The relationship between hepatitis B virus (HBV) infection, severity of liver disease, frequency of infection, and degree of gastric lesions was not yet fully investigated in Egyptian patients. The present work was performed on 100 Egyptian patients with HBV from the National Hepatology and Tropical Medicine Institute and 70 healthy volunteers as control group. The participants were subjected to full medical history taking, clinical examination, and laboratory investigations. All patients were positive for HBV surface antigen (HBV sAg), HBV DNA, and negative for hepatitis C virus antibodies. The severity of the liver disease was assessed using Child-Pugh scoring system. Screening of all participants for Ag in stool was performed. Biopsy specimens were taken from the gastric lesions of -infected patients for histopathological examination. The mean age of the patients and control group were 34.9 and 33.4 years, respectively. The levels of the liver enzymes were statistically higher in HBV patients than the control group. Ag in stool was detected in 45.7% of the control group, and a higher percentage (60%) was detected in the patients group. Chronic gastritis with glandular atrophy and metaplasia was found in 15.6% of patients of Child-Pugh A, 70% of Child-Pugh B, and 100% of Child-Pugh C. It could be concluded that the prognosis of the liver disease significantly influences the severity of the gastric pathology in infection.

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Background Hepatocellular carcinoma (HCC) comprises 5.6% of all cancers worldwide representing the sixth most common cancer. It is also the fourth most common cause of cancer-related mortality. Angiogenesis is a main factor in the development of HCC. Vascular endothelial growth factor (VEGF) is considered as the force for physiological and pathological angiogenesis, and overexpression of VEGF is prominent in HCC. We aimed to study the effect of direct-acting antivirals (DAAs) on VEGF considered as the key regulator of angiogenesis in HCC. This cross-sectional study involved fifty patients who were divided into two groups: group I—twenty-five chronic hepatitis C virus (HCV) patients as (cases) subjected to treatment with direct-acting antiviral drugs for 3 months; group II—twenty-five chronic HCV patients developed HCC as (controls). Serum VEGF level was measured in of group I at baseline, at end of treatment, and 3 months after the end of treatment by sofosbuvir 400 mg plus daclatasvir 60 mg for 3 months in the HCV patient group, also VEGF was assessed in group II with HCC. Results Serum VEGF was high in both groups, but it was higher in the HCC group with a statistically significant difference (p < 0.001), also serum VEGF in the HCV group decreased after 3 months at the end of DAA treatment from 209.5 ± 137.6 to 44.1 (31.8–55.3) mg/ml, and all patients who received DAAs achieved sustained virologic response (SVR). Conclusion We found that change in serum VEGF in HCV patients treated with DAAs in this study cannot explain the risk of HCC after treatment by DAAs.

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