Portal hypertensive colopathy is associated with portal hypertension severity in cirrhotic patients

AIM： To assess the prevalence of portal hypertension （PH） related colorectal lesions in liver transplant candidates, and to evaluate its association with the severity of PH. METHODS： Between October 2004 and December 2005, colonoscopy was performed in 92 cirrhotic liver transplant candidates. We described the lesions resulting from colorectal PH and their association with the grade of PH in 77 patients who underwent measurement of hepatic venous pressure gradient （HVPG）. RESULTS： Mean age was 55 years and 80.7% of patients were men. The main etiology of cirrhosis wasalcoholism （45.5%）. Portal hypertensive colopathy （PHC） was found in 23.9%, colonic varices in 7.6% and polyps in 38% of patients （adenomatous type 65.2%）. One asymptomatic patient had a well-differentiated adenocarcinoma. The manifestations of colorectal PH were not associated with the etiology of liver disease or with the Child-Pugh grade. Ninety percent of patients with colopathy presented with gastroesophageal varices （GEV）, and 27.5% of patients with GEV presented with colopathy （P = 0.12）. A relationship between higher values of HVPG and presence of colopathy was observed （19.9：1：6.2 mmHg vs 16.8 ± 5.4 mmHg, P = 0.045）, but not with the grade of colopathy （P = 0.13）. Preneoplastic polyps and neoplasm （P = 0.02） and spontaneous bacterial peritonitis （P = 0.006） were more prevalent in patients with colopathy. We did not observe any association between previous β-blocker therapy and the presence of colorectal portal hypertensive vasculopathy. CONCLUSION： PHC is common in cirrhotic liver transplant candidates and is associated with higher portal pressure.

Portal hypertensive colopathy in patients with liver cirrhosis

AIM: In patients with liver cirrhosis and portal hypertension, portal hypertensive colopathy is thought to be an important cause of lower gastrointestinal hemorrhage. In this study, we evaluated the prevalence of colonic mucosal changes in patients with liver cirrhosis and its clinical significance. METHODS: We evaluated the colonoscopic findings and liver function of 47 patients with liver cirrhosis over a 6-year period. The main cause of liver cirrhosis was post-viral hepatitis (68%) related to hepatitis B (6%) or C (62%) infection. All patients underwent upper gastrointestinal endoscopy to examine the presence of esophageal varices, cardiac varices, and congestive gastropathy, as well as a full colonoscopy to observe changes in colonic mucosa. Portal hypertensive colopathy was defined endoscopically in patients with vascular ectasia, redness, and blue vein. Vascular ectasia was classified into two types: type 1, solitary vascular ectasia; and type 2, diffuse vascular ectasia. RESULTS: Overall portal hypertensive colopathy was present in 31 patients (66%), including solitary vascular ectasia in 17 patients (36%), diffuse vascular ectasia in 20 patients (42%), redness in 10 patients (21%) and blue vein in 6 patients (12%). As the Child-Pugh class increased in severity, the prevalence of portal hypertensive colopathy rose. Child-Pugh class B and C were significantly associated with portal hypertensive colopathy. Portal hypertensive gastropathy, esophageal varices, ascites and hepatocellular carcinoma were not related to occurrence of portal hypertensive colopathy. Platelet count was significantly associated with portal hypertensive colopathy, but prothrombin time, serum albumin level, total bilirubin level and serum ALT level were not related to occurrence of portal hypertensive colopathy. CONCLUSION: As the Child-Pugh class worsens and platelet count decreases, the prevalence of portal hypertensive colopathy increases in patients with liver cirrhosis. A colonoscopic examination in patients with liver cirrhosis is indicated, especially those with worsening Child-Pugh class and/or decreasing platelet count, to prevent complications such as lower gastrointestinal bleeding.