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Coronavirus causes an outbreak of viral pneumonia that spread throughout the world. Liver injury is becoming more widely recognized as a component of the clinical picture of COVID-19 infection. We aimed to review this relation in a concise way. This review article includes a large number of patients from both western and eastern countries with no clear difference of liver affection. The more severe and frequent liver injury, the more severe COVID-19 infection. Up to half of patients developed hepatitis with serum ALT elevation. Both hepatocellular and/or ductular injury were observed as evidenced by alkaline phosphatase elevation. Increase incidence of morbidity and mortality had been recorded in patients with CLD. Cirrhosis mortality extended in line with the Child-Turcotte-Pugh class. The incidence of ACLF in CLD patients with COVID 19 is not clear. There are no significant associations with the etiology of liver disease and death in cirrhosis. COVID-19 hinders HCV elimination by 2030. Patients should continue their medications if already receiving treatment. Patients with occult or resolved HBV and COVID-19 who are receiving immunosuppressive agents should use antiviral therapy to prevent viral flare-ups.

Background Eosinophilic gastroenteritis (EGE) is defined by the presence of gastrointestinal symptoms, with an abnormal eosinophilic infiltrate of the intestine wall and exclusion of other causes of secondary eosinophilia. EGE has three clinical presentations, depending on the depth of eosinophilic infiltration of the bowel wall. It individualizes into three types, namely mucosal, muscular, and subserosal. Eosinophilic ascites, which is caused by edema and eosinophilic inflammation of the serosal layer of the small bowel wall, is the most uncommon presentation of EGE. Case summary A 30-year-old Egyptian woman presented with pain in the epigastrium and diffuse abdominal distension. Past medical history comprised allergy to iron injections (for iron deficiency anemia). Clinical examination showed moderate abdominal distention (palpation) and shifting dullness (percussion) suggestive of moderate ascites; mild right pleural effusion was also suspected, but findings were otherwise unremarkable. Abdominal and pelvic examinations by ultrasound and contrast-enhanced computed tomography showed moderate ascites, mild right pleural effusion, and diffuse thickening of the antrum and small bowel loops. Endoscopy of the upper gastrointestinal tract revealed mild diffuse hyperemia of the esophagus, stomach and duodenum, with no relevant findings in the histopathology of biopsy specimens taken from these sites. Laboratory results showed eosinophilia in the peripheral blood and marked increase of eosinophils in the ascitic fluid. Treatment with corticosteroids resulted in normalization of the laboratory test results, and the ascites resolved within a week of initiation of therapy. Conclusion Eosinophilic ascites, characterized by increased eosinophils in peripheral blood and ascitic fluid, showed dramatic response to steroid therapy.

Background: Antibiotic resistance of Helicobacter pylori (H. pylori) treatment is on the rise, and is affecting the efficacy of current used therapeutic regimens. Aim: We aimed to enhance the understanding of antimicrobial resistance rates of H. pylori strains recovered from patients at Theodor Bilharz Research Institute Hospital in Egypt, as a mandatory step before starting treatment. Subjects and methods: Mutant genes conferring metronidazole, amoxicillin, clarithromycin, and tetracycline resistance were detected in 60 H. pylori strains recovered from patients who underwent upper endoscopic examination. Patients were considered to be infected with H. pylori when rapid urease test and detection of 16S rRNA in gastric biopsies recorded positive. Molecular detection of resistant genes to metronidazole (rdx gene) and amoxicillin (pbp1A gene) was carried out by conventional PCR followed by sequencing of PCR products. While detection of 23S rRNA gene conferring clarithromycin resistance and detection of 16S rRNA mutation gene conferring tetracycline resistance were carried out by real-time PCR. Results: H. pylori resistance rates to metronidazole, and amoxicillin were 25% and 18.3% respectively. While for clarithromycin and tetracycline, point mutations in 23S rRNA types A2142G and A2143G and in 16S rRNA of H. pylori were assessed by real time PCR assay respectively. Resistance mutant genes were found to be 6.7% of clarithromycin and 1.7% of tetracycline. Combined resistance rates to metronidazole and amoxicillin was (11.6%) followed by metronidazole and clarithromycin (5%), while patterns of clarithromycin and amoxicillin (1.6%), metronidazole, clarithromycin and amoxicillin (1.6%) were revealed. Conclusion: Data concerning antimicrobial resistance genes play an important role in empiric treatment of H. pylori infection. According to our results, H. pylori resistance to metronidazole and amoxicillin was relatively high. Clarithromycin is still a good option for first line anti-H. pylori treatment. Combined resistant strains are emerging and may have an effect on the combination therapy. Keywords: H. pylori, Antimicrobial resistance, Gene mutations, Rdx gene, Clarithromycin resistance, Tetracycline resistance

Background: Helicobactor pylori (H. pylori) virulence markers would be useful to predict peptic ulcer disease (PUD) or gastric cancer. Aim: In Egypt, since inadequate data are present regarding H. pylori virulence–related genes in different age group patients with gastro-duodenal diseases, it becomes crucial to study the clinical status of cagA, vacA and iceA1 genotypes of H. pylori strains recovered from patients with dyspepsia. Subjects and methods: The study included 113 dyspeptic patients who were exposed to upper gastrointestinal endoscopic examination. Four antral biopsies were obtained from each patient for the analysis of H. pylori infection by rapid urease test and detection of 16S rRNA. Results: Sixty (53.1%) patients were confirmed to be infected with H. pylori. Upon endoscopy, gastritis was revealed in 27 patients (45%) and10 patients (16.7%) had PUD. Of the 60 H. pylori strains, 39 (65%) had at least one virulence gene. Six different genotypic forms were recognized; vacA (9/60), iceA1 (1/60), vacA/cagA (7/60), vacA/iceA1 (13/60), vacA/cagA/iceA1 (8/60) only one of cagA/iceA type and we could not detect cagA. The overall vacA, iceA1and cagA genes identified were 61.6%, 38.8%, 26.6% respectively, by PCR-based molecular testing. The vacA gene status was highly significant related to gastritis patient (P ≤ 0.036). The vacA s1m1 and s2m2 alleles were significantly found in 50% of H. pylori infected patients with PUD and with gastritis 57.1% respectively (P ≤ 0.01). Conclusion: In conclusion, the main genotype combinations in the studied Egyptian patients were; vacAs2m2/iceA1, vacAs1m1/cagA, mostly associated with gastritis, and vacAs1/cagA/icA, mainly in PUD. The less virulent (s2, s2m2) H. pylori genotypes were found in patients aged over 43 years. Keywords: Helicobactor pylori, vacA, cagA, icA1, Peptic ulcer disease, PCR–based genotyping, Gastric biopsies

Helicobactor pylori (H. pylori) has been strongly associated with gastritis, peptic ulcer and is linked to an increased risk of gastric cancer. The cytotoxin-associated gene product (cagA) and the vacuolating cytotoxin (vacA) have been implicated as two major virulence factors of H. pylori. Since there is an increasing evidence that genetic variability of H. pylori may have clinical importance, we aimed to evaluate different vacA genotypes and reveal its relationship with endoscopic and transmission electron microscopy (TEM) findings among H. pylori infected Egyptian patients. Forty H. pylori infected patients possessing vacA gene who underwent upper endoscopic examination were considered to be infected with H. pylori when rapid urease test and detection of 16S rRNA in gastric biopsy recorded positive. Both vacA and cagA genotypes were detected by polymerase chain reaction (PCR). The TEM was performed to assess the ultra-structure of the gastric mucosa. Four vacA genotypes were identified, the most prominent was the s2/m2 allele combination (52.5%) followed by s1/m1 (27.5%), s1/m2 (17.5%) and s2/m1 genotype was found just in one H. pylori strain (2.5%). There were significant correlations between vacA s2/m2 and gastritis (65.2%), and vacA s1/m1 and peptic ulceration (57%). The cagA gene was associated with 38% of vacA genotypes and 60% of which were significantly associated with vacA s1/m1 genotype with the development of severe gastritis reaching up to gastric ulcer. The TEM revealed H. pylori spiral and coccoid forms, cytoplasmic vacuolar degeneration caused by vacA, swollen mitochondria and dilated rough endoplasmic reticulum. In Egypt where prevalence of H. pylori infection is high, genotyping of H. pylori virulence factors can help to predict patients who are at a high risk of related gastroduodenal diseases. Although H. pylori with vacA s2/m2 genotype is mostly related to low level of virulent strains yet, significant crosstalk between H. pylori strains harboring both vacA s1/m1 and cagA gene provides crucial insights into virulence of high level. Key words: Helicobactor pylori, vacA genotyping, cagA, gastritis, peptic ulcer.

Introduction: Treatment of HCV using a combination of pegylated interferon (PEG-IFN) and ribavirin fails in about 40% of the patients with HCV genotype 4 infections, and it is physically and economically demanding. Thus, it is highly important to identify factors that can help to predict the likelihood that a patient will respond to this treatment. Methods: In this study, five miRNAs, i.e., miRNA-122, miRNA-199, miRNA-192, miRNA-30, and miRNA- 128, were selected according to previous studies that demonstrated their noticeable functions in viral replication, indicating that they potentially could be used by host cells to control viral infections. The five miRNAs were measured using real-time, reverse transcription-polymerase chain reactions. The data were analyzed using the ttest and chi-squared test. Results: We found that the expression level of miRNA-122 was significantly increased in the responders’ group (p < 0.01) over that in the non-responders’ groups before and after treatment; both increased significantly (p < 0.01) compared with the normal control group. Conclusion: miR-122 might be a useful predictor for virological responses to treatment with PEG-interferon plus ribavirin therapy in patients with HCV.

Background: Infection with Helicobacter pylori (H. pylori) causes persistent gastritis that may progress to fatal gastric cancer. The cytotoxin-associated gene A protein (CagA), encoded by the cytotoxin-associated gene A (cagA) is the main virulence factor associated with more severe clinical outcomes. It is further divided into Western-type CagA and East Asian-type CagA. The East Asian-type CagA induces more cytoskeleton changes and is more likely to be associated with gastric cancer. Aim of the study: In the current study we aimed to identify the most prevalent H. pylori cagA genotype among Egyptian patients suffering from dyspepsia and to examine its possible correlation with the associated clinical condition. Patients and methods: Four biopsies were obtained from the antrum and angularis from each of 113 adult patients, who underwent upper endoscopy at the Endoscopy Unit, Theodor Bilharz Research Institute (TBRI) Hospital for the analysis of H. pylori by rapid urease test and detection of 16S rRNA. Nested PCR assay was used to determine cagA genotype. Results: Sixty (53.1%) dyspeptic patients were found infected with H. pylori. Although Egypt has a high prevalence of H. pylori infection, low prevalence of cagA was detected (26.5%). Western type cagA is the predominant type (62.5%) while East Asian type was not detected and others (37.5%) remain uncharacterized. Western-genotype cagA genotype was found in 80% of patients with peptic ulcer disease and 40% of patients with gastritis. Conclusion: Absence of the more virulent East Asian cagA genotype, which is the strongest risk factor for gastric carcinogenesis, may explain the very low gastric cancer rate among Egyptian population compared to other parts of the world. This finding demands further molecular studies using whole genome sequencing and more samples to determine the exact uncharacterized cagA genotype to identify the actual risk in developing gastroduodenal diseases in Egypt. Keywords: Helicobacter pylori, Endoscopic findings, Western type cagA, East-Asian cagA, Peptic ulcer, Gastritis

Introduction: Liver fibrosis is the excessive accumulation of extracellular matrix that occurs by activation of hepatic stellate cells (HSCs), which has been identified as the major driver of liver fibrosis. Several studies confirmed that miRNAs have regulatory effects on the activation of HSCs by affecting the signaling pathways. The aim of this study was to develop non-invasive diagnostic markers by measuring different circulating miRNAs in serum as predictor markers for early diagnosis of liver fibrosis and its progression. Methods: In this case-control study, we enrolled 66 subjects with chronic hepatitis C (CHC) with early stage of fibrosis and 65 subjects with CHC with late-stage fibrosis. Also, 40 subjects were included as normal controls. The six main miRNAs, i.e., miR-138, miR-140, miR-143, miR-325, miR-328, and miR-349, were measured using the reverse transcription-polymerase chain reaction. Results: In the cases of CHC both with early and late stage of fibrosis, the circulating levels of the six main miRNAs were significantly higher than the levels in the control group. ROC analysis indicated that the sensitivity and specificity of miR-138 were 89.3% and 71.43%, respectively, in the early stage of fibrosis. In the late stage, the sensitivity and specificity of miR-138 were 89.3 and 93.02%, respectively, whereas, for miR-143, they were 75.0 and 88.4%, respectively. Conclusions: Circulating miR-138 could serve as a non-invasive biomarker for the detection of early fibrosis. Also, miR-138 and miR-143 could be specific biomarkers for indicating the late stage of liver fibrosis

BACKGROUND: Hepatitis C virus (HCV) genotype 4 is a common infection in Egypt and is the leading cause of liver disease.OBJECTIVE: To study the efficacy and safety of a novel 20 kD pegylated interferon alpha-2a derived fromHansenula polymorphain combination with ribavirin for the treatment of Egyptian patients with genotype 4 chronic hepatitis C (CHC).METHODS: One hundred seven patients with genotype 4 CHC were involved in the present study. Liver biopsy was performed in all patients. All patients received a fixed weekly dose of 160 μg of a novel pegylated interferon in combination with ribavirin in standard and adjusted doses. Serum HCV RNA levels were assessed by a real-time sensitive polymerase chain reaction assay at four, 12, 48 and 72 weeks after the start of therapy. Patients demonstrating an early virological response (EVR) completed a 48-week course of treatment.RESULTS: The overall sustained virological response (SVR) was 60.7%. The SVR in patients with a rapid virological response was significantly higher (91.7%) than in patients with complete EVR (67.74%) (P=0.033) and partial EVR (56.14%) (P=0.003). SVR was also significantly higher in patients with a low degree of liver fibrosis according to Metavir score (F1 and F2) (67.57%) compared with those with a high degree of liver fibrosis (F3 and F4) (45.45%) (P=0.017). The baseline viral load had no impact on SVR in the present series nor were any serious adverse events reported.CONCLUSION: The novel pegylated interferon alpha-2a assessed in the present study was effective for the treatment of patients with genotype 4 CHC, and was safe and well tolerated.

Introduction Whey protein contains biologically active ingredients that can prevent and attenuate disease besides being nutritive. The aim of the study was to clarify the effects of oral administration of whey protein on viral load and host defence mechanisms, in particular, phagocytic function of neutrophils, selected immunomodulatory cytokines and serum inflammatory markers, in compensated chronic hepatitis C virus (HCV) patients. Material and methods Twenty-seven HCV patients (20 males and 7 females) recruited from the hepatology clinic of the Theodor Bilharz Research Institute (TBRI) were given whey protein concentrate (WPC) twice daily for two months. In addition, 15 age and sex matched healthy participants were included in the study, as a control group. Neutrophil phagocytic activity, serum intercellular adhesion molecule (sICAM), interleukin-2 (IL-2), nitric oxide (NO), as well as HCV-RNA levels and routine investigations were determined for patients, before and after WPC supplementation and once for the control group. Results There was a significant decrease in viral load and markers of active inflammation, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), while serum albumin, total leucocyte counts and absolute neutrophil counts showed significant elevation accompanied by improvement of neutrophil phagocytic activity after WPC supplementation compared to pre-treated levels. The oral WPC supplementation was well tolerated without any serious adverse events. Conclusions Oral supplementation of WPC has promising results as a new therapeutic strategy against HCV and its sequelae by decreasing the viral load and active inflammation as well as improving the synthetic capacity of the liver and the phagocytic function of neutrophils, in these patients.

A decade ago, a study revealed that praziquantel (PZQ) failed to cure 1.6% of those with intestinal schistomiasis in five villages of the Nile delta region. The recommended dosage of PZQ is a single 40 mg/kg oral dose, and each of these patients continued to pass viable Schistosoma mansoni eggs despite three successive doses at or above this level. The eggs passed by these uncured villagers produced adult worms that were, in most cases, significantly less responsive to PZQ in vitro. This report investigates the current sensitivity of S. mansoni infections to PZQ after 10 years of therapeutic pressure in the same villages, testing the hypothesis that the number of drug failures would have increased as continued drug pressure selected for worms with diminished sensitivity to PZQ. The data show that these villages have experienced a significant decrease in the prevalence and intensity of S. mansoni infections, with present infection rate of 10.9%, compared with 25.1% in 1994. The first treatment resulted in normal range of cure rates, between 73.8 and 92.3% in each of the five villages in the study. After three successive doses (40, 40, and 60 mg/kg, the same treatment protocol applied a decade ago) there were no uncured patients remaining in the study. This shows that there has not been an increase of drug failure, despite 10 years of therapeutic pressure in these villages where there had been resistant infections and worms with decreased response to PZQ.

The role of insulin resistance (IR) in chronic hepatitis C genotype 4 (CHC-4) patients is still under assessment. The aims of this study are to assess the prevalence and predictors of IR and its influence along with clinical, metabolic, virological, and histological factors on the severity of liver fibrosis in 100 Egyptian patients with CHC-4.In 100 untreated patients with CHC-4, IR was assessed using the Homeostasis Model Assessment and defined greater than 3. By logistic regression (LR), independent factors associated with IR and significant fibrosis (SF=fibrosis, Metavir score≥F2) were assessed in nondiabetic and noncirrhotic patients.One hundred patients were included; 54% were men and 46% were women. The mean age of the patients was 40.46±9.41 years. Of the total patients, 55% were overweight and 28% were obese. Metabolic syndrome was observed in 26% of patients; five of them were known to be diabetic. All patients were genotype 4. Most of our patients had mild viremia (2 00 000 IU/ml), whereas only 16% had higher viral load (2 00 000 IU/ml). There was no correlation between IR and hepatitis C virus viremia (r=-0.069; P=0.492). Necroinflammation was moderate-severe (A2-A3) in 25% of patients. SF (F2-F4) was found in 46% of patients and 11% had cirrhosis (F4). Most of our patients, 54%, had moderate steatosis and 21% had severe steatosis. IR was present in 46% of patients; 39 (42.9%) were nondiabetic, which is correlated significantly with BMI (r=0.395; P0.01). IR was found to increase significantly with the fibrosis stage (P=0.001), insignificant fibrosis, 18.5%, SF (F2-F4), 71.4%, and cirrhosis (F4), 100%. By LR, IR was independently and significantly associated with age more than 40 years, obesity (BMI30 kg/m), SF, and severe steatosis (30%). IR was also significantly associated with metabolic syndrome. SF was present in 46 patients (46%). It was associated with IR, moderate-severe necroinflammation, and severe steatosis. By LR, in noncirrhotic patients, SF was associated with age more than 40 years, obesity (BMI30 kg/m), moderate/severe liver inflammation, and severe steatosis.In CHC-4 patients, IR is highly prevalent and independently associated with age, obesity, SF, and severe steatosis. Management of IR might significantly improve the prognosis of CHC-4 patients.

The policy of elective repair of umbilical hernia in cirrhotic ascitic patients has long been a subject of debate and is still a major health problem. This study evaluated the role and outcome of elective mesh repair of umbilical hernia in cirrhotic ascitic patients, compared with the conventional two layers fascial repair technique. Forty cases with a small to medium sized umbilical hernia defects in ascitic cirrhotic patients were divided into two groups (GIGII) of 20 patients each. After proper control of ascites in both groups, patients in GI were subjected to elective umbilical hernia onlay mesh repair. In GII, hernias were managed by conventional two layers fascial repair. In GI, transient early postoperative ascitic fluid leakage occurred in 3 (15%) cases and mild superficial wound infection in 5 (25%) cases which was controlled by antibiotics. Two (10%) cases developed hernia recurrence during follow up period. In GII, ascitic leakage occurred in 6 (30%) cases that responded well to conservative management except only one case needed re-exploration and repair reenforcement. Drainage was significantly less than in GI in amount (P0.05) and duration (P0.01), wound infection occurred in 3 (15%) cases but were superficial and controlled conservatively. Recurrence occurred in 7 cases (35%). Elective mesh repair of umbilical hernia with ascites in cirrhotic patients proved to be a safe, simple and effective technique with perioperative antibiotics and proper aseptic procedure.

This trial investigated the anti-schistosomal activity of mirazid in comparison with that of praziquantel in Schistosoma mansoni-infected Egyptian patients. The sample population was composed of 1,131 individuals (459 school children and 672 household members). Screening for S. mansoni was conducted using the standard Kato Katz technique. Four slides from a single stool sample were examined before treatment, and four slides per sample from stool samples obtained on three consecutive days were examined post-treatment. All positive eligible subjects were randomly assigned into two groups, the first received mirazid at a dose of 300 mg/day for three consecutive days, and the second received praziquantel at a single dose of 40 mg/kg. All treated subjects were examined 4-6 weeks post-treatment. Mirazid showed low cure rates of 9.1% and 8.9% in S. mansoni-infected school children and household members, respectively, compared with cure rates of 62.5% and 79.7%, respectively, in those treated with praziquantel. Therefore, we do not recommend mirazid as an agent to control schistosomiasis.