Effect of early propranolol administration on portal hypertensive gastropathy in cirrhotic rats

AIM:To investigate any protective effect of early propranolol administration in the development of portal hypertensive gastropathy in cirrhotic rats. METHODS:For the development of liver cirrhosis and portal hypertensive gastropathy,60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein,followed by phenobarbital and carbon tetrachloride(CCl4) administration.After two weeks of CCl4 administration, the rats were randomly separated into two groups.In group A,propranolol was continuously administered intragastrically throughout the study,whereas in group B normal saline(placebo)was administered instead. Hemodynamic studies and vascular morphometric analysis of gastric sections were performed after complete induction of cirrhosis. RESULTS:Vascular morphometric studies showed higher numbers of vessels in all mucosal layers in the control group.Statistical analysis revealed a significantly higher total vascular surface in the control group compared to the propranolol group,but with no statistically significant difference between the mean vascular surfaces between the groups.Our study clearly shows that the increased mucosal blood flow is manifested by a marked increase of vessel count. CONCLUSION:Early propranolol's administration in portal hypertensive cirrhotic rats seems to prevent intense gastric vascular congestion that characterizes portal hypertensive gastropathy.

Helicobacter pylori and portal hypertensive gastropathy

To the Editor:H. pylori lives in the gastric epithelial cells, sometimes in gastric glands.Whetherornottheproliferationandbiologicalbehavior of H. pylori can be influenced by the status of the gastric mucosa is still unknown. Portal hypertensive gastropathy (PHG) is a blood drainage obstructive disease. In this pathologic environment, gastric mucosa may be further impaired when patients are infected with H. pylori. The role of H. pylori in the pathogenesis of PHG and

Accuracy of virtual chromoendoscopy in differentiating gastric antral vascular ectasia from portal hypertensive gastropathy:A proof of concept study

BACKGROUND Accurate detection of gastric antral vascular ectasia(GAVE)is critical for proper management of cirrhosis-related gastrointestinal bleeding.However,endoscopic diagnosis of GAVE can be challenging when GAVE overlaps with severe portal hypertensive gastropathy(PHG).AIM To determine the added diagnostic value of virtual chromoendoscopy to high definition white light for real-time endoscopic diagnosis of GAVE and PHG.METHODS We developed an I-scan virtual chromoendoscopy criteria for diagnosis of GAVE and PHG.We tested our criteria in a cross-sectional cohort of cirrhotic adults with GAVE and PHG when high-definition white light endoscopy(HDWLE)diagnosis was in doubt.We then compared the accuracy of I-scan vs HDWLE alone to histology.RESULTS Twenty-three patients were included in this study(65.2%Caucasians and 60.9%males).Chronic hepatitis C was the predominant cause of cirrhosis(43.5%)and seven adults(30.4%)had confirmed GAVE on histology.I-scan had higher sensitivity(100%vs 85.7%)and specificity(75%vs 62.5%)in diagnosing GAVE compared to HDWLE.This translates into a higher,albeit not statistically significant,accuracy of I-scan in detecting GAVE compared to HDWLE alone(82%vs 70%).I-scan was less likely to lead to an accurate diagnosis of GAVE in patients on dialysis(P<0.05)and in patients with elevated creatinine(P<0.05).Iscan had similar accuracy to HDWLE in detecting PHG.CONCLUSION This pilot work supports that virtual chromoendoscopy may obviate the need for biopsies when the presence of GAVE is in doubt.Larger studies are needed to assess the impact of virtual chromoendoscopy on success of endoscopic therapy for GAVE.

Shared changes in angiogenic factors across gastrointestinal vascular conditions:A pilot study

BACKGROUND Neovascularisation is common to a variety of gastrointestinal(GI)disorders with differing aetiologies and presentations;usually affecting adults above 60 years.Shared angiogenic factors modulated by disease specific elements could be a common denominator and represent novel diagnostic and therapeutic targets.As yet,assessment of angiogenic factors across several GI vascular disorders associated with recurrent bleeding and anaemia has not been reported.AIM To assess serum levels of angiogenic factors in several intestinal vascular disorders.METHODS A case control study was performed in Tallaght University Hospital in patients with endoscopically proven small bowel angiodysplasia(SBA),portal hypertensive gastropathy(PHG),gastric antral vascular ectasia(GAVE)and nonbleeding,non-anaemic controls.Using enzyme-linked immunosorbent assay,concentrations of Angiopoietin 1(Ang-1),Ang-2 and vascular endothelial growth factor(VEGF)were measured from 2 serum tubes of blood following informed consent.The relative expression of Ang-1 and Ang-2 and Ang-1/2 ratio was calculated and compared between groups.Statistical analysis was applied using a t-test,and a P value of<0.05 was considered significant.RESULTS To date 44 samples were tested:10 SBA,11 PHG,8 GAVE and 15 controls.Mean age 60(range 20-85)years and 20(45%)were males.Controls were significantly younger(49 years vs 66 years,P=0.0005).There was no difference in VEGF levels between the groups(P=0.6).SBA,PHG and GAVE Ang-1 levels were similar and were significantly lower than controls,(P=0.0002,95%CI:241 to 701).Ang-2 levels were statistically higher in PHG and GAVE groups compared to controls(P= 0.01, 95%CI: 77.8 to 668) and as a result, also had a lower Ang-1/2 ratioscompared to controls. While SBA Ang-2 levels were higher than controls, this didnot reach statistical significance. Neither age nor haemoglobin level, which wassimilar between disease groups, could explain the difference. In addition, themedian Ang-1/Ang-2 ratio for all patients was found to be significantly lowercompared to controls, 8 vs 28 respectively, P = 0.001, 95%CI: -27.55 to -7.12.CONCLUSIONOur novel pilot study suggests common alterations in Ang-1 and Ang-2 levelsacross several GI vascular disorders. Differences in Ang-1/Ang-2 ratios amongvascular disorders compared to controls suggest disease-specific modulation.