The management of acute esophageal variceal bleeding remains a clinical challenge. Band ligation is the main therapeutic option, but it may be technically difficult to perform in active bleeders. This may necessitate an alternative therapy for this group of patients. This study was conducted to assess the safety and efficacy of sclerotherapy versus cyanoacrylate injection for management of actively bleeding esophageal varices in cirrhotic patients. This prospective study included 113 cirrhotic patients with actively bleeding esophageal varices. They were randomly treated by endoscopic sclerotherapy or cyanoacrylate injection as banding was not suitable for those patients due to profuse bleeding making unclear endoscopic visual field. Primary outcome was incidence of active bleeding control and secondary outcomes were incidence of six weeks rebleeding, complications, and mortality among the studied patients. Initial bleeding control was significantly higher in cyanoacrylate versus sclerotherapy groups (98.25, 83.93% respectively, P = 0.007). No significant differences between sclerotherapy and cyanoacrylate groups regarding rebleeding (26.79, 19.30% respectively, P = 0.344), complications, hospital stay or mortality rate were observed. Based on this single-center prospective study, both of these therapies appear to have relatively favorable outcomes, although cyanoacrylate injection may be superior to sclerotherapy for initial control of active bleeding. [ClinicalTrials.gov Identifier: NCT03388125 ]–Date of registration: January 2, 2018 “Retrospectively registered”.

Introduction: Diabetic nephropathy (DN) represents one of the main causes of end-stage renal disease in type 2 diabetes mellitus (DM) patients. Galectin-3 has been implicated in pathogenesis of many pathological conditions. To date, there are limited data regarding the relationship between galectin-3 and DN. Aim of the study: Evaluation of serum galectin-3 as a novel prognostic biomarker in patients with DN. Patients and methods: This prospective study was carried out in the Internal Medicine and Clinical Pathology Departments, Tanta University Hospital, Egypt, from March 2015 to March 2018 on 300 patients with type 2 DM. Patients were divided into three groups: group I included 100 patients with albumin/creatinine ratio (ACR) 300 mg/g (macroalbuminuria). All patients were subjected to the following: full history taking, clinical examination, and laboratory evaluation (HbA1c, creatinine, estimated glomerular filtration rate, ACR, and serum galectin-3). Results: The mean levels of galectin-3 were significantly higher in patients with macroalbuminuria than in those with microalbuminuria and normoalbuminuria. Galectin-3 was a significant predictor for progression to microalbuminuria, macroalbuminuria, dialysis, and death among patients with type 2 DM. Conclusion: Based on this single center prospective study, serum galectin-3 is considered a significant predictor for DN progression among patients with type 2 DM.

Introduction: The onset of the Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) is caused by acquired somatic mutations in target myeloid genes “driver mutations”. The CCL2 gene is overexpressed by non-Hodgkin lymphomas and multiple solid tumors. Aim of the study: to evaluate the possible association of CCL2 rs1024611 SNP and its expression level and the risk of developing Philadelphia-negative MPNs. Patients and methods: A total of 128 newly diagnosed Philadelphia-negative MPN patient and 141 healthy subjects were evaluated for the genotype distribution of CCL2 rs1024611 and CCL2 expression levels. Results: The CCL2 rs1024611 G/G genotype was more frequent and significantly frequent among PMF and Post-PV/ET-MF patients and the mean CCL2 expression levels were significantly higher in PMF and Post-PV/ET-MF compared to the healthy subjects. The CCL2 rs1024611 SNP was significantly correlated to the CCL2 gene expression level and fibrosis grade. ROC analysis for the CCL2 gene expression level that discriminates MF patients from PV + ET patients revealed a sensitivity of 80.43% and a specificity of 73.17% with an AUC of 0.919 (p < 0.001). Conclusion: The CCL2 rs1024611 polymorphism could be an independent risk factor for developing MF (PMF and Post-PV/ET-MF). Moreover, CCL2 gene expression could be potential genetic biomarker of fibrotic progression.

Introduction: Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and/or pulmonary embolism (PE), is a common, acute, multifactorial disease with a five-years cumulative incidence of recurrence of approximately 25%. Actually, no single genetic defect can predict the risk of recurrence of VTE. Therefore, individual genetic risk profiling could be useful for the prediction of VTE recurrence. Aim of the study: To assess the combined effect of the common prothrombotic genotypes on the risk of recurrence of VTE in recently diagnosed unprovoked VTE patients. Patients and methods: This population based, prospective follow-up study was carried out from January 2015 to December 2020 in (internal medicine, cardiovascular medicine and anesthesia and ICU departments, Tanta University Hospital, Egypt) on 224 recently diagnosed unprovoked VTE patients. Whole blood was collected by standard venipuncture at the time of admission prior to the beginning of anticoagulant therapy. Genomic DNA was extracted and was genotyped for the 5-SNPs Genetic risk score (GRS), previously validated for first venous thrombosis (FVL rs6025, PTM rs1799963, ABO rs8176719, FGG rs2066865 and FXI rs2036914). Results: The main important finding in the present study was that patients having ≥3 risk alleles were associated with higher risk of VTE recurrence compared to those having ≤2 risk alleles (the reference group) (HR 2.5, 95% CI 1.48–4.21) (p = 0.001). Patients with GRS ≥ 3 had a significantly shorter time recurrence free survival (43.07 months) compared to the low risk group of patients with GRS (0–2) (p < 0.001). Conclusion: GRS model could be an effective and useful model in risk stratification of VTE patients, and genetic risk profiling of VTE patients could be used for the prediction of recurrence of VTE.

Background and Aims. Currently, it is well known that Helicobacter pylori- (H. pylori-) related peptic ulcer is one of the main causes of nonvariceal bleeding in cirrhotic patients. However, there is a lack of data to identify the exact effect ofH. pyloriinfection on variceal bleeding. This study was conducted to identify the impact ofH. pyloriinfection on gastric variceal bleeding in cirrhotic patients.Patients and Methods. 76 cirrhotic patients with gastric varices were included in this prospective study and divided into 2 groups: nonbleeding gastric varices (32 patients) and bleeding gastric varices (44 patients). The fasting serum gastrin level was measured. Mucosal biopsies from the gastric body and antrum were examined to determine the patterns of gastritis and the presence ofH. pylori.Results. The frequency ofH. pyloriinfection in the studied patients was 59.2%. There were significant differences between both groups regarding liver decompensation (P=0.001), red color sign over gastric varices (P=0.0011), prevalence ofH. pyloriinfection (P=0.0049), histological patterns of gastritis (P=0.0069), and serum gastrin level (P=0.0200). By multivariate analysis, Child C cirrhosis, red color sign over gastric varices, andH. pylori-induced follicular gastritis were independent risk factors for bleeding from gastric varices.Conclusion.H. pylori-induced follicular gastritis is considered as an additional risk factor for bleeding from gastric varices.