Background: In the cirrhotic patients, the activity of Helicobacter Pylori (H Pylori) urease was believed as a source of gastric ammonia. Objective: To evaluate the role of H pylori in pathogenesis of hepatic encephalopathy (HE). Patients and Methods: This case control study was carried out on 100 patients, 18 years old or more and both sexes. Patients were divided into 3 groups; group A (n = 40): Liver cirrhosis (LC) (Child C) and positive H pylori, group B (n = 40): LC (Child C) and negative H pylori and group C (n = 20): Healthy persons as a control group. Stool H Pylori antigen, arterial blood ammonia and plasma endotoxins were done. Results: Mean value ± SD of serum ammonia was 97.28 ± 31.66 ng/dL in group A, 65.45 ± 14.91 ng/dL in group B and 48.6 ± 11.66 ng/dL in group C. There was a significant increase in group A than B and C, and in group B than C. Mean value ± SD of plasma endotoxin was 0.55 ± 0.11 ng/dL in group A, 0.34 ± 0.12 ng/dL in group B and 0.25 ± 0.09 ng/dL in group C. There was a significant increase in group A than B and C, and in group B than C. HE significantly increased in group A (55.0%) than group B (17.5%). Conclusion: Cirrhotic patients (Child C) with positive H pylori were associated with higher incidence of HE, higher levels of ammonia and endotoxins than patients with negative H pylori.