Proton Pump Inhibitor Plus Propranolol Versus Proton Pump Inhibitor Alone on Peptic Ulcer Healing in Patients With Liver Cirrhosis

Proton Pump Inhibitor Plus Propranolol Versus Proton Pump Inhibitor Alone on Peptic Ulcer Healing in Patients With Liver Cirrhosis: a Randomized Trail

Proton pump inhibitor plus propranolol versus proton pump inhibitor alone on peptic ulcer healing in patients with liver cirrhosis: a randomized trail

Portal hypertension is responsible for the development of portosystemic collaterals. The hemodynamic alternations may result in mucosal and vascular changes along gastrointestinal (GI) tract as well. According to several epidemiological studies, cirrhotic patients are at a higher risk of developing peptic ulcers, delayed healing, and a higher frequency of ulcer recurrence. The death rate from peptic ulcer disease in cirrhotic patients has been reported to be five times higher than that of the general population. The exact mechanism remains incompletely understood, but may be related to impaired mucosal defense mechanisms. Aggressive factors such as Helicobacter pylori and gastric acid may not be the predominant etiology in such circumstances. Sarfeh et al. found gastric mucosa of portal hypertensive rats, compared with that of controls, has distinctive functional and histologic abnormalities that can explain its increased susceptibility to erosive injury. Auroux et al. found gastroduodenal ulcer was independently associated only with the severity of the hypertensive gastropathy in cirrhotics. Chen et al. found portal hypertension with a hepatic venous pressure gradient > 12 mmHg may be an important factor contributing to the increased prevalence of gastric ulcer observed in patients with liver cirrhosis. Thereby, we presumed that clinically significant portal hypertension may play a role in development of peptic ulcer in cirrhotic patients. Lebrec et al. elucidated non-selective beta-blocker (NSBB) could significantly decrease portal pressure and lower the risk of GI bleeding in patients with cirrhosis. Kitano et al. found portal hypotensive treatment with NSBB, reduces ethanol-induced gastric mucosal damage in portal hypertensive rats and improves endoscopic signs of portal hypertensive gastropathy in cirrhosis patients. We designed a 2-year randomized trial to evaluate the effectiveness of proton pump inhibitor with or without propranolol on ulcer healing and the incidence of ulcer bleeding in patients with cirrhosis and peptic ulcers.

Inclusion Criteria:

• Between 20 and 85 years old
• Liver cirrhosis associated with esophageal varices or gastric varices
• Gastric ulcer or duodenal ulcer ,size bigger or egual than 0.5 cm

Exclusion Criteria:

• Acute bleeding
• Steroid or NSAID user
• Pregnancy, or the patients with other terminal illness (such as other terminal cancers, heart failure, renal failure...)
• Propranolol contraindications (such as atrioventricular block, heart failure, chronic obstructive pulmonary disease, asthma, poorly controlled diabetes, severe peripheral arterial disease...)