing PC and whether they could detect survival or not. PATIENTS AND METHODS: The study included a total of 47 PC cases that were histopathologically proven to have PC, and 37 controls that were attending at the same time for investigation but proved that they were all PC free. Pre-diagnostic concentrations of vitamin D and VDR polymorphism Fok1 were assessed from all participants in the study. RESULTS: There was a 1.5-fold increase in the serum level of vitamin D in PC patients when compared to non-PC subjects. Regarding VDR Fok1, polymorphism distribution in PC was CC (Wild Type) 26 (55.3%), CT 16 (34%), and TT 5 patients (10.7%). For the control group, CC was found in 24 (64.8%), CT in 12 (32.4%), and TT genotype was found only in one individual 1 (2.8%) with no statistically significant difference between the two studied groups (P 0.72). CONCLUSION: Low serum vitamin D or VDR-SNP is not a risk factor for PC in Egyptian patients. Recommendations to increase vitamin D concentrations in healthy persons for the prevention of cancer and improving overall survival should be carefully considered.
ABSTRACT
Background: The liver has been recognized as a major target of injury in patients with insulin resistance or the metabolic syndrome. Insulin resistance is associated with fat accumulation in the liver, a condition called nonalcoholic fatty liver disease (NAFLD). NAFLD is a clinicopathologic entity that includes a spectrum of liver damage ranging from simple steatosis to nonalcoholic steatohepatitis (NASH), advanced fibrosis, and rarely, progression to cirrhosis. Recent studies emphasize the role of insulin resistance, oxidative stress and subsequent lipid peroxidation, proinflammatory cytokines, adipokines and mitochondrial dysfunction in the development and progression of NAFLD. About 20% all adults have NAFLD and 2% to 3% of adults have NASH. A strong correlation exists between overweight, in particular visceral fat accumulation, and prevalence of NASH. Aim: "This study aimed at assessing the effect of insulin resistance in a sample of Egyptian patients with non-Alcoholic fatty liver". Methods: This study was conducted on 2 groups 104 NAFLD as diagnosed by ultrasound examination and 21 healthy participants as control group. All the participants were subjected to an abdominal ultrasonography, liver enzymes, lipid profile (triglycerides, HDL, LDL cholesterol), glucose and fasting insulin. Results: The blood sugar and fasting insulin levels were significantly higher in NAFLD patients than control group (172.81±35.47 mg/ml vs 101.33±11.95 mg/ml and11.72±4.7 U/ml vs 5.93±4.68) respectively. 88.5% of NAFLD patients were obese (BMI ≥ 30) and 11.5% were over weight (BMI < 30) while 23.8% were obese and 76.2% were overweight for control group. HOMA-IR was significantly higher in NAFLD patients than in healthy controls (5.02±2.39 vs. 1.41±1.20; P<0.001). We found 81.7% of the studied patients fulfilled the metabolic syndrome criteria while 9.5% for controls. HOMA-IR ROC curve showed 94.23% sensitivity and 85.71 specificity in NAFLD group. Fasting Insulin ROC curve showed 91.35% sensitivity and 80.95% specificity in NAFLD group. Conclusion: Patients with NAFLD have higher insulin resistance and have higher lipid profile, ALT & AST levels compared with their control group. Also the Ratio of the metabolic syndrome was higher in the NAFLD patients (81.7%).
ABSTRACT
Background: Obesity, insulin resistance and dyslipidemia are the most significant risk factors of non-alcoholic fatty liver disease (NAFLD) in children, and a major cause of liver-related morbidity. The aim of this study was to evaluate the serum levels of adiponectin, leptin and fasting insulin in obese children with NAFLD to explore the role of adiponectin in the pathogenesis of this disease. Materials and Methods: The fasting serum levels of adiponectin, leptin, glucose, insulin, ALT, AST, total bilirubin, direct bilirubin, albumin, alkaline phosphatase, creatinine, cholesterol, triglycerides, HDL, LDL, GGT and CRP were measured in a group of 50 NAFLD children after making ultrasonography and 40 other participants were considered as a control group with comparable age, sex and body-mass index. Results: Plasma adiponectin was found significantly low in NAFLD children than its level in control group (3.23± 2.5 vs 11.0 ± 2.95 ng/dl). Moreover, NAFLD group had significantly higher insulin resistance, fasting insulin 11.4± 4.9 vs 4.7±3.1 mu/l levels in comparison with control group. Regarding serum leptin, there was no significant difference. An inverse correlation was observed between adiponectin and homeostatic model assessment (HOMA-IR), fasting insulin, leptin, triglycerides, ALT, AST, GGT and BMI. Conclusion: This data supports a role for low circulating adiponectin value in the pathogenesis of NAFLD and its association with insulin resistance.
ABSTRACT
Non alcoholic fatty liver (NAFLD) is accumulation of fat in the liver cells of peoples who drink little or no alcohol causing mild steatosis with mostly no signs, symptoms or complication but this may progress to steatohepatitis (NASH) and may liver cirrhosis then failure. NAFLD is recognized as the most common type of chronic liver disease in Western countries and the leading cause of cryptogenic cirrhosis. Insulin resistance (IR) is a key factor in the pathogenesis of NAFLD, the latter being considered as the hepatic component of IR or metabolic syndrome (MetS). Although the pathogenesis of NAFLD is not fully elucidated, a complex interaction between adipokines and cytokines produced by adipocytes and/or inflammatory cells infiltrating adipose tissue appears to play a crucial role in MetS and NAFLD and its progress. A number of factors are linked with NAFLD such as obesity, type 2 diabetis mellitus (T2DM), hyperlipidemia, gastric bypass, and its progress to NASH correlate with certain cytokines secreted like adiponectin, interlukin-6 (IL-6), and C- reactive protein CRP. Adiponectin is a novel adipocyte-specific protein, which, it has been suggested, plays a role in the development of insulin resistance and atherosclerosis. The role of (IL-6) in liver pathology is very complex, and its participation in the development of NAFLD remains unclear. IL-6 is a key element in the acute phase response, mediating the synthesis of several acute phase proteins (such as CRP and serum amyloid A). Thus, we cannot exclude the possibility that IL-6 might also play an indirect deleterious role in NAFLD pathogenesis. In diet-induced obese mice, treatment with IL-6 antibodies improved sensitivity to insulin. Objective: This study aim is to evaluate the level of adiponectin, IL-6 and CRP in Egyptian patients with NAFLD. Methods: This study was conducted on 2 groups 104 NAFLD as diagnosed by ultrasound examination and 21 healthy participants as control group. All the subjects were subjected to an abdominal ultrasonography, liver enzymes ALT & AST, lipid profile (triglycerides, HDL, LDL, cholesterol, CRP, IL-6 & Adiponectin). Results: Plasma adiponectin levels were significantly lower in NAFLD patients than control gp (3.05±2.65μg/ml vs 10.52±3.35 (μg/ml). IL-6 level was higher in NAFLD than control gp but not significant (114.24±22.32pg/ml vs 104.9±19.98pg/ml). CRP was significantly higher in NAFLD than control gp (17.86±11.59mg/L vs 5.4±3.81mg/L). Adiponectin ROC curve showed an AUROC curve in NAFLD gp (0.918 p=0.0001). IL-6 ROC curve showed an AUROC curve in NAFLD gp (0.703 p=0.0003). CRP ROC curve showed an AUROC curve in NAFLD gp (0.853 p=0.0001). Conclusion: Patients with NAFLD have lower adiponectin levels and higher IL-6 and CRP levels compared with their control group.