Use of hemostatic powder in bleeding portal hypertensive gastropathy.
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ABSTRACT:
SUBMITTER: Ishaq S
PROVIDER: S-EPMC5992334 | biostudies-literature | 2017 Sep
REPOSITORIES: biostudies-literature
Publications
Use of hemostatic powder in bleeding portal hypertensive gastropathy.
Ishaq Sauid S Kuwai Toshio T Siau Keith K
VideoGIE : an official video journal of the American Society for Gastrointestinal Endoscopy 20170901 9
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Project description:Background and aimsPortal hypertensive gastropathy (PHG) is common in patients with cirrhosis and may cause bleeding. This study systematically explored the independent impact of patient characteristics, portal hypertension and hepatic dysfunction on PHG severity and associated anemia.MethodsPatients with cirrhosis undergoing endoscopy were included in this retrospective analysis and PHG was endoscopically graded as absent, mild or severe. Clinical and laboratory parameters and hepatic venous pressure gradient (HVPG) were assessed with respect to an association with severity of PHG.ResultsA total of 110 patients (mean age: 57 years, 69% male) with mostly alcoholic liver disease (49%) or viral hepatitis (30%) were included: 15 (13.6%) patients had no PHG, 59 (53.6%) had mild PHG, and 36 (32.7%) had severe PHG. Severe PHG was significantly associated with male sex (83.3% vs. 62.2% in no or mild PHG; p = 0.024) and higher Child-Turcotte-Pugh (CTP) stage (CTP-C: 38.9% vs. 27.0% in no or mild PHG; p = 0.030), while MELD was similar (p = 0.253). Patients with severe PHG had significantly lower hemoglobin values (11.2 ± 0.4 g/dL vs. 12.4 ± 0.2 g/dL; p = 0.008) and a higher prevalence of iron-deficiency anemia (IDA: 48.5% vs. 26.9%; p = 0.032). Interestingly, HVPG was not significantly higher in severe PHG (median 20 mm Hg) vs. mild PHG (19 mm Hg) and no PHG (18 mm Hg; p = 0.252). On multivariate analysis, CTP score (odds ratio, OR: 1.25, 95% confidence interval, CI 1.02-1.53; p = 0.033) was independently associated with severe PHG, while only a trend towards an independent association with IDA was observed (OR: 2.28, 95% CI 0.91-5.72; p = 0.078).ConclusionThe CTP score but not HVPG or MELD were risk factors for severe PHG. Importantly, anemia and especially IDA are significantly more common in patients with severe PHG.
| S-EPMC6978296 | biostudies-literature
Project description: Not available
| S-EPMC8182254 | biostudies-literature
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| S-EPMC5992094 | biostudies-literature
Project description:Background and objectivesThis study aimed to test the safety and efficacy of Hemospray® for emergency control of acute variceal bleeding (AVB) due to portal hypertension in cirrhotic patients.Patients and methodsThis single-arm, prospective trial, conducted at two hospitals in Belgium and Egypt, included patients admitted to the emergency room with hematemesis and/or melena and known or suspected liver cirrhosis. All patients received urgent hemodynamic stabilization, octreotide (50 mcg bolus then 25 mcg/hour for 24 hours) and intravenous ceftriaxone (1 g/hour). Endoscopy to confirm AVB and Hemospray® application (if indicated) was performed within six hours of admission. Patients were kept under observation for 24 hours and underwent second endoscopy and definitive therapy (band ligation and/or cyanoacrylate injection in cases of gastric varices) the next day.ResultsThirty-eight patients were admitted for suspected AVB, and 30 of these had confirmed AVB (70% male; mean age 59.5 years (range, 32.0-73 years)). Child-Pugh class C liver disease was present in 53.4%. Esophageal varices were observed in 83.4% of patients, gastric varices in 10%, and duodenal varices in 6.6%. Spurting bleeding at the time of endoscopy was observed in 43.4%. One patient developed hematemesis six hours after Hemospray® application and underwent emergency endoscopic band ligation. No major adverse events or mortalities were observed during 15-day follow-up.ConclusionHemospray® application was safe and effective at short-term follow-up for emergency treatment of AVB in cirrhotic patients.
| S-EPMC4480536 | biostudies-literature
Project description:This study investigated the impact of partial splenic embolization (PSE) on portal hypertensive gastropathy (PHG). We retrospectively analyzed endoscopic findings and the portal venous system of 31 cirrhotic patients with PHG. The improved group was defined as the amelioration of PHG findings using the McCormack classification. Child-Pugh scores of the improved group (18 of 31 patients) were significantly lower compared with those of the non-improved group (p = 0.018). The changes in the diameters of the portal trunk and those of the spleno-portal junction and spleen hilum in the splenic vein of the improved group were significantly larger than those of the non-improved group (p = 0.007, p = 0.025, and p = 0.003, respectively). The changes in the diameters of the portal vein and splenic hilum of the splenic vein showed significant correlations with Child-Pugh score (r = 0.386, p = 0.039; r = 0.510, p = 0.004). In a multivariate analysis of baseline factors related to the improved group, Child-Pugh grade A was significantly associated with the improvement of PHG (odds ratio 6.875, p = 0.033). PSE could be useful for PHG, especially in patients with Child-Pugh grade A, at least in the short term.
| S-EPMC10094775 | biostudies-literature
Project description: Not available
| S-EPMC6317971 | biostudies-literature
Project description:Mucosal apoptosis has been demonstrated to be an essential pathological feature in portal hypertensive gastropathy (PHG). p53-upregulated modulator of apoptosis (PUMA) was identified as a BH3-only Bcl-2 family protein that has an essential role in apoptosis induced by a variety of stimuli, including endoplasmic reticulum (ER) stress. However, whether PUMA is involved in mucosal apoptosis in PHG remains unclear, and whether PUMA induces PHG by mediating ER stress remains unknown. The aim of the study is to investigate whether PUMA is involved in PHG by mediating ER stress apoptotic signaling. To identify whether PUMA is involved in PHG by mediating ER stress, gastric mucosal injury and apoptosis were studied in both PHG patients and PHG animal models using PUMA knockout (PUMA-KO) and PUMA wild-type (PUMA-WT) mice. The induction of PUMA expression and ER stress signaling were investigated, and the mechanisms of PUMA-mediated apoptosis were analyzed. GES-1 and SGC7901 cell lines were used to further identify whether PUMA-mediated apoptosis was induced by ER stress in vitro. Epithelial apoptosis and PUMA were markedly induced in the gastric mucosa of PHG patients and mouse PHG models. ER stress had a potent role in the induction of PUMA and apoptosis in PHG models, and the apoptosis was obviously attenuated in PUMA-KO mice. Although the targeted deletion of PUMA did not affect ER stress, mitochondrial apoptotic signaling was downregulated in mice. Meanwhile, PUMA knockdown significantly ameliorated ER stress-induced mitochondria-dependent apoptosis in vitro. These results indicate that PUMA mediates ER stress-induced mucosal epithelial apoptosis through the mitochondrial apoptotic pathway in PHG, and that PUMA is a potentially therapeutic target for PHG.
| S-EPMC3973242 | biostudies-other
Project description: Not available
| S-EPMC7332663 | biostudies-literature
Project description:OBJECTIVES:The objective of this study was to determine the incidence and risk factors associated with new-onset and worsening portal hypertensive gastropathy (PHG) in patients with chronic hepatitis C (CHC). METHODS:A total of 831 CHC patients with bridging fibrosis or cirrhosis at the time of entry were prospectively monitored for clinical and histological liver disease progression while receiving either low-dose peginterferon ?2a or no antiviral therapy in the HALT-C (Hepatitis C Antiviral Long-term Treatment against Cirrhosis) trial. Upper endoscopy with grading of PHG was performed at baseline and at year 4 of the study. The presence and severity of PHG were determined using the NIEC (New Italian Endoscopy Conference) criteria, and worsening PHG was defined as a score increase of ?1 point. RESULTS:During a median follow-up of 3.85 years, 50% of 514 subjects without PHG developed new-onset PHG, whereas 26% of 317 patients with baseline PHG had worsening PHG. Independent predictors of new-onset PHG included higher alkaline phosphatase and being diabetic, whereas predictors of worsening PHG were Caucasian race, lower albumin, as well as higher serum aspartate transaminase/alanine transaminase ratio and homeostatic model assessment levels. New-onset and worsening PHG were significantly associated with clinical and histological progression. They were also associated with new-onset and worsening gastroesophageal varices. CONCLUSIONS:New-onset and worsening PHG develop at a rate of 12.9% per year and 6.7% per year, respectively, in non-responder CHC patients with advanced fibrosis. If confirmed in other studies, endoscopic surveillance for PHG may need to be tailored to individual patient risk factors.
| S-EPMC3772514 | biostudies-literature
Project description:BackgroundPortal 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.MethodsWe 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.ResultsLFQ analyses identified 423 significantly differentially expressed proteins. 17 proteins that significantly elevated in the gastric mucosa of PHG patients were further validated using PRM.ConclusionsThis 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).
| S-EPMC8111717 | biostudies-literature