Helicobacter pylori and non-alcoholic fatty liver disease: Is there a relationship?

Non-alcoholic fatty liver disease (NAFLD) is distinguished by liver injury due to metabolic stress, identified by diffuse hepatocyte macrovascular fatty lesions [1]. The prevalence of NAFLD is rising yearly, with a worldwide incidence rate between 20% and 30% [2]. Complex hereditary variables, improper lipid metabolism, and insulin resistance are the key characteristics of the etiology of NAFLD [3]. The research has revealed that aberrant lipid metabolism in the liver can result in dysbacteriosis in the intestinal flora; abnormality of the flora eventually encourages lipid deposition in the liver. Additionally, there is mounting proof that NALFD is linked to abnormalities in the gut flora, particularly Helicobacter pylori (H, pylori) [4]. Gram-negative bacillus, termed H pylori, has colonized the deep layers of the gastric mucosa. [5]. The global infection rate for H pylori is about 50% or higher [6]. According to research, H pylori causes gastric cancer, gastrointestinal lymphoma, peptic ulcers, and chronic gastritis [7]. Additionally, some researchers indicate a connection between H pylori and liver cancers, diabetes, and improper lipid metabolism [8]. Some studies have discovered that infection by H pylori is one of the elements for NAFLD to progress and that getting rid of H pylori can partially stop the evolution of NAFLD [9].

The gamma-glutamyl transpeptidase to platelet ratio (GPR) and the gammaglutamyl transpeptidase to albumin (GAR) versus fibroscan as indicators of hepatic fibrosis in Non-Alcoholic Fatty Liver Disease Patients

Background: Identifying patients at risk with Non-alcoholic fatty liver disease (NAFLD) related fibrosis is crucial. Many noninvasive fibrosis markers were developed recently in chronic hepatitis C and B patients, but a few were evaluated in NAFLD. Aim: to assess the accuracy of the gamma-glutamyl transpeptidase and the other noninvasive markers gamma-glutamyl transpeptidase-to-platelet ratio and gammaglutamyl transpeptidase-to-albumin ratio (GPR and GAR) versus fibroscan as indicators of hepatic fibrosis in NAFLD patients. Patients and Methods: A total of 100 NAFLD patients were examined by abdominal ultrasound and then fibroscan to assess liver steatosis and fibrosis. They were grouped into the early fibrosis group and the advanced fibrosis group. Demographic data and laboratory investigation were collected. GPR and GAR were calculated. The correlation between them and liver stiffness measurement (LSM) was reported. The accuracy of predicting liver fibrosis was assessed. Results: There was a significant positive correlation between GPR and GAR and the degree of fibrosis. GPR (P <0.001*) and GAR (P <0.001*) were independent predictors for advanced hepatic fibrosis by multiple linear regression analysis. Fibrosis score was used as the dependent variable, with the other studied biomarkers as independent variables. The AUCs of GPR and GAR were 0.790 and 0.949 in assessing liver fibrosis, respectively. Conclusion: GPR and GAR were positively correlated with hepatic fibrosis and may be used as a novel, simple, accurate, and low-cost parameter for diagnosing hepatic fibrosis in NAFLD patients.

Fibrofast and fibrosis-4 versus fibroscan as indicators of hepatic fibrosis in non-alcoholic fatty liver disease patients: A cross sectional Study

Aims: Non-alcoholic fatty liver disease (NAFLD) is a broad category for a disease spectrum that includes simple steatosis, which can proceed to non-alcoholic steatohepatitis, cirrhosis, and, finally, hepatocellular carcinoma. Owing to the invasive nature of liver biopsy, the need for non-invasive tools were required for diagnosis. Objective: To compare the performance of simple biochemical scores (fibroblast) FIB-5 and (fibrosis-4) FIB-4 with fibroscan to differentiate mild to moderate fibrosis (MF; F0 to F2) from advanced fibrosis (AF; F3 to F4) in patients with NAFLD. Patients and methods: This cross-sectional study was done on 116 NAFLD patients. All patients were scanned with the FibroScan examination. FIB-5 and FIB-4 were calculated for all patients. Results: The mean kPa score (liver stiffness measurement score) of the patients belonging to advanced fibrosis [9.53 ± 1.05]. The FIB-4 score was significantly higher in patients with advanced fibrosis (1.54 ± 0.38) compared with patients with mild to moderate fibrosis (1.18 ± 0.44), p-value = 0.001, whereas the FIB-5 score was insignificant between patients. Conclusion: FIB-4 is superior to FIB-5 as a non-invasive simple marker in diagnosing advanced fibrosis in NAFLD patients.

The relationship between vitamin D deficiency and NAFLD in sample of Egyptian type 2 diabetic patients

Background: vitamin D deficiency has a strong association with insulin resistance and NAFLD.Objective: to assess vitamin D levels in patients having type2 diabetes with NAFLD and to study its relationship withinsulin resistance. Patients and methods: a case­control study conducted on 50 subjects who were divided into 2 groups: 35 patients having T2DM and NAFLD (group 1) and 15 healthy subjects served as control (group 2). Fasting plasma glucose (FBG), 2 hour post prandial (2hrpp), and fasting plasma insulin (FPI) were measured with calculation of HOMA-IR. Fasting lipids, Hb A1c, calcium, phosphorus, urea, creatinine, serum alanine aminotranseferase (ALT), aspartate aminotransaminase (AST) were also measured. BMI was calculated, serum 25 (OH)D was measured with ELISA and abdominal ultrasonography was done for all participant. Results: the study showed lower level of vitamin D in patients with T2DM and NAFLD 10.6 (5.5-21.3) as compared to control group 31 (27-39.7). While non-significant difference was found between male and female regarding 25(OH) D level and HOMA-IR. There was significant negative correlation between vitamin D level and HOMA-IR. Conclusion: Vitamin D level was associated with presence of NAFLD. There was strong relation between vitamin D level and insulin resistance as vitamin D deficiency was associated with higher levels of HOMA-IR. Obesity may be related to low vitamin D level, but no difference in VD level between males and females was found

Transforming growth factor beta one and non alcoholic fatty liver disease

Background and study aim: Hepatic steatosis reflects an imbalance between the uptake and synthesis of fatty acids by the liver and their oxidation and export. The mechanism of cell injury remains unclear. Transforming growth factor ­ beta 1 (TGF-ß1) as a proinflammatory cytokine has become an important issue in the context of pathogenesis and progression of non alcoholic fatty liver disease (NAFLD). This study was planned to assess the value of TGF-ß1 in different forms of NAFLD.Patients and methods:This study included 62 patients; 20 patients with benign steatosis (group 1), 20 patients with non alcoholic steatohepatitis (NASH) (group 2) and 22 patients with cirrhosis (group 3), as well as 7 healthy subjects who served as a control group. Each group was subclassified according to the presence of obesity, type 2 diabetes mellitus and hypertriglyceridemia. All participants were subjected to abdominal ultrasound, ultrasound guided needle liver biopsy and routine laboratory investigations e.g. complete blood picture, liver function tests, fasting and 2 hours postprandial blood glucose and serum triglycerides.Results : Serum TGF-ß1 in the benign steatosis group was insignificantly different from the control group, while NASH and cirrhosis groups had significantly higher levels compared to control and benign steatosis groups (P<0.001). TGF-ß1 in NASH group was significantly higher than in cirrhosis group (428.78 ± 117.15 vs 260.42 ± 110.22 ng/ml, P=0.032). In benign steatosis group, TGF-ß1 was insignificantly different among subgroups. In NASH and cirrhotic patients, TGF-ß1 was significantly higher in dyslipidemic subgroups.Conclusion : Serum level of TGF-ß1 was higher in patients with severe forms of NAFLD (NASH and cirrhosis) than in patients with benign steatosis