"Portal hypertensive gastropathy" from_date:2012

Portal Hypertensive Gastropathy and MELD-Na Score Predict Recurrent Gastrointestinal Bleeding After TIPSS: An ALTA Group Study. Transjugular intrahepatic portosystemic shunt (TIPSS) is highly effective for treatment of variceal bleeding; however, factors contributing to rebleeding complications remain unclear. In this study, we aim to determine risk factors for recurrent portal hypertensive with rebleeding. We identified 476 patients, predominately middle-aged (mean age 57), male (62%) and White (65%), with mean MELD-Na 16. 16% (n = 77) had a rebleeding event; these patients were more likely to be male (p = 0.016), with higher serum creatinine (p = 0.005), MELD-Na (p = 0.0002), portal hypertensive gastropathy on pre-TIPSS upper endoscopy (p = 0.000) and with higher incidence of TIPSS revision (p

Risk factors for portal hypertensive gastropathy. Portal hypertensive gastropathy (PHG) is often underestimated in clinical diagnosis. Gastrointestinal bleeding in cirrhosis of PHG accounts for approximately 10% of upper gastrointestinal bleeding. However, the relationship between PHG and gender, laboratory parameters, liver function and varices is still controversial. In the present study, we

Irsogladine maleate alters expression of a tight junction protein in portal hypertensive gastropathy. Portal hypertensive gastropathy (PHG) is characterized by noninflammatory edema and vasodilatation of the lamina propria of the mucosal epithelium. In addition, the alterations of intercellular junction proteins and dilatation of the endothelial gaps have been reported. In this study, we

Blood Ammonia Level Correlates with Severity of Cirrhotic Portal Hypertensive Gastropathy Portal hypertensive gastropathy (PHG) is a common anomaly with potential for bleeding found in portal hypertension. Blood ammonia levels correlate well with liver disease severity and existence of portosystemic shunts. Increased ammonia results in vasodilation and hepatic stellate cell activation causing and exacerbating portal hypertension. To assess the relation of blood ammonia to the presence and severity of portal hypertensive gastropathy in cirrhosis. This cross-sectional study included 381 cirrhotics undergoing screening for esophageal varices (EV) divided into a portal hypertensive gastropathy group (203 patients with EV and PHG), esophageal varix group (41 patients with EV but no PHG), and control group

Noninvasive Clinical Predictors of Portal Hypertensive Gastropathy in Patients with Liver Cirrhosis Portal hypertensive gastropathy (PHG) is described endoscopically as "mosaic-like appearance" of gastric mucosa with or without the red spots. It can only be diagnosed by upper gastrointestinal (GI) endoscopy. The aim of this study was to determine the diagnostic accuracy of platelet count

Use of hemostatic powder in bleeding portal hypertensive gastropathy

PGE2/EP4 receptor attenuated mucosal injury via β‐arrestin1/Src/EGFR‐mediated proliferation in portal hypertensive gastropathy Portal hypertensive gastropathy (PHG) is a serious complication of liver cirrhosis and a potential cause of bleeding in patients with cirrhosis. Suppressed mucosal epithelial proliferation is a crucial pathological characteristic of PHG. Our studies demonstrated

Portal hypertensive gastropathy as a prognostic index in patients with liver cirrhosis. Portal hypertensive gastropathy (PHG) is a frequently overlooked complication of liver cirrhosis (LC). The clinical implications of PHG as a prognostic factor of LC or a predictive factor for the development of hepatocellular carcinoma (HCC) have not been established. The aim of this study was to assess

The Portal Hypertensive Gastropathy: A Case and Review of Literature Upper gastrointestinal bleeding is a cause of high risk for morbidity and mortality. It has been debated in alcoholic cirrhosis, if alcohol exerts an exclusive and causal role upon gastropathy or whether it is linked to cirrhotic portal hypertension. The authors describe an autopsy report regarding mortality caused by gastric

Efficacy of argon plasma coagulation in the management of portal hypertensive gastropathy Evaluation of the outcome and experience in 2 years of management of portal hypertensive gastropathy (PHG) by argon plasma coagulation (APC) in a cohort of Egyptian cirrhotic patients. This study was conducted over a 2-year period from January 2011 to February 2013. Upper gastrointestinal endoscopy

Pleuritic chest pain from portal hypertensive gastropathy in ESRD patient with autosomal dominant polycystic kidney disease misdiagnosed as pericarditis. Portal hypertensive gastropathy (PHG) is a gastric mucosal lesion complicating portal hypertension, with higher prevalence in decompensated cirrhosis. PHG can sometimes complicate autosomal dominant polycystic kidney disease (ADPKD) due

Portal hypertensive gastropathy and gastric antral vascular ectasia. Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are two types of upper gastrointestinal bleeding that may present similarly, but are managed very differently. This article reviews the pathogenesis and guidelines in management of both of these conditions with emphasis on recent advances

Review article: the management of portal hypertensive gastropathy and gastric antral vascular ectasia in cirrhosis. Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are important causes of both acute and chronic gastrointestinal bleeding in patients with cirrhosis. To review the current management of PHG and GAVE. PubMed was searched for English language articles using the key words 'GAVE', 'gastric antral vascular ectasia', 'cirrhosis', 'gastrointestinal bleeding', 'acute', 'chronic', 'portal hypertensive gastropathy', 'watermelon stomach', 'radiofrequency ablation', 'band ligation', 'thermoablation' and 'TIPSS'. GAVE and PHG are both encountered in patients with cirrhosis. They can be seen in asymptomatic patients and in those with either acute or chronic

Helicobacter pylori and portal hypertensive gastropathy: any new information?

Helicobacter pylori infection in patients with liver cirrhosis: prevalence and association with portal hypertensive gastropathy The role of () in the pathogenesis of portal hypertensive gastropathy (PHG) in cirrhotic patients is poorly defined. The aim of this study was toinvestigate the prevalence of infection and its association with PHG in patients with liver cirrhosis. Seroprevalence

Transient elastography to rule out oesophageal varices and portal hypertensive gastropathy in HIV-infected subjects with liver cirrhosis. It is recommended that patients with cirrhosis undergo endoscopic screening to rule out the presence of gastroesophageal varices: a noninvasive predictive method to identify cirrhotic patients with a very low risk of esophageal varices could potentially avoid unnecessary endoscopies. We studied in 85 HIV-infected patients with cirrhosis the association between the absence of esophageal varices and portal hypertensive gastropathy, assessed by endoscopy, and liver stiffness measurement by transient elastography. We analyzed other parameters related to portal hypertension and hepatic function. Values of transient elastography and platelet count were significantly

, radiation proctitis, gut angiodysplasia, hereditary haemorrhagic telangiectasia, gastric antral vascular ectasia (GAVE), portal hypertensive gastropathy, refractory radiation proctitis, obscure source), or iv. Life-long spontaneous impairment of haemostasis, or v. A vascular abnormality predisposing to potentially life-threatening haemorrhage, or vi. Irreversible hepatic disease with coagulopathy anticoagulation therapy without remedial cause, or (ii) History of intracranial, intraocular, spinal, retroperitoneal or atraumatic intra-articular bleeding, or (iii) Chronic, irreversible, recurrent gastrointestinal bleeding of any cause (eg, radiation proctitis, gut angiodysplasia, hereditary haemorrhagic telangiectasia, gastric antral vascular ectasia (GAVE), portal hypertensive gastropathy, refractory

. ‡ Portal hypertension is defined by any 1 of the following criteria: 1. Persistent splenomegaly either by physical exam or by imaging; 2. Persistent hypersplenism (platelet count <150 × 109/L); 3. Esophageal or gastric varices or portal hypertensive gastropathy; 4. Hepatic venous pressure gradient >10 mm Hg. 156 www.jpgn.orgESPGHAN/NASPGHAN

intrahepatic portosystemic stenting in Portal Hypertensive Gastropathy. J Coll Physicians Surg Pak. 2009;19(9):584–5. PubMed Google Scholar 38. Mezawa S, Homma H, Ohta H, Masuko E, Doi T, Miyanishi K, Takada K, Kukitsu T, Sato T, Niitsu Y. Effect of transjugular intrahepatic portosystemic shunt formation on portal hypertensive gastropathy and gastric circulation. Am J Gastroenterol. 2001;96(4):1155–9 . Article CAS PubMed Google Scholar 39. Urata J, Yamashita Y, Tsuchigame T, Hatanaka Y, Matsukawa T, Sumi S, Matsuno Y, Takahashi M. The effects of transjugular intrahepatic portosystemic shunt on portal hypertensive gastropathy. J Gastroenterol Hepatol. 1998;13(10):1061–7. Article CAS PubMed Google Scholar 40. Gjeorgjievski M, Cappell MS. Portal hypertensive gastropathy: a systematic review