Is There an Association between Variceal Bleed and Helicobacter pylori Infection in Cirrhotic Patients with Portal Hypertension?

Objectives: The objective of this study was to find the association of H. pylori in patients with variceal bleeding as well as rebleeding in cases of cirrhosis with portal hypertension. Methods: This was a prospective cohort of patients with bleeding esophageal varices. The primary outcome was correlation between prevalence of H. pylori and the incidence of bleeding/ rebleeding from varices and with encephalopathy. The secondary outcome were correlation between the site of bleeding with H. pylori infection and the association of pepsinogen I & II and the ratio of pepsinogen I/II with bleeding. Results: A total of 190 patients were assessed for eligibility, out of which 159 patients were included in this study. 124 out of 159 patients (77.9%) had alcohol-related liver disease. 8 out of 159 patients had HBV-related liver disease. 7 patients with varices had neither bled at presentation nor did bleed in the follow-up period. A total of 78 out of 159 (49.05%) patients were H.pylori-infected. Patients with esophageal varices [Adjusted Risk (AR)=0.7] and H.pylori infection (AR=0.7) had a lower risk of variceal rebleeding. Among the patients negative for H.pylori, pepsinogen I was higher in patients with rebleeding (30.7 vs 14.4; p<0.001). Among H.pylori positive patients, the ratio of pepsinogen I/II was higher in patients with rebleeding (2.9 vs 1.3; p=0.023). Conclusion: H.pylori infection was associated with a lower risk of rebleeding in cases of cirrhosis with portal hypertension. Irrespective of the status of H.pylori infection, rebleeding was associated with more gastric acid output demonstrated by the level of pepsinogen. Keywords: Pepsinogen; hepatic encephalopathy; gastric acid output, Helicobacter pylori

Dihydroquercetin (taxifolin) attenuates dexamethasone activity on prostaglandin E-2 but potentiates thromboxane-A2 action in gastric acid secretion in wistar rats

The activity of dexamethasone and taxifolin {(2R, 3R)-2-(3, 4-Dihydroxyphenyl)-3,5,7-trihydroxy-2,3-dihydrochromen-4-one}supplementation on prostaglandin E2 and thromboxane A2 in gastric acid secretion and anti-ulcer was studied. Twenty male Wistar rats (180g-200g body weight) were used. The rats were randomly selected into four groups containing 5 rats each. Group 1 was the control group fed on normal rat feed. Group 2 received 3mg/kg of Dexamethasone (intraperitoneally) at one day interval. Group 3 received 3mg/kg of Dex. intraperitoneally and 1mg/kg body weight of taxifolin orally while group 4 received 1mg/kg body weight of taxifolin. At the end of 6 weeks, basal and peak gastric acid output was measured by continuous perfusion of rats stomach under anaesthesia with normal saline at the rate of 1ml/min. Gastric acid, mucus secretion, ulcer index, PGE-2 and thromboxane A2 activity were determined according to standard procedures. Results showed a significantly (p<.05) decreased prostaglandin and mucus secretion level and a raised thromboxane concentrations and gastric acid output in dexamethasone administration. Taxifolin significantly (p<.05) lowered thromboxane A2 concentration in Dex treatment while increasing the prostaglandin E2 level. We conclude that Taxifolin decreases dexamethasone- induced gastric acid secretion, increases prostaglandin activity but reduces thromboxane concentration.