Peptic Ulcer Diseases in Patients with Liver Cirrhosis and Portal Hypertension: Experience in a Tertiary Level Hospital in Bangladesh

Introduction: Cirrhosis of liver and peptic ulcer disease (PUD) are very common in Bangladesh. PUD may coexist with cirrhosis and portal hypertension. Haematemesis and melaena in cirrhosis of liver are not always from ruptured oesophageal varices; rather it may be due to bleeding peptic ulcer disease. Objective: To find the prevalence of PUD among patients with liver cirrhosis and portal hypertension. Materials and Methods: This cross sectional, descriptive study was conducted on 96 patients of cirrhosis of liver diagnosed with oesophageal varices at endoscopy unit of Kurmitola general hospital, during endoscopic evaluations in 4 months period from september 2017 to december 2017. Results: Total cirrhotic patients enrolled were 96 (M=61, F=35), mean age was 51.8 ± 14.2 yrs (18-86years). Hepatitis B virus (HBV) was the leading cause of cirrhosis in 54.1%, Hepatitis C virus (HCV) 5.2 %, proven non-alcoholic steatohepatitis (NASH) were 11.5% and rest were from unknown aetiology. Their average Child-Turcotte-Pugh (CTP) score were 8.6 (12-5), 37.6% associated with portal hypertensive gastropathy. Grade-III oesophageal varices found in 52 patients, whereas grade-II in 25 patients. Among this 96 patients 39 (40.6%) revealed peptic ulcer disease more in the form of gastric ulcer (n=23) than duodenal ulcer (n=10) and both (n=6). Most of the ulcers belonged to Forrest class III (76.9%). Conclusions: Variceal bleeding and portal hypertensive gastropathy are the common causes of bleeding and anaemia in patients with cirrhosis of liver. Peptic ulcer disease has been found to be one of the potential causes of haematemesis, melaena, and anaemia among these patients in Bangladesh. Large multicenter controlled studies are needed to confirm the reports. JAFMC Bangladesh. Vol 16, No 2 (December) 2020: 68-71

Gastric mucosal function in portal hypertensive gastropathy secondary to schistosomal hepatic fibrosis: effect of sclerotherapy

Gastric mucosal function in portal hypertensive gastropathy secondary to schistosomal hepatic fibrosis [SHF] was evaluated. Group I comprised 20 patients with no bleeding;10 had portal hypertensive gastropathy [PHG]. Group II comprised 20 patients with bleeding. Free acidity, total acidity, basal acid output, serum pepsinogen I, gastric mucosal blood flow [GMBF] and gastrin were significantly lower in group II, whereas serum gastrin and somatostatin staining were significantly higher. No histopathological changes were noted between both groups, In conclusion, bleeding caused by SHF results in hypoacidity, hypergastrinaemia and hypopepsinogenaemia. Estimated GMBF distinguishes patients with PHG and those who are bleeders

Upper GI Bleeding Secondary to Radiation Gastritis in a Patient with Preexisting Portal Hypertensive Gastropathy

We commonly see patients presenting with either portal hypertensive gastropathy (PHG) or radiation gastritis. Radiation-induced hemorrhagic gastritis is an unusual lethal complication postradiation. Patients with preexisting PHG have very friable mucosa that can easily bleed after radiation for cancer treatment. There is an increased risk of bleeding with both entities present together. Our aim is to focus on treatment and possible prevention of gastrointestinal bleeding in patients with preexisting PHG undergoing radiation therapy for newly diagnosed cancer. Several therapies like prednisolone, argon plasma coagulation, laser coagulation have been proposed. There are no set guidelines for treatment. In these patients, if radiation therapy is indicated either for hepatic or gastrointestinal malignancy, it is suggested to premedicate with proton pump inhibitors or sucralfate. We describe a case of 73-year-old female who presented with upper gastrointestinal bleeding. She had liver cirrhosis secondary to nonalcoholic fatty liver disease and diagnosed with pancreatic cancer, for which she received chemoradiation. She was found to have both radiation gastritis and PHG with diffuse erythematous, edematous, congested mucosa with diffuse oozing blood in the antrum making it very challenging to treat.

Discovery and validation of novel protein markers in mucosa of portal hypertensive gastropathy

Background Portal hypertension induced esophageal and gastric variceal bleeding is the main cause of death among patients of decompensated liver cirrhosis. Therefore, a standardized, biomarker-based test, to make an early-stage non-invasive risk assessment of portal hypertension, is highly desirable. However, no fit-for-purpose biomarkers have yet been identified. Methods We conducted a pilot study consisting of 5 portal hypertensive gastropathy (PHG) patients and 5 normal controls, sampling the gastric mucosa of normal controls and PHG patients before and after endoscopic cyanoacrylate injection, using label-free quantitative (LFQ) mass spectrometry, to identify potential biomarker candidates in gastric mucosa from PHG patients and normal controls. Then we further used parallel reaction monitoring (PRM) to verify the abundance of the targeted protein. Results LFQ analyses identified 423 significantly differentially expressed proteins. 17 proteins that significantly elevated in the gastric mucosa of PHG patients were further validated using PRM. Conclusions This is the first application of an LFQ-PRM workflow to identify and validate PHG–specific biomarkers in patient gastric mucosa samples. Our findings lay the foundation for comprehending the molecular mechanisms of PHG pathogenesis, and provide potential applications for useful biomarkers in early diagnosis and treatment. Trial registration and ethics approval: Trial registration was completed (ChiCTR2000029840) on February 25, 2020. Ethics Approvals were completed on July 17, 2017 (NYSZYYEC20180003) and February 15, 2020 (NYSZYYEC20200005).

Discovery and Validation of Novel Protein Markers in Mucosa of Portal Hypertensive Gastropathy

Background: Portal hypertension induced esophageal and gastric varix bleeding is the main cause of death among patients of decompensated liver cirrhosis. Therefore, a standardized, biomarker-based test, to make an early-stage non-invasive risk assessment of portal hypertension, is highly desirable. However, no fit-for-purpose biomarkers have yet been identified. Methods: We conducted a pilot study consisting of 5 portal hypertensive gastropathy (PHG) patients and 5 normal controls, sampling the gastric mucosa of normal controls and PHG patients before and after endoscopic cyanoacrylate injection, using label-free quantitative (LFQ) mass spectrometry, to identify potential biomarker candidates in gastric mucosa from PHG patients and normal controls. Then we further used parallel reaction monitoring (PRM) to verify the abundance of the targeted protein. Results: LFQ analyses identified 423 significantly differentially expressed proteins. 17 protein that significantly elevated in the gastric mucosa of PHG patients were further validated using PRM. Conclusions: This is the first application of an LFQ-PRM workflow to identify and validate PHG–specific biomarkers in patient gastric mucosa samples. Our findings lay the foundation for comprehending the molecular mechanisms of PHG pathogenesis, and provide potential applications for useful biomarkers in early diagnosis and treatment.Trial Registration: Trial registration was completed (ChiCTR2000029840) on February 25, 2020.