Introduction: Obesity is the major pathogenesis of the non-alcoholic fatty liver disease (NAFLD). The combination of low-level laser therapy (LLLT) and Mediterranean diet (MD) is a new approach for improving liver function. Methods: 60 obese older adults (65-75 years old) with NAFLD were randomly assigned equally to two groups: a study group and a control group. The study group received LLLT and MD, while the control group followed MD only. These findings evaluated the changes in the level of liver enzymes, serum lipid profile, and anthropometric measurements (body mass index [BMI] and waist circumference [WC]) after 12 weeks of intervention. Results: Both study and control groups showed a significant reduction in the levels of liver enzymes, serum lipid profile, BMI, and WC (P<0.001 and P <0.01 respectively); however, the study group showed more significant results compared to the control group (P<0.01). Conclusion: LLLT and MD may be considered as a treatment approach for NAFLD in older adults to improve their liver function, control dyslipidemia, and help in losing weight.

Background and study aim: Baveno VI consensus recommended the use of noninvasive predictors of EV to avoid unnecessary endoscopies. Von Willbrand factor (VWF) and VITRO score, (VWF/ platelet count), are both correlated to liver cirrhosis and fibrosis. The aim of this study was to evaluate the role of VWF and VITRO score as predictors of esophageal varices and their bleeding.Patients and Methods: Seventy seven patients were included in this study. They were randomly selected from cirrhotic patients admitted to endoscopy unit for the first time. They were allocated into two groups; group I: patients who have esophageal varices, group II: patients with no esophageal varices.Results: VWF Ag and VITRO score were significantly higher in the varices group (group I). VWF Ag level was 169.3±20.2 in group I vs 146.8±35.5 µg/dL in group II p<0.001. VITRO score was 2.2±1.1 in group I vs 1.6±0.7 µg/10 8 platelet p=0.05. We found that at cut off value of 153% VWF can predict the presence of EV with sensitivity 88.1% and specificity of 61.1% and AUC= 0.66 p=0.04. VITRO score can predict the presence of varices with sensitivity of 69.5% and specificity of 50% at a cut off value 1.5 AUC=0.065 P=0.05. Conclusion:VWF and VITRO score rise significantly in patients with esophageal varices. Both markers can be reliable in prediction of the presence of EV's. VWF Ag can be reliable marker in prediction of risky and bleeding varices.

Introduction: The Baveno VI consensus recommended the use of noninvasive predictors to identify patients at high risk of esophageal varices (EV) in whom endoscopic evaluation is most needed. Kallistatin is a protein molecule synthesized by the liver, and its level declines with the deterioration of liver functions. We aim to explore the role of kallistatin as a predictor of esophageal varices. Methods: This case-control study included 70 cirrhotic patients (35 patients with EV and 35 patients without EV). The laboratory investigations and upper GI endoscopy were performed, and the serum kallistatin level was measured in all patients.Results: The mean level of serum kallistatin was significantly lower in patients with varices (12.2 ± 5.6 vs 16.9 ± 4.8 µg/ml, p = 0.009). It also shows a significant decline in patients with large varices. Kallistatin can predict the presence of EV and large EV at cut off values of 15.8 and 8.9 µg/ml, respectively, with sensitivity and specificity of 71.4% and 54.3% for EV and 50% and 94.8% for large EV. Discussion: Kallistatin is a promising marker that can be used to predict the presence of esophageal varices especially when they are large and risky.

Background and study aim: Hepatic encephalopathy (HE) is a complex and variable neuropsychiatric syndrome that is seen in patients with acute and chronic liver diseases. Diabetes mellitus (DM) is more prevalent in patients with post HCV cirrhosis. Because diabetes mellitus may be associated with delayed gastrointestinal transit and promoting constipation, increasing intestinal bacterial overgrowth and increasing glutaminase activity, we speculated that its presence in patients with HCV related cirrhosis would predispose to and exacerbate hepatic encephalopathy. Patients and Methods: This study included 264 patients with severely decompensated post-HCV cirrhosis, 132 diabetic cirrhotic patients and 132 non-diabetic cirrhotic patients as control group. History is taken for all patients regarding the number of attacks of encephalopathy he experienced in the past three months, the duration of diabetes and the anti-diabetic medication he uses. All patients in the study performed liver function tests, abdominal ultrasound, complete blood count and HBA1c level for diabetic patients as well as psychometric tests for hepatic coma. Results: Diabetic patients had higher frequency of all grades of hepatic encephalopathy mean number of attacks for each patient in the past three months is 1.9±0.3 vs 0.8±0.1 in non-diabetics with unclear precipitating factor in 43% of diabetic patients versus 23% in non-diabetic patients. Patients on oral hypoglycemic drugs represented 14.3% of diabetic patients. Patients with HBA1c >11% were 43% among patients on oral hypoglycemic drugs vs 23% with insulin. Patients on oral hypoglycemic drugs had higher frequency of hepatic coma. The mean number of attacks experienced by each patient rises with increased concentration of HBA1c from 0.8±0.2 at level <7% to 6.4±3for level >11%. The mean number of attacks increased with the duration of diabetes from 1±0.4 for <5 years to 6.4±3.1for >15 years. Conclusion: The frequency of HE was higher in diabetic patients without other obvious precipitating factor. Patients with uncontrolled diabetes and patients on oral hypoglycemic drugs, and those with longer duration of diabetes seem to have higher risk of developing HE.

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