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OBJECTIVE: Bile reflux gastritis is caused by the backward flow of duodenal fluid into the stomach. A retrospective cohort study was performed to estimate the prevalence and risk factors of bile reflux gastritis postcholecystectomy, and to evaluate the endoscopic and histopathologic changes in gastric mucosa. METHODS: Patients with refractory upper abdominal pain right below the ribs with symptoms of bloating, burping, nausea, vomiting, and bile regurgitation during the period from January 2018 to December 2020, submitted to Zagazig University Hospitals were enrolled in this study. The studied 64 patients were divided into two groups; the control group (CG): 30 subjects who had never undergone any biliary interventions, and the post-cholecystectomy group (PCG): 34 patients who had undergone cholecystectomy. RESULTS: The prevalence of bile reflux gastritis was (16.7%) and (61.8%) in CG and PCG, respectively. Diabetes, obesity, elevated gastric bilirubin, and elevated stomach pH were all risk factors for bile reflux gastritis in both groups (r = .28,.48,.78,.57 respectively). Age, sex, epigastric pain, heartburn, vomiting, and the existence of bile reflux gastritis, on the other hand, had no correlation. DISCUSSION: After a cholecystectomy, bile reflux gastritis is prevalent, especially among obese and diabetic patients.

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Background and purpose: Multidrug and toxin extrusion transporter 1 (MATE1), encoded by the SLC47A1 gene and single nucleotide polymorphisms of organic cation transport 1, may impact metformin's responsiveness and side effects. Inward-rectifier potassium channel 6.2 (Kir 6.2) subunits encoded by KCNJ11 may affect the response to sulfonylurea. This study aimed to evaluate the association between SLC22A1 rs72552763 and rs628031, SLC47A1 rs2289669 and KCNJ11 rs5219 genetic variations with sulfonylurea and metformin combination therapy efficacy and safety in Egyptian type 2 diabetes mellitus patients. Experimental approach: This study was conducted on 100 cases taking at least one year of sulfonylurea and metformin combination therapy. Patients were genotyped via the polymerase chain reaction-restriction fragment length polymorphism technique. Then, according to their glycated hemoglobin level, cases were subdivided into non-responders or responders. Depending on metformin-induced gastrointestinal tract side effects incidence, patients are classified as tolerant or intolerant. Findings/Results: KCNJ11 rs5219 heterozygous and homozygous mutant genotypes, SLC47A1 rs2289669 heterozygous and homozygous mutant genotypes (AA and AG), and mutant alleles of both polymorphisms were significantly related with increased response to combined therapy. Individuals with the SLC22A1 (rs72552763) GAT/del genotype and the SLC22A1 (rs628031) AG and AA genotypes were at a higher risk for metformin-induced gastrointestinal tract adverse effects. Conclusion and implications: The results implied a role for SLC47A1 rs2289669 and KCNJ11 rs5219 in the responsiveness to combined therapy. SLC22A1 (rs628031) and (rs72552763) polymorphisms may be associated with increased metformin adverse effects in type 2 diabetes mellitus patients.

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<br><b>Introduction:</b> Biliary gastropathy is a disease characterized by upper abdominal pain, frequent heartburn, nausea, and vomiting of bile. It is caused by the backward flow of duodenal fluid into the stomach and esophagus.</br> <br><b>Aim:</b> A retrospective cohort study was performed to estimate the prevalence and risk factors of bile reflux gastritis secondary to cholecystectomy and to evaluate the endoscopic and histopathologic changes in gastric mucosa caused by bile reflux gastritis.</br> <br><b>Materials and methods:</b> The study involved 64 patients with epigastric pain and/or dyspeptic symptoms during the period from January 2018 to December 2020 who presented to Zagazig University Hospitals. The subjects were divided into two groups: the control group (CG), with 30 subjects who had never undergone any biliary interventions, and the post-cholecystectomy group (PCG), consisting of 34 patients who had undergone cholecystectomy.</br> <br><b>Results:</b> The prevalence of bile reflux gastritis was 16.7% in the CG and 61.8% in the PCG. In both groups, diabetes, obesity, increased gastric bilirubin, and increased gastric pH were risk factors for bile reflux gastritis (r = 0.28, 0.48, 0.78, and 0.57, respectively). However, there were no correlations between age, sex, epigastric pain, heartburn, vomiting, and the presence of bile reflux gastritis.</br> <br><b>Discussion:</b> Bile reflux gastritis is a common complication following cholecystectomy and is more common among obese and diabetic patients.</br>.

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BACKGROUND: Bile reflux gastropathy is caused by the backward flow of duodenal fluid into the stomach. A retrospective cohort study was performed to declare if the therapeutic biliary interventions cause bile reflux gastropathy, and to estimate its prevalence and risk factors, and to evaluate the gastric mucosa endoscopic and histopathologic changes. METHODS: 62 patients, with epigastric pain and/or dyspeptic symptoms, were grouped into, Group 1 : (34) patients that had undergone cholecystectomy and Group 2 : (28) patients who had undergone at least one of the following procedures for the treatment of benign pathology: endoscopic sphincterotomy and endoscopic stenting. Their ages ranged from 27 to 59 years. All participants had undergone gastroscopy for gastric aspirate analysis as well as gastric mucosa biopsy for histopathological examination. RESULTS: the prevalence of bile reflux gastropathy was (21.34%) after therapeutic biliary interventions with a P-value of 0.000. In both groups, diabetes, obesity, increased gastric bilirubin, and increased gastric pH were risk factors for bile reflux gastropathy (r = 0.27, 0.31, 0.68, 0.59 respectively), while age, sex, epigastric pain, heartburn, vomiting were mot. CONCLUSION: bile reflux gastropathy is common after therapeutic biliary interventions being more among obese and diabetic patients.

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BACKGROUND: Though direct-acting antiviral agents (DAAs) therapy is associated with a high cure rate of hepatitis C virus infection, a potential risk of serious adverse events (SAEs) exists. The aim of this study was to determine the incidence and predictors of morbidity and mortality related to DAAs therapy. METHODS: This prospective study was conducted on a real word cohort of 1562 treatment naïve chronic hepatitis C (CHC) Egyptian patients, who received 12-weeks therapy with sofosbuvir (SOF) plus daclatasvir (DCV) ± ribavirin (RBV). The incidence and predictors of SAEs and mortality during treatment course and over the following 12 weeks were recorded. RESULTS: The mean age of study participants was 51.38 ± 9.70 years (55.22%, males). Liver cirrhosis was defined in 72.4% of participants. SAEs were recorded in 120 participants (7.68%), including hepatic decompensation, gastrointestinal bleeding, anemia and hepatocellular carcinoma. Nine patients (0.58%) died and 69 patients (4.42%) discontinued therapy due to SAEs. Severity of cirrhosis was the significant predictor of morbidities and mortality. Hepatic decompensation was predicted by baseline serum albumin [cutoff value: 3.00 g/dL, area under the receiver operating characteristic curve (AUROC): 0.953] and serum bilirubin (cutoff value: 1.75 mg/dL, AUROC: 0.940). CONCLUSION: The risk of morbidity and mortality related to SOF/DCV ± RBV therapy in CHC patients is small and is significantly linked to advanced cirrhosis.

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The aim of this study was to assess the efficacy and safety of two protocols for retreatment of a cohort of Egyptian patients with chronic hepatitis C (CHC) who relapsed after NS5A inhibitor-based therapy. We conducted a prospective cohort study to assess the safety and efficacy of 12 weeks' retreatment with either combination of sofosbuvir/daclatasvir/simeprevir plus ribavirin (SOF/DCV/SMV/RBV, n = 45) or sofosbuvir/ombitasvir/paritaprevir/ritonavir plus ribavirin (SOF/OBV/PTV/r/RBV, n = 163) in patients who had previously failed NS5A inhibitors-based regimens. The primary end point was SVR 12 weeks after the end of treatment (SVR12). Safety follow-up data were recorded for 60 weeks after the end of treatment. Two hundred-eight patients were included in the study. Of them, 53.4% of patients were females and 40.4% had liver cirrhosis. The most common prior drug combinations were sofosbuvir/daclatasvir (n = 94) and sofosbuvir/daclatasvir plus ribavirin (n = 109). The overall SVR12 rates were 98.1%. In SOF/DCV/SMV/RBV group, 95.6% achieved SVR12, while in SOF/OBV/PTV/r/RBV group, the SVR12 rates were 98.8%. SVR12 was higher in cirrhotic patients (84/84) than noncirrhotic (120/124), P value = .0149. Regarding the safety outcomes, anaemia and fatigue were significantly higher in SOF/OBV/PTV/r/RBV group. Hepatocellular carcinoma (HCC) was reported in eight (3.8%) patients (four in each group). Of them, death was confirmed in four patients. Retreatment of Egyptian CHC relapsed patients with either sofosbuvir/daclatasvir/simeprevir plus ribavirin or sofosbuvir/ombitasvir/paritaprevir/ritonavir plus ribavirin is highly effective and well-tolerated for both noncirrhotic and compensated cirrhotic patients. Incidental de novo HCC and hepatic decompensation are comparable in the two groups.

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The reappearance of HCV infection months or years after sustained virologic response (SVR) may be due to the persistence of HCV in tissue cells in spite of being undetected in serum. This situation is known as occult hepatitis C infection (OCI). We aimed to assess the prevalence of OCI in Egyptian patients with chronic hepatitis C (CHC) who achieved SVR after treatment with direct-acting antiviral agents (DAA). We carried out a cross-sectional study at the Advanced Center for Liver Diseases of Zagazig University Hospitals and Al-Ahrar Viral Hepatitis Treatment Center, Sharkia Governorate, Egypt. One hundred and fifty adult patients with CHC, who achieved SVR 12-24 weeks after end of treatment with sofosbuvir/daclatasvir ± ribavirin (139 patients, 92.67%), sofosbuvir/ledipasvir ± ribavirin (eight patients, 5.33%), sofosbuvir/simeprevir (two patients, 1.33%), and ombitasvir/ paritaprevir/ritonavir + ribavirin (one patient, 0.67%), according to the Egyptian National Committee for Control of Viral Hepatitis, were included in the study. We tested these patients for HCV RNA in peripheral blood mononuclear cells (PBMCs) immediately after confirmation of SVR12-24 weeks. Statistical analysis was performed by means of the Shapiro-Wilk test, Mann-Whitney U test, Chi-square test, and Fisher's exact test. Seventeen patients (11.33%) were positive for PBMNCs HCV RNA. The prevalence of OCI was highest in patients treated with simeprevir/sofosbuvir (2/2 patients). There is a substantially high prevalence of OCI after treatment with DAAs. We recommend dual testing for HCV RNA in both serum and PBMCs at the end of treatment of HCV infection with DAAs and during validation of the SVR following the initial response.

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AIM: Assessment of short term changes in portal blood flow and long term changes in liver functions in cirrhotic patients who chose to fast during the month of Ramadan in summer. BACKGROUND: During Ramadan, healthy Muslims obligated to fast from predawn to sunset. PATIENTS AND METHODS: Forty cirrhotic patients intended to fast during the month of Ramadan in the year 2014, were examined by Congestion index (CI) as a non-invasive indicator of short term changes in the portal blood flow, while liver function tests were determined as an indicator of long term changes in liver functions. RESULTS: A total of 38 patients completed the whole month fasting and two patients discontinued fasting due to variceal bleeding. The complicated patients were 7. CI showed a statistically significant increase from fasting to postprandial status (P<0.001), with statistically significant increases from fasting to postprandial status in Child class A (P<0.001), and B (P<0.001). We did not find a statistical significance between patients with complications and those without complications (P=0.6). There was a statistically significant rise in the serum bilirubin after Ramadan. Deterioration noticed as advanced Child classes, development of lower limb edema, increasing ascites, increasing jaundice and overt encephalopathy. CONCLUSION: Cirrhotic patients showed significant short-term changes in the portal blood flow. However, these changes are not linked to complications or deterioration of liver functions and accommodated especially in patients with Child class A and B. Child class C patients should not fast.

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Background. Endoscopic surveillance for early detection of dysplastic or neoplastic changes in patients with Barrett's esophagus (BE) depends usually on biopsy. The diagnostic and therapeutic role of endoscopic mucosal resection (EMR) in BE is rapidly growing. Objective. The aim of this study was to check the accuracy of biopsy for precise histopathologic diagnosis of dysplasia and neoplasia, compared to EMR in patients having BE and related superficial esophageal lesions. Methods. A total of 48 patients with previously diagnosed BE (36 men, 12 women, mean age 49.75 ± 13.3 years) underwent routine surveillance endoscopic examination. Biopsies were taken from superficial lesions, if present, and otherwise from BE segments. Then, EMR was performed within three weeks. Results. Biopsy based histopathologic diagnoses were nondysplastic BE (NDBE), 22 cases; low-grade dysplasia (LGD), 14 cases; high-grade dysplasia (HGD), 8 cases; intramucosal carcinoma (IMC), two cases; and invasive adenocarcinoma (IAC), two cases. EMR based diagnosis differed from biopsy based diagnosis (either upgrading or downgrading) in 20 cases (41.67%), (Kappa = 0.43, 95% CI: 0.170-0.69). Conclusions. Biopsy is not a satisfactory method for accurate diagnosis of dysplastic or neoplastic changes in BE patients with or without suspicious superficial lesions. EMR should therefore be the preferred diagnostic method in such patients.

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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

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