Background: Non-alcoholic fatty liver disease (NAFLD) is a very common disease that affects 25-30% of the population in western countries. Many studies have observed the importance of H. pylori infection in the development of insulin resistance, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis, and liver fibrosis and cirrhosis. However, the evidence from different studies was controversial. The present study aimed to investigate the relationship between H. pylori infection and NAFLD in a developing country. Patients and Methods: This cross-sectional study included all the attending outpatient clinics at four Major University hospitals and two research and clinical institutes in a developing country in the period between June and October 2019. Patients were assessed for the diagnosis of H. pylori infection as detected by H. pylori antigen in stool; they were also assessed for the diagnosis of NAFLD by ultrasound, fibroscan, and CAP. Results: The study was conducted on 646 patients; H. pylori infection was found to be present in 538 patients (83.3%). NAFLD (diagnosed by both U/S and Fibroscan with CAP), ALT, AST, hepatomegaly, hypertension, fasting blood sugar were significantly higher in H. pylori +ve group than H. pylori −ve group. After performing Linear regression of independent risk factors of NAFLD to prove or to refute the role of Helicobacter; H. pylori positivity, total cholesterol, degree of fatty liver by ultrasound, fasting blood sugar and diastolic blood pressure were independent risk factors for NAFLD. Conclusion: Helicobacter pylori infection was independent risk factors for NAFLD and correlated with increased degree of steatosis.

Acute upper gastrointestinal bleeding (UGIB) affects large number of elderly with high rates of morbidity and mortality. Early identification and management of the factors predicting in-hospital mortality might decrease mortality. This study was conducted to identify the causes of acute UGIB and the predictors of in-hospital mortality in elderly Egyptian patients.286 elderly patients with acute UGIB were divided into: bleeding variceal group (161 patients) and bleeding nonvariceal group (125 patients). Patients’ monitoring was done during hospitalization to identify the risk factors that might predict in-hospital mortality in elderly.Variceal bleeding was the most common cause of acute UGIB in elderly Egyptian patients. In-hospital mortality rate was 8.74%. Increasing age, hemodynamic instability at presentation, co-morbidities (especially liver cirrhosis associated with other co-morbidity) and failure to control bleeding were the predictors of in-hospital mortality.Increasing age, hemodynamic instability at presentation, co-morbidities (especially liver cirrhosis associated with other co-morbidity) and failure to control bleeding should be considered when triaging those patients for immediate resuscitation, close observation, and early treatment.

Background and aimsEgypt is considered to have the highest rate of hepatitis C virus (HCV) prevalence worldwide. However, HCV prevalence is currently declining due to the improvement of health education programs, improved environmental sanitation, and the introduction of novel treatment regimens. The aim of this work was to determine the HCV seroprevalence among Menoufia University students.MethodsThe current study included 48,972 students from Menoufia University, Egypt. Blood sample was obtained from every patient for HCV seromarker testing. In anti-HCV-positive subjects, quantitative PCR for HCV RNA was done.ResultsOverall, HCV antibody prevalence rate was 1%. This prevalence was higher in females (304/27,421; 1.1%) than in males (194/21,371; 0.9%). HCV-RNA PCR was positive in 355/48,972 (0.7%); the percentage of HCV PCR positive among the anti-HCV-positive was 71.3% (355/498 patients), with a higher prevalence among females than in males but without statistical significance. In addition, rural areas showed more prevalent HCV seroprevalence than urban areas.ConclusionThese prevalence rates for HCV infection are lower than that previously reported in the same age group denoting a new evidence for the reduction of prevalence and a hope for successful eradication of HCV in the forthcoming years.

BackgroundThe COVID-19 pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected over 100 million people causing over 2.4 million deaths over the world, and it is still expanding. Although, ACE2 has been identified as the principal host cell receptor of 2019-nCoV, and it is thought to play a critical role in the virus's entrance into the cell and subsequent infection, many cells can be infected by COVID-19 while also expressing little or no ACE2. Unlike other viral infections, COVID-19 is characterized by widespread and severe systemic manifestations, immune dysregulation and multi-organ involvement. In addition, the range of serious inflammatory, neuropsychiatric and autoimmune diseases called post-COVID syndromes are now left behind as disease tables. This wide and diverse spectrum of diseases seen in COVID-19 cannot be explained by the mechanism of viral tropism mediated by ACE2 and TMPRSS2 receptors. It is possible that different receptor and signaling mechanisms that cannot be explained by the viral tropism mechanism play a role in the pathogenesis of acute systemic effects and chronic post-COVID syndromes in COVID-19. It was showed that COVID-19 infection leads to a loss of smell (anosmia) but the COVID-19 entry receptors, angiotensin-converting enzyme 2 (ACE2), is not expressed in the receptor of olfactory neurons, or its generation is limited to a minor fraction of these neurons. Moreover It was demonstrated that COVID-19 could infect lymphocyte through its ACE2 receptors, but numerous studies found that lymphocytes don't express ACE2 receptors or express it with a little, insufficient amount. It is clear from the information and findings presented and addressed in our article that COVID-19 not only binds to ACE2, but also to additional receptors, leading to more disease lethality and existence of covid-19 symptoms which remain unexplained. As a result, discovering and identifying these receptors could lead to the development of new treatments that could suppress COVID-19 and reduce its severity and pathogenicity. Herein, we insilico discovered that blocking of STRA6 by the SARS-CoV-2 spike protein could disrupt the retinoid signaling mechanism and leads to pathogenetic consequences through some other inflammatory pathways.MethodsThe STRA6 receptor protein were submitted to the server for functional interaction associated network between partners for the STRING (Research Online of Interacting Genes/Proteins Data Basis version 10.0)13 .Docking study of each Spike -ACE 2 and STRA6 receptor protein were carried out using HDOCK server (http://hdock.phys.hust.edu.cn/). The binding mode of Spike -ACE 2 and STRA6 receptor protein is retrieved form the PDB https://www.rcsb.org/ with accession number (7DMU , 5sy1)ResultsOur results showed that COVID-19 Spike protein exhibited a high binding affinity for human STRA6 and a low binding energy with it. The docking score of COVID-19 spike protein with STRA6( -354.68) kcal/mol was higher than the docking score of spike protein with ACE2 (-341.21 ) kcal/mol. Spike protein Receptor Binding Domain(RDB) of COVID-19 strongly and efficiently binds to STRA6 receptor, definitely to the RDB vital residues of RBP-binding motif located in STRA6 receptor. The docking of STRA6 target protein with spike viral protein revealed the involvement of the spike protein into the extracellular and membrane part of the STRA6 receptor and amino acids residues of STRA6 along with spike protein which make interactions and play an important role in formation of complexes. The corresponding distances about the residue contacts between proteins STRA6- Spike protein complex are documented here where the STRA6- Spike protein complexes binding site are the RDB of the CHOLESTEROL in STRA6 receptor which bind with interface residue( ARG 511A , VAL 512A THR 515A ALA 516A ASN 519A with interface residue degree (2.965 , 3.595 , 3.286 , 4.592 , and 4.235) representatively, also the ability of the spike to bind to RDB of the STRA 6 protein in the ILE 131C , MET 145C , HIS 86A with interface residue( 4.961 , 4.953 and 3.271) representatively. STRA6- Spike protein complex with PDB ID (5SY1 , 6LZG).ConclusionsSTRA6 is a critical regulator of many biological processes thorough initiating cellular retinol uptake, in different organs and tissues as in immune cells for improving the immune system homeostasis in various populations. Our docking study reveals that COVID-19 spike protein binds directly to the integral membrane receptor (STRA6) in addition to its binding sites of the cholesterol. STRA6 mediates cellular uptake of retinol (vitamin A) by recognizing a molecule of RBP-retinol to trigger release and internalization of retinol . Therefore COVID-19 may leads to downregulation of STRA6 receptor leading to inhibition the regulatory function of retinoic acid and cholesterol helping in existing symptoms and complications including lymhopenia, Nuerogical disorders, Ineffective RIG-I pathway, Interferon inhibition, Cytokine storm, Diabetes, Hormonal imbalance, Thrombosis, and Smell loss. Therefore, we believe that this novel discovery that STRA6 receptor acts as a novel binding receptor for COVID-19 could explain COVID-19 severity and its common symptoms with unknown aetiology . Moreover, retinoic acid metabolism was found to be defective in COVID-19 (cytokine storm), sepsis, ARDS and SIRS .As a result reconstitution of the retinoid signaling may prove to be a valid strategy for COVID-19 management. We suggest that Vitamin A metabolites ,especially, retinoic acid will be promising and effective treatments for COVID-19 infection and its unknown aetiology symptoms. It worth mentioning that aerosolized all- trans retinoic acid and 13 cis retinoic acid is currently under clinical investigation (ClinicalTrials.gov Identifier: NCT05002530, NCT04353180)

Background and aim Liver transplantation (LT) has emerged as an established therapeutic option for patients with chronic liver disease. Patients with end-stage liver disease are at high risk of infection with multidrug-resistant organisms, which may affect the outcome of LT. The aim of this study was to evaluate the impact of pre-transplant infection on the outcome of living-donor LT. Methods Prospective follow-up was done for 50 patients with chronic liver disease who had had LT performed from September 2013 to December 2017. We divided patients into group 1 (patients who had had infection within 3 months before transplantation with adequate treatment [n=20]), and group 2 (patients without infection [n=30]). Both groups were followed for 4 months post-operatively. Results Patients with high Model for End-Stage Liver Disease scores were more susceptible to infection pre- and post-operatively, and chest infection was the most common infection pre-transplant. There were no significant statistical differences regarding hospital and ICU stay and post-operative course between the groups, but the mortality rate was higher in group 1 (40%) than in group 2 (23.3%), and the causes of mortality in the group 1 were mainly due to medical causes (infections and sepsis, 75%) versus 28.6% in group 2. Conclusion Liver-cell failure and concomitant infection 3 months before LT with adequate treatment had no significant statistical differences regarding hospital, ICU stay, or medical complications, but post-operative infection and mortality rate were more frequent in group 1 and the causes of mortality were mainly medical.