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Does Helicobacter pylori affect portal hypertensive gastropathy?  [cached]
Al Mofleh Ibrahim
Saudi Journal of Gastroenterology , 2007,
Abstract: Helicobacter pylori (H. pylori) is a major etiological factor of peptic ulcer disease (PUD). It is supposed to be a risk factor for the more frequently encountered PUD in patients with liver cirrhosis. Several investigators have evaluated the effect of H. pylori on liver cirrhosis, portal hypertensive gastropathy (PHG) and encephalopathy with controversial results. Some reports have shown a higher seroprevalence and suggested a synergistic effect of H. pylori on liver cirrhosis and PHG. However, this increased prevalence is associated with a negative histology and is not influenced by the cause of cirrhosis, PHG, Child class or gender. Most studies have not found any correlation between H. pylori and PHG. In contrast, other studies have reported a markedly lower prevalence of H. pylori in cirrhotics with duodenal ulcer compared to controls. The aim of this article is to review the relationship between H. pylori infection and portal hypertensive gastropathy and the role of H. pylori eradication in cirrhotic patients.
Prevalence of gastric varices and portal hypertensive gastropathy in patients with Symmers periportal fibrosis  [cached]
Mudawi Hatim,Ali Yasir,El Tahir Mohamed
Annals of Saudi Medicine , 2008,
Abstract: Background and Objective: Symmers′ periportal fibrosis secondary to schistosomiasis is a common cause of portal hypertension worldwide. Data on the prevalence of gastric varices and portal hypertensive gastropathy in this group of patients with portal hypertension is relatively scarce. The aim of this study was to determine the prevalence of gastric varices and portal hypertensive gastropathy in patients presenting with portal hypertension secondary to Symmers′ periportal fibrosis. Patients and Methods: In a prospective study, upper gastrointestinal endoscopy was carried out to determine the prevalence of gastric varices and portal hypertensive gastropathy in patients with portal hypertension secondary to Symmers′ periportal fibrosis. Results: Of 143 patients studied, 24 patients (16.8%) had gastric varices (grade I in 10.5%, grade II in 6.3%) and 31 patients (21.7%) had portal hypertensive gastropathy (mild in 11.2%, severe in 10.5%). Gastric varices were more prevalent in patients with grade I and II esophageal varices and portal hypertensive gastropathy was more prevalent in those with grade III and IV esophageal varices, but the differences were not statiscally signiffant. Conclusion: We concluded that both gastric varices and portal hypertensive gastropathy seem to have a lower prevalence in patients with portal hypertension secondary to Symmers′ periportal fibrosis when compared to reported data in patients with portal hypertension secondary to liver cirrhosis and non-cirrhotic portal fibrosis.
Portal hypertensive colopathy is associated with portal hypertension severity in cirrhotic patients  [cached]
Antonio Diaz-Sanchez, Oscar Nu?ez-Martinez, Cecilia Gonzalez-Asanza, Ana Matilla, Beatriz Merino, Diego Rincon, Inmaculada Beceiro, Maria Vega Catalina, Magdalena Salcedo, Rafael Ba?ares, Gerardo Clemente
World Journal of Gastroenterology , 2009,
Abstract: 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 was alcoholism (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 ± 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 gastropat a clinically significant puzzle  [cached]
Eleftheriadis E.
Annals of Gastroenterology , 2007,
Abstract: SUMMARY In this review the updated information concerning the influence of portal hypertension on gastric mucosa is presented. The term portal hypertensive gastropathy [PHG] defines a wide spectrum of endoscopic lesions that appear in the gastric mucosa of cirrhotic patients and which should be differentiated from gastric antral vascular ectasia. These endoscopic findings correspond to dilated mucosal and submucosal vessels in the absence of inflammation. There is wide variation in the prevalence of PHG, but its natural history in not clearly documented. Endoscopic variceal obliteration may contribute to the development or aggravation of these lesions. Similar influence of portal hypertension seems to be extended in the lower gastrointestinal tract. With regard to gastric mucosal hemodynamics, it is not known whether active congestion or passive congestion causes gastric mucosal hyperhemia. The pathogenesis of PHG in not well known, but both venous congestion related to raised portal pressure and increased gastric blood flow seem to be crucial factors for its development. Gastric mucosal defense mechanisms are impaired in PHG. Bleeding is its unique clinical manifestation and occurs in patients with severe lesions. Pharmacological, surgical and interventional radiological procedures are available for the treatment of bleeding PHG, but the treatment needs to be improved. Key words: Portal hypertensive gastropathy, portal hypertensive vasculopathy, liver cirrhosis, portal hypertension
Manifestations of severe portal hypertension: Validation of a non-invasive score in cirrhotic patients
Afonso,Miguel; Pinto,Joana; Veloso,Ricardo; Freitas,Teresa; Carvalho,Jo?o; Fraga,José;
Jornal Português de Gastrenterologia , 2012,
Abstract: background and aims: current guidelines recommend that cirrhotic patients should undergo upper gastrointestinal endoscopy for screening of esophageal varices. several studies evaluated the ability of non-invasive markers to predict the presence of esophageal varices. we aimed to test the validity of platelet count-to-spleen diameter ratio (pc/sd) to predict the presence of esophageal varices as well as endoscopic signs of severe portal hypertension (large varices, red signs on esophageal varices and severe portal hypertensive gastropathy) using the 909 cut-off value. patients and methods : retrospective study of 170 cirrhotic patients, who underwent screening for esophageal varices. liver cirrhosis etiology, laboratory, ultrasonography and endoscopy data were analyzed. stats: mann-whitney test, x2, roc curves. results: 170 patients (55 female) were included. one hundred and three (60,6%) had esophageal varices (34,1% large; 11,8% with red signs). ninety-seven patients (57,1%) had portal hypertensive gastropathy (phg): with severe phg in 38 (22,3%). pc/sd <909 was documented in 93 patients. it was significantly associated with the presence of esophageal varices (p<0,001; auroc= 0,84) and high-risk esophageal varices (large varices or red signs - p<0,001; auroc= 0,8). the score was also significantly associated with the presence of severe portal hypertensive gastropathy (p<0,001; auroc= 0,63). conclusions: pc/sd is significantly associated with the presence of esophageal varices and portal hypertensive gastropathy. a pc/sd ≥909 is a good predictor of the absence of high-risk varices or severe portal hypertensive gastropathy
Clinical Manifestations of Portal Hypertension  [PDF]
Said A. Al-Busafi,Julia McNabb-Baltar,Amanda Farag,Nir Hilzenrat
International Journal of Hepatology , 2012, DOI: 10.1155/2012/203794
Abstract: The portal hypertension is responsible for many of the manifestations of liver cirrhosis. Some of these complications are the direct consequences of portal hypertension, such as gastrointestinal bleeding from ruptured gastroesophageal varices and from portal hypertensive gastropathy and colopathy, ascites and hepatorenal syndrome, and hypersplenism. In other complications, portal hypertension plays a key role, although it is not the only pathophysiological factor in their development. These include spontaneous bacterial peritonitis, hepatic encephalopathy, cirrhotic cardiomyopathy, hepatopulmonary syndrome, and portopulmonary hypertension.
Manifestations of severe portal hypertension: Validation of a non-invasive score in cirrhotic patients Manifesta es de hipertens o portal grave: Valida o de score n o invasivo  [cached]
Miguel Afonso,Joana Pinto,Ricardo Veloso,Teresa Freitas
Jornal Português de Gastrenterologia , 2012,
Abstract: BACKGROUND AND AIMS: Current Guidelines recommend that cirrhotic patients should undergo upper gastrointestinal endoscopy for screening of esophageal varices. Several studies evaluated the ability of non-invasive markers to predict the presence of esophageal varices. We aimed to test the validity of platelet count-to-spleen diameter ratio (PC/SD) to predict the presence of esophageal varices as well as endoscopic signs of severe portal hypertension (large varices, red signs on esophageal varices and severe portal hypertensive gastropathy) using the 909 cut-off value. PATIENTS AND METHODS : Retrospective study of 170 cirrhotic patients, who underwent screening for esophageal varices. Liver cirrhosis etiology, laboratory, ultrasonography and endoscopy data were analyzed. STATS: Mann-Whitney test, X2, ROC curves. RESULTS: 170 patients (55 female) were included. One hundred and three (60,6%) had esophageal varices (34,1% large; 11,8% with red signs). Ninety-seven patients (57,1%) had portal hypertensive gastropathy (PHG): with severe PHG in 38 (22,3%). PC/SD <909 was documented in 93 patients. It was significantly associated with the presence of esophageal varices (P<0,001; AUROC= 0,84) and high-risk esophageal varices (large varices or red signs - P<0,001; AUROC= 0,8). The score was also significantly associated with the presence of severe portal hypertensive gastropathy (P<0,001; AUROC= 0,63). CONCLUSIONS: PC/SD is significantly associated with the presence of esophageal varices and portal hypertensive gastropathy. A PC/SD ≥909 is a good predictor of the absence of high-risk varices or severe portal hypertensive gastropathy INTRODU O E OBJECTIVOS: O rastreio de varizes esofágicas através de endoscopia digestiva alta está recomendado nos doentes com cirrose hepática. Vários estudos têm avaliado a aplicabilidade de marcadores n o-invasivos na previs o de varizes do esófago. Neste trabalho, os autores pretenderam testar a validade da raz o contagem de plaquetas/diametro bipolar do ba o para prever a presen a de varizes do esofago e manifesta es de hipertens o portal grave (varizes esofágicas grandes ou com sinais vermelhos e gastropatia de hipertens o portal grave), utilizando o valor de cut-off 909. PACIENTES E MéTODOS: Estudo retrospectivo de 170 pacientes com cirrose hepática, que realizaram endoscopia digestiva alta para rastreio de varizes do esófago. Foram registados dados clínicos, laboratoriais, imagiológicos e endoscópicos. ANáLISE ESTATíSTICA: teste de Mann-Whitney, X2, curvas ROC. RESULTADOS: Foram incluídos 170 pacientes (55 mulheres). Cento e t
Colonoscopy-based diagnosis of portal hypertensive colopathy in cirrhotic patients and relation to hepatic disease pathogenesis  [cached]
CHEN Linyan
Journal of Clinical Hepatology , 2013,
Abstract: ObjectiveTo evaluate the rate of colonoscopy-based diagnosis of portal hypertensive colopathy (PHC) in patients with cirrhosis and evaluate associations with the hepatic disease pathogenic features. MethodsTwenty-three cirrhotic patients who underwent colonoscopy between January 2009 and May 2012 were enrolled in the study. The colonoscopy examination results, Child-Pugh scores, esophageal varices stages, and aspartate aminotransferase to platelet ratio index (APRI) values were recorded for each patient. The significance of inter-group differences was assessed by Chi-squared test or Fisher′s exact test. ResultsThe most common colonoscopy finding was PHC (9/23, 39.1%). Only 8.7% (2/23) of patients had completely normal findings. Occurrence of PHC was associated with moderate to severe esophageal varices (P=0.086) but not with severe liver fibrosis, either by APRI index or Child-Pugh score. ConclusionThe majority of cirrhosis patients had anomalous colonoscopy findings, and more than one-third had PHC. Colonoscopy should be considered for cirrhotic patients to identify previously undiagnosed PHC and initiate timely treatment.
PPIs are not associated with a lower incidence of portal-hypertension-related bleeding in cirrhosis  [cached]
Mauricio Garcia-Saenz-de-Sicilia, Francisco Sanchez-Avila, Norberto C Chavez-Tapia, Gustavo Lopez-Arce, Sandra Garcia-Osogobio, Roberto Ruiz-Cordero, Felix I Tellez-Avila
World Journal of Gastroenterology , 2010,
Abstract: AIM: To determine if proton pump inhibitor use in cirrhotic patients with endoscopic findings of portal hypertension is associated with a lower frequency of gastrointestinal bleeding.METHODS: Patients with cirrhosis and endoscopic findings related to portal hypertension, receiving or not receiving proton pump inhibitor (PPI) therapy, were included retrospectively. We assigned patients to two groups: group 1 patients underwent PPI therapy and group 2 patients did not undergo PPI therapy.RESULTS: One hundred and five patients with a median age of 58 (26-87) years were included, 57 (54.3%) of which were women. Esophageal varices were found in 82 (78%) patients, portal hypertensive gastropathy in 72 (68.6%) patients, and gastric varices in 15 (14.3%) patients. PPI therapy was used in 45.5% of patients (n = 48). Seventeen (16.1%) patients presented with upper gastrointestinal bleeding; in 14/17 (82.3%) patients, bleeding was secondary to esophageal varices, and in 3/17 patients bleeding was attributed to portal hypertensive gastropathy. Bleeding related to portal hypertension according to PPI therapy occurred in 18.7% (n = 9) of group 1 and in 14% (n = 8) of group 2 (odds ratio: 0.83, 95% confidence interval: 0.5-1.3, P = 0.51).CONCLUSION: Portal hypertension bleeding is not associated with PPI use. These findings do not support the prescription of PPIs in patients with chronic liver disease with no currently accepted indication.
Zolmitriptan: A Novel Portal Hypotensive Agent Which Synergizes with Propranolol in Lowering Portal Pressure  [PDF]
Mercedes Reboredo, Haisul C. Y. Chang, Roberto Barbero, Carlos M. Rodríguez-Ortigosa, Francisco Pérez-Vizcaíno, Asunción Morán, Mónica García, Jesús M. Banales, Norberto Carre?o, Félix Alegre, Ignacio Herrero, Jorge Quiroga, Jesús Prieto, Bruno Sangro
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0052683
Abstract: Objective Only a limited proportion of patients needing pharmacological control of portal hypertension are hemodynamic responders to propranolol. Here we analyzed the effects of zolmitriptan on portal pressure and its potential interaction with propranolol. Methods Zolmitriptan, propranolol or both were tested in two rat models of portal hypertension: common bile duct ligation (CBDL) and CCl4-induced cirrhosis. In these animals we measured different hemodynamic parameters including portal venous pressure, arterial renal flow, portal blood flow and cardiac output. We also studied the changes in superior mesenteric artery perfusion pressure and in arterial wall cAMP levels induced by zolmitriptan, propranolol or both. Moreover, we determined the effect of splanchnic sympathectomy on the response of PVP to zolmitriptan. Results In both models of portal hypertension zolmitriptan induced a dose-dependent transient descent of portal pressure accompanied by reduction of portal flow with only slight decrease in renal flow. In cirrhotic rats, splanchnic sympathectomy intensified and prolonged zolmitriptan-induced portal pressure descent. Also, propranolol caused more intense and durable portal pressure fall when combined with zolmitriptan. Mesenteric artery perfusion pressure peaked for about 1 min upon zolmitriptan administration but showed no change with propranolol. However propranolol enhanced and prolonged the elevation in mesenteric artery perfusion pressure induced by zolmitriptan. In vitro studies showed that propranolol prevented the inhibitory effects of β2-agonists on zolmitriptan-induced vasoconstriction and the combination of propranolol and zolmitriptan significantly reduced the elevation of cAMP caused by β2-agonists. Conclusion Zolmitriptan reduces portal hypertension and non-selective beta-blockers can improve this effect. Combination therapy deserves consideration for patients with portal hypertension failing to respond to non-selective beta-blockers.
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