Hypertensive Gastropathy Research Articles

1958 An Unusual Ca(u)se of Upper Gastrointestinal Bleeding

INTRODUCTION: Duodenal varices (DVs) represent 17% of ectopic varices (EVs), have a 4-fold increased bleeding risk when compared to esophago-gastric varices (EGVs), and mortality rate up to 40%. There are no guidelines on the ideal management of DVs. We report a case of massive hemorrhage secondary to DV managed successfully with transjugular intrahepatic portosystemic shunt (TIPS). CASE DESCRIPTION/METHODS: A 69-year-old gentleman presented with hematemesis, hematochezia, dizziness and near-syncope. He was diagnosed with cryptogenic cirrhosis, non-alcoholic steatohepatitis in the past after negative autoimmune and infectious work-up. Prior doppler ultrasound showed elevated portal flow velocity; esophagogastroduodenoscopy (EGD) a month prior revealed portal hypertensive gastropathy (PHG) but no EGVs, and normal duodenum. Given prior hepatic encephalopathy, TIPS was not performed. He had abdominal surgeries in the past. He was hemodynamically unstable with benign abdominal exam. Labs revealed acute blood loss anemia with Hgb 9.1 (baseline 13), thrombocytopenia and coagulopathy. Following initial resuscitation with fluids, blood products, octreotide and pantoprazole infusion, urgent EGD was performed. There were no EGVs, but features of diffuse PHG, as well as a compressible mucosal bulge with a nipple sign representing a varix in the second portion of the duodenum were seen. Given the insufficient evidence to support endoscopic therapy in ectopic varices, interventional radiology was consulted. CT angiogram demonstrated patent portosystemic veins. TIPS was performed with a decrease in portal gradient from 16 to 2 mmHg. Rifaximin, lactulose and zinc were commenced. He remained hemodynamically stable following this and did not require further intervention. A year later, he remains free of further bleeding episodes or hepatic encephalopathy. DISCUSSION: Bleeding DVs are rare and potentially life-threatening. Diagnosis should be suspected in all cases of gastrointestinal hemorrhage, particularly in the absence of EGV or another source. Standard management has not yet been established. TIPS is a relatively safe and effective means of controlling acute DV bleeding. EVs may re-bleed despite a reduction of portosystemic pressure gradient < 12 mmHg or by 25–50% of baseline; hence the “12 mmHg rule” does not apply. Our patient recovered successfully following TIPS without needing additional therapy. Reducing the pressure gradient to very low values can result in successful outcomes with TIPS in DVs.

3127 Blakemore? Wait More!

INTRODUCTION: This is a case of a decompensated cirrhotic patient with a non-variceal upper GI bleed that was nearly treated with placement of a Sengstaken-Blakemore tube, which would likely have perforated her acutely ischemic esophagus. CASE DESCRIPTION/METHODS: A 62-year-old woman with decompensated alcoholic cirrhosis and a history of esophageal varices was brought to the ED for “coffee ground” emesis and lethargy. She relapsed into drinking alcohol two weeks before presentation and shortly thereafter developed abdominal pain. Three days before admission, she developed non-bloody emesis. On the day of presentation she had at least 10 episodes of clear emesis that eventually turned black. She had a history of esophageal varices requiring banding, most recently 5 years prior to admission. Her most recent EGD was 3 years ago, which was significant for portal hypertensive gastropathy and small varices that did not require banding. Initial vital signs were significant for a HR of 110 and BP of 77/37. Abdominal exam demonstrated normoactive bowel sounds, diffuse tenderness to palpation, no guarding, and no rebound tenderness. In the ED, patient had at least 2000 cc of “coffee ground” emesis and she was intubated for airway protection. Placement of a Blakemore tube was considered but ultimately decided against given that observed emesis was not bright red and emergent endoscopy would soon be performed. Initial labs were significant for: Hgb 14.4 platelets 106 lactate 24 pH 6.9 INR 1.5 creatinine 3.4 total bilirubin 2.8 AST 281 ALT 168. Emergent EGD in the MICU revealed no esophageal or gastric varices, however severe erosive esophagitis and acute esophageal necrosis with a “black esophagus.” Patient underwent a chest CT and cardiothoracic surgery consultation. After a brief stay in the MICU with supportive care, patient was ultimately extubated, her diet cautiously advanced and she was discharged to home. DISCUSSION: This case illustrates the need to think critically about the etiology of a brisk GI bleed, as not all significant GI bleeds in cirrhotic patients are related to varices. A clinical clue indicating that this may not have been an active variceal bleed was that the large-volume emesis was coagulated rather than fresh blood. Furthermore, the objective data reflected a state of severe hypovolemia and ischemia but no anemia in spite of recurrent hematemesis. Placement of a Blakemore tube in the setting of acute esophageal necrosis could have resulted in a catastrophic outcome of esophageal rupture.

3007 Santorinirrhage Due to Hemosuccus Pancreaticus as a Rare Manifestation of Upper Gastrointestinal Bleeding

INTRODUCTION: Hemosuccus pancreaticus (HP), bleeding from the pancreatic duct into the gastrointestinal (GI) tract via ampulla of vater, is extremely rare. Some causes include pancreatitis, pseudoaneurysm of the peri-pancreatic vessels, or malignancy. The rarity with which this condition is encountered makes HP difficult to diagnose. We present a case of HP with bleeding from the minor duodenal papilla from a pancreatic pseudocyst. CASE DESCRIPTION/METHODS: A 39-year-old male with alcohol use disorder and chronic pancreatitis presented to the hospital with complaints of abdominal pain and melena. Labs showed significant anemia: hemoglobin, 6.90 g/dL. He was admitted for blood transfusions and further investigation. Endoscopic evaluation showed portal hypertension gastropathy, without evidence of gross bleeding. CT abdominal scan showed cystic lesions at the pancreatic tail and within the pancreatic body (Figure 1). Endoscopic ultrasound fine needle aspiration biopsy of the cystic lesion was done. Fluid analysis was consistent with pancreatic pseudocyst with elevated amylase. He was discharged home in stable condition with gastroenterology follow-up. He returned to the hospital with recurrent episodes of melena and transfusion-dependent anemia. He had IR guided transjugular intrahepatic portosystemic shunt from right hepatic vein to right portal vein. He continued to have episodes of melena with new coffee-ground hematemesis. Repeat endoscopy was performed with frank bleeding noted from the minor duodenal papilla (Figure 2). MRI was unable to confirm pancreas divisum due to pancreatic atrophy and poor visualization of the pancreatic duct. CT abdominal scan now showed hemorrhage within the two pancreatic cysts. Mesenteric angiogram was performed which showed pseudoaneurysm off proximal splenic artery and gastroepiploic artery both of which were embolized (Figure 3). His abdominal distension and pain improved significantly after the procedure with no more episodes of melena or hematemesis. He was discharged home without recurrence of symptoms. DISCUSSION: Our case illustrates the diagnostic dilemma of obscure upper GI bleeding. HP with bleeding from the duct of Santorini has been reported twice. All hemodynamically stable patients with HP should undergo endoscopic, radiographic, and angiographic evaluation. Therapeutic options consist of selective embolization or surgery. A multidisciplinary team approach with a precise protocol is paramount to drastically reduce the mortality and morbidity of patients.

1970 Spontaneous Page Kidney as a Cause of Gastric Variceal Bleed

INTRODUCTION: Gastric variceal bleeding occurs in 15–50% of patients with non-cirrhotic portal venous thrombosis but can also occur in cases of splenic vein thrombosis (SVT) due to the formation of isolated gastric varices (IGV). We present the first reported case of a page kidney causing splenic vein compression, thrombosis, and subsequent gastric variceal bleeding. CASE DESCRIPTION/METHODS: A 31-year-old stuntman presented with epigastric pain and worsening exertional dyspnea over 3 weeks. History was notable for melena and anemia with no reported ulcers on endoscopy. On admission, he had hemoglobin of 4.1 g/dl with severe iron deficiency and elevated reticulocyte count. There was no serologic evidence of hepatic or renal disease. A computed tomography (CT scan) of the abdomen revealed a large left-sided perirenal collection consistent with page kidney, splenomegaly and decreased caliber of the mid and distal splenic vein suggestive of nonocclusive SVT. His liver was normal. Initial endoscopy revealed an IGV type 1 and mild portal hypertensive gastropathy (Figure 1). CT angiography did not reveal a splenorenal shunt to pursue a balloon retrograde transvenous obliteration (BRTO). While admitted, he developed hematemesis and worsening anemia. Ultimately, underwent IR splenic vein stenting with a bare-metal stent and subsequent decompression of the gastric varices with brisk flow of the portal vasculature (Figure 2). DISCUSSION: Gastric varices are classified primarily by location with most involving the gastroesophageal junction due to portal hypertension. The incidence of bleeding is highest in IGV, typically associated with SVT. Common etiologies of SVT include pancreatitis, malignancy or trauma. Our case described an extrinsic splenic vein compression and subsequent thrombosis due to a sub-capsular renal hematoma possibly of unclear etiology. Treatment for GV often depends on local expertise, but commonly consists of cyanoacrylate injection, banding (especially in type 1 gastro-esophageal varices), transjugular intrahepatic portosystemic shunt (TIPS) placement, BRTO, and even splenectomy. More recently, in cases of IGV due to isolated SVT, splenic vein stenting has been increasingly utilized. In our case, TIPS would not address the pre-hepatic portal hypertension and cyanoacrylate was not available. Splenic vein stenting was thus chosen to decompress the IGV with excellent response seen on subsequent follow-up (Figure 1).

The Efficacy of Argon Plasma Coagulation versus Carvedilol for Treatment of Portal Hypertensive Gastropathy

Background/Aim: Several treatment options have been developed for portal hypertensive gastropathy (PHG); medications and endoscopic management. The aim of this study was to evaluate the efficacy and safety of argon plasma coagulation (APC) versus Carvedilol in treatment of a cohort of Egyptian patients with severe PHG. Methods: A total of 130 patients with severe PHG were enrolled; 10 patients were excluded due to death and failure to complete the treatment sessions accordingly, 120 patients were included. Patients were divided into 2 groups: Group A (n = 52) treated with APC; Group B (n = 68) treated with oral Carvedilol. Success was defined as stabilization of hemoglobin (Hb) over 100 g/dL or Hb increase >10% from pretreatment level and reduction of blood transfusion requirements over the following 3 months after the start of therapy. Upper gastrointestinal endoscopy was performed to assess the degree and site of PHG. APC was conducted to areas with mucosal ectatic vascular lesions. Results: PHG was mostly fundic (36.35%) in APC group and (36.76%) in Carvedilol group (p = 0.56). Throughout follow-up period, there was significant increase in Hb level, serum iron, and serum ferritin with a significant decrease in total iron-binding capacity (TIBC) in APC group as compared to Carvedilol group (p < 0.001). Additionally, there was gradual increase in the mean Hb, serum iron, and serum ferritin and gradual decrease of TIBC in Carvedilol group. Accordingly, there was an overall improvement of iron deficiency anemia (IDA) in both groups; however, it was significantly better in APC group than in Carvedilol group. No major adverse events were detected in both the groups. Conclusion: APC significantly improves IDA and decreases transfusion requirements in patients with severe PHG as compared to oral Carvedilol with small risk of adverse events. Furthermore, the combination of APC and Carvedilol unless contraindicated could have a synergistic effect in controlling severe PHG.

Pediatric non-cirrhotic portal fibrosis: role of endoscopic management in determining long-term outcome.

Non-cirrhotic portal fibrosis (NCPF) is a rare cause of pediatric portal hypertension. There is abundant literature in adults but paucity of data in children. We aimed to evaluate and compare the endoscopic and long-term outcomes of children with NCPF. Consecutive children (≤ 18years) diagnosed with NCPF evaluated for clinical and endoscopic profile and outcome. The cohort underwent 3weekly endoscopic sessions until esophageal variceal eradication followed by 6-12monthly endoscopic surveillance. Non-bleeders and bleeders were compared for endoscopic outcome. Forty-five NCPF children with median age of 14.5 (6-18) years and symptom duration 12 (1-120) months presented with spleen-related issues (78%), esophageal varices (96%), primary gastric varices (56%), and portal hypertensive gastropathy (89%). Thirty-three patients undergoing endotherapy (secondary prophylaxis n = 22, primary prophylaxis n = 11) showed primary eradication of varices after 5 (2-12) sessions. 36% showed recurrence of esophageal varices in 11 (6-42) months and secondary gastric varices developed in 12%. Overall 87% patients required endoscopic intervention at onset or follow-up. Poor outcome was observed in ten patients (n = 9 bleeders). Three children died of variceal bleeding before endoscopic eradication of esophageal varices. Three developed decompensation after a median follow-up of 48 (3-120) months and referred for liver transplantation. Four patients required surgery for portal hypertension. Overall, endoscopic outcome of NCPF is favorable. One-third patients have recurrence of esophageal varices. Small proportion of bleeders have poor outcome.

Prevalence of Portal Hypertensive Gastropathy in Chronic Liver Disease and Correlation with the Severity of Liver disease.

BackgroundPortal hypertensive gastropathy (PHG) is an underappreciated condition in patients with chronic liver disease (CLD). It is a common endoscopic finding in CLD patients, but its relation with esophageal varices (EV) and the severity of the liver disease is controversial. Herein, we aimed to study the prevalence of PHG in CLD patients and to determine its association with EV and the severity of the liver disease.MethodsThis descriptive, cross-sectional, analytical study was conducted at the Hepatology department, Bir Hospital Kathmandu from 19th March to 30th June 2019. A total of 404 patients with CLD of various etiology fulfilling the inclusion criteria were approached, and informed consent was taken before enrolling in the study. All patients underwent EGD, and the findings related to EV and PHG were noted. The severity of PHG was graded according to the McCormack classification and EV were graded according to the American Association for the study of liver diseases guideline. The severity of liver disease was stratified based on Child-Pugh class and Model for End-Stage Liver Disease (MELD score). Data was entered on Statistical Package for the Social Sciences (SPSS) Version 25 for further analysis.ResultsOf 404 CLD patients, the mean (±SD) age was 49.14 (±10.5) years. Portal hypertensive gastropathy was observed in 269 (66.6%) patients, of which 80.6% (217) had mild PHG while 19.4% (52) had severe PHG. EV were present in 362 (89.6%) patients. One hundred and thirty-two (36.5%) had small EV, and 230 (63.5%) had large EV. No significant association was observed between grades of gastropathy and size of varices (p = 0.36). There was a non-significant association with the MELD score and other biochemical parameters. However, there were significant associations between Child-Pugh class and PHG and Child-Pugh class and PHG severity, p = 0.001 and p = 0.01 (p <0.05), respectively.ConclusionsIn our study, the prevalence of PHG in the Nepalese population in CLD is 66.6 %. PHG is significantly associated with the severity of CLD in terms of Child-Pugh class but not associated with MELD. Also, no association has been found with the size of varices.

IL-6-Driven FasL Promotes Nf-κBp65/PUMA-Mediated Apoptosis in Portal Hypertensive Gastropathy

Background: Mucosal epithelial apoptosis with non-specific inflammation is an essential pathological characteristic in portal hypertensive gastropathy (PHG). However, whether a coordinated crosstalk between myeloid cells and epithelial cells involved in PHG remains unclear. Methods: Gastric injury and mucosal apoptosis were examined in patients with PHG and the PHG model of p65ΔM/ΔM (myeloid cells specific NF-κBp65 deletion) and p65f/f (floxed p65) mice, PUMA-WT (PUMA wild-type) and PUMA-KO (PUMA knockout) mice. The interaction of IL-6, Fas, FasL, NF-κBp65 and PUMA expression was investigated, and the mechanisms underlying IL-6-regulated gastric epithelial apoptosis were analysed. Findings: IL-6, which is induced in the mucosa of PHG patients and mice, promotes FasL production via enhancing NF-κBp65 activation in myeloid cells, while blockage of IL-6 signaling by Tocilizumab or deletion of NF-κBp65 in myeloid cells attenuates the inflammatory response and Fas/FasL-mediated epithelial apoptosis in PHG. IL-6-driven FasL from myeloid cells combines with epithelial Fas receptor to encourage NF-κBp65/PUMA-mediated epithelial apoptosis in PHG, and inhibition of NF-κBp65 or knockout of PUMA dramatically alleviates Fas/FasL network-mediated epithelial apoptosis in PHG. Interpretation: These results indicate that IL-6 drives FasL generation via NF-κBp65 in myeloid cells to promote Fas/NF-κBp65/PUMA-mediated epithelial apoptosis in PHG. Funding: This work was supported by grants from the National Natural Science Foundation of China (U1501224, 81700536), the Natural Science Foundation Team Project of Guangdong Province (2018B03031200), the Science and Technology Developmental Special Foundation of Guangdong Province (2017B020226003), the Basic Research Programme of Young Teachers' Training Project of Sun Yat-sen University (17ykpy51), the Science and Technology Planning Projects of Guangzhou City (201604020118, 201604020002). Declaration of Interest: The authors declare that there are no conflicts of interest. Ethical Approval: The study protocol and the acquisition of the tissue samples were approved by the Institutional Review Board of The Third Affiliated Hospital of Sun Yat-Sen University.

Hemolytic Anemia following Stent-Graft Transjugular Intrahepatic Portosystemic Shunt Creation.

Transjugular intrahepatic portosystemic shunt (TIPS) creation is a minimally invasive technique aimed at managing the complications of portal hypertension. Initially performed in the setting of variceal bleeding, the role of TIPS has expanded to treatment of medically refractory ascites, portal hypertensive gastropathy, hepatic hydrothorax, Budd-Chiari syndrome, portal vein thrombus, and hepatorenal syndrome. Potential complications from TIPS are well documented, and include hepatic encephalopathy, hepatic failure, and TIPS dysfunction. Hemolytic anemia is a lesser known complication related to TIPS creation. In this article, a case of hemolytic anemia following TIPS creation using a Viatorr stent-graft in described.

Five-year-term results in cirrhotics without varices, either affected or not by portal hypertensive gastropathy.

Information is lacking on the appearance of varices in cirrhotics, either affected or not by portal hypertensive gastropathy (PHG). We assessed whether the absence or presence and the grade of PHG influenced the development of varices in cirrhotics without varices over time. Forty cirrhotics without varices affected or not by PHG at baseline underwent follow-up endoscopy after 5 years. One-tailed t-test and the χ-test were used to evaluate variable comparison and the presence of associations. Multivariate logistic regression analysis and the analysis of variance test were carried out to compare the variables and identify predictors of varices. The Child-Pugh score at baseline and after 5 years was significantly different (5.72±0.98 vs. 6.25±1.67, P<0.001). After 5 years, 10 (25%) cirrhotics were affected by varices, whereas 30 (75%) patients remained without varices. PHG was associated significantly with varices (P=0.001), proving to be a significant predictive independent factor for their development over time (F=4.765, significant=0.004; analysis of variance test, P<0.001). A link between the duration of PHG and the development of varices is likely. An early therapeutic management of PHG might delay the development of varices in cirrhotics.

Utility of histology for the diagnosis of portal hypertensive gastroenteropathy. Concordance between the endoscopic image and gastrointestinal biopsies. Role of the CD34 marker

Abstract Introduction Upper gastroscopy in patients with cirrhosis often reveals non-specific lesions, which are usually oriented as portal hypertensive gastropathy (PHG). However, the diagnosis of PHG can be difficult, both from an endoscopic and histological point of view. The study of CD34 expression, which enhances the endothelial cells of the microvasculature, could help the differential diagnosis. The objectives of this study were to evaluate the correlation between endoscopy and histology in the diagnosis of PHG and to assess the utility of CD34 in the diagnosis of PHG. Material and methods The results of immunostaining with CD34 gastric fundus biopsies from 100 cirrhotic patients and 20 controls were compared with the endoscopic images. Results The correlation between the histology and the endoscopic diagnosis of PHG was very low (kappa = 0.15). In addition, the measurement of the diameter of the gastric vessels enhanced by the use of immunohistochemical staining (CD34) did not show good correlation with the endoscopic diagnosis (p = 0.26) and did not provide relevant information for the histological diagnosis of PHG either. Discussion The correlation between histology and endoscopy is low for the diagnosis of PHG. The use of immunostaining for CD34 does not seem to improve the diagnostic yield of the histological study.

Predictive and Prognostic Value of Von Willebrand Factor in Patients with Cirrhosis and Esophageal Varices

Background and study aim: Von Willebrand factor (vWF) is released by activated endothelial cells and plays a crucial role in the development of portal hypertension. vWF levels correlate with liver function and venous hepatic pressure gradient (VHPG) and independently predict clinical outcome. The aim was to evaluate serum vWF levels as a predictor for esophageal varices and prognosis in patients with liver cirrhosis. Patients and Methods: Sixty two patients with liver cirrhosis, divided into two groups according to presence (group I) or absence (group II) of varices were included, In addition, twenty healthy persons served as control group (group III). All patients were submitted to full history taking, clinical examination, laboratory investigations and abdominal ultrasonography. The severity of liver disease was estimated by Modified Child-Pugh and Model for End Stage Liver Disease (MELD) scores. All patients were underwent upper gastrointestinal endoscopy and vWF assay. Results: vWF values were significantly higher in group I (p1=0.001), than controls (p2=0.000), but no significant difference between group II and control group (p3= 0.59). Receiver operating characteristics (ROC) curve analysis of vWF revealed that, vWF at cutoff value of 173.8 µg/ml; the sensitivity for detection of esophageal varices was 80.8%, specificity 76.0%, positive predictive value (PPV) was 93.9%, negative predictive value (NPV) was 55.6%; area under the curve was 86.6.There was significant positive correlation between vWF and Child, MELD, esophageal varices grade and severity of portal hypertensive gastropathy. Conclusion: vWF is a good predictor for development of esophageal varices and correlated well with prognosis in patients with cirrhosis.

Long-term outcome of endoscopic variceal band ligation of esophageal varices in patients with chronic liver disease.

There are scanty data on the long-term outcome of endoscopic variceal band ligation (EVL) for esophageal varices. Adult patients suffering from a chronic liver disease (CLD) undergoing EVL of esophageal varices of grade 2 and above between January 2006 andDecember 2015 were followed upfor the recurrence of varices, worsening of portal hypertensive gastropathy (PHG), rebleeding, and mortality. EVL was done as primary prophylaxis of bleeding in 72 and as secondary prophylaxis in 175 patients. All received propranolol after EVL if there was no contraindication. Two hundred and forty-seven CLD patients (mean age 51.83 ± 11.28years, 179 males) underwent 306 EVL sessions. The most common etiology was alcohol (53%). Sixty-eight percent of patients had grade 3 esophageal varices 76.5%had PHG. There was no immediate post-EVL bleeding or 30-day mortality. Variceal obliteration was achieved in 100% with 19% recurrence within amean period of53.74 ± 27.2months. PHG worsened in 49.7%. Overall, rebleeding occurred in 13.8%, 4.3% from recurrent varices. There was no difference in variceal recurrence (16.7% vs. 20%) and incidence of rebleeding (9.7% vs. 13.7%) between patients undergoing EVL for primary and secondary prophylaxis. Cumulative rebleeding rates after 1, 5, and 9years were 1.6%, 9.2%, and 11.4%, respectively. The overall mortality was 85%, mostly from progressive CLD, and only 8.6% was due to rebleeding. On subgroup analysis, the factors significantly associated with rebleeding was Child-Pugh class C and worsened PHG those with mortality were alcohol and Child-Pugh class C. EVL is effective in the long-term for both primary and secondary prophylaxis of esophageal variceal bleeding.

Outcome of Esophageal Variceal Ligation in Cirrhotic Patients: Experience in a Tertiary Care Hospital in Dhaka

Background: Bleeding from esophageal varices in cirrhosis is an emergency condition. Esophageal varices band ligation has shown better results in terms of variceal obliteration as well as having fewer side effects like ulceration, perforation and stricture formation.&#x0D; Methods: This observational study was conducted at the gastroenterology department of BIRDEM general hospital, from September 2014 to March 2015. Subjects were eligible if they had a diagnosis of cirrhosis based on history, physical examination, biochemical parameters and presence of esophageal varices in upper gastrointestinal endoscopy. All patients were tested to determine the cause of liver cirrhosis. All patients under-went upper gastrointestinal endoscopy after consent. Esophageal variceal ligation was done at appropriate situation and patients were followed up later on. SPSS 23 was used for statistical analysis.&#x0D; Results: The sample size was 69. The cumulative mean age was 55.58±14.462 years (range: 20-90), with gender-based mean age of 54.76±15.704 years for males and 57.22±11.739 years for female. Mild portal hypertensive gastropathy (PHG) was found 31 (44.9%) patient and severe PHG 36 (52.2%). Patients were followed up for mean period of 8.52±3.6 months. Variceal obliteration was achieved in 25 (36.2%) patients, while 06 (8.7%) cases developed re-bleeding during the study period and this type of patients were managed by other modalities or combination therapies. Recurrence of varices occurred in 13 (18.8%). 25 (36.2%) patients reduction of varix size occured after esophageal variceal ligation (EVL), 32 (46.4%) required second session and 12 (17.4%) required more than second session (Table-2). Thirty nine (56.5%) patients experienced minor adverse events like GI discomfort (retrosternal pain or dysphagia), while severe adverse events were noticed in 13 (18.8%) patients. Fundal varix was found among 8 (11.6%) patient on follow up endoscopy and GAVE found in 6 (8.69%) patients. All patient developed PHG during follow up endoscopy.&#x0D; Conclusion: Band ligation eradicates esophageal varices with less complications and a lower re-bleeding rate, but at the same time eradication is associated with more frequent development of PHG and fundal varices.&#x0D; Birdem Med J 2019; 9(1): 63-69

High prevalence of asymptomatic peptic ulcers diagnosed during screening endoscopy in patients with cirrhosis.

Background:Peptic ulcer disease (PUD) is more prevalent in cirrhotics and this may aggravate prognosis. We investigated the prevalence of PUD in cirrhotics and its potential association with Helicobacter pylori (H. pylori) infection, the underlying etiology and severity of liver disease, and other manifestations of portal hypertension (PH).Methods:We enrolled consecutive asymptomatic cirrhotic patients who underwent screening endoscopy in a tertiary hospital during a 12-month period. We recorded the presence of PUD and the endoscopic findings associated with PH. H. pylori infection was documented through either histology or CLO-test. The diagnosis of cirrhosis was based on elastography, liver biopsy or a combination of clinical, biochemical and imaging data.Results:One hundred patients (M/F: 54/46, mean age: 61±14 years) were included in the analysis. Viral hepatitis (37%) and alcohol (22%) were the most common causes of cirrhosis. Child-Pugh stage was A/B/C: 60/35/5. PUD was found in 19 patients (14 gastric, 5 duodenal). H. pylori infection was diagnosed in 54%. Varices were detected in 59% (39% needed treatment). PH gastropathy was present in 81% (severe in 33%). The presence of PUD was unrelated to the etiology and the severity of liver disease or to other endoscopic manifestations of PH. No correlation was found between PUD and H. pylori infection.Conclusions:A high prevalence of PUD was observed in our cirrhotic patients, although they were asymptomatic and had no known risk factors of ulcerogenicity. The value of screening endoscopy for the early diagnosis and treatment of PUD in cirrhotics deserves further investigation.

The role of portal congestion index in prediction of esophageal varices in hepatitis C virus-infected patients

Objective To assess the role of portal congestion index (PCI) in prediction of esophageal varices (EV) in hepatitis C virus (HCV)-infected patients. Background Portal hypertension (PH) often develops in HCV-infected patients. EV rupture leads to variceal bleeding, the most lethal complication of cirrhosis. Duplex Doppler ultrasonography of portal vein is a noninvasive method to assess blood flow velocity and portal vein cross-sectional area as a parameter for PH. Patients and methods This study was conducted on 200 HCV-infected patients (116 with EV and 84 without EV). Patients were subjected to complete blood picture, liver and kidney functions, serum electrolytes, viral markers, abdominal ultrasonography, upper gastrointestinal tract endoscopy, and duplex Doppler evaluation of portal vein with calculation of PCI. Results There was a highly significant difference between HCV-infected patients with and without EV regarding PCI (P = 0.0001). At cutoff point of PCI 0.11, the sensitivity, specificity, and accuracy to predict EV were 93, 85.7, and 90%, respectively, with area under the curve 0.889. There was a statistically highly significant positive correlation between PCI and presence of fundal varices and PH gastropathy (P = 0.0001). There was a statistically significant positive correlation between PCI and grades of EV (P = 0.012). Conclusion PCI is useful as a noninvasive predictor of EV in HCV-infected patients.

Expression of Vascular Endothelial Growth Factor in the Gastric Mucosa of Patients with Portal Hypertensive Gastropathy

Background and study aim: Portal hypertensive gastropathy (PHG) is a common finding in patients with cirrhosis and portal hypertension that occurs in between 7% and 98% of cases. High levels of vascular endothelial growth factor (VEGF) in mesentery suggested their contribution in portal hypertension secondary to liver cirrhosis. VEGF participates in regulation of angiogenesis in gastric wall in portal hypertension. The aim was to evaluate the serum concentration of VEGF and gastric mucosal expression of VEGF and its possible association with PHG. Patients and Methods: Serum levels and gastric mucosal expression of VEGF were measured in fifty seven patients with liver cirrhosis and portal hypertensive gastropathy as well as eleven patients with liver cirrhosis without portal hypertensive gastropathy and another twenty one persons served as control group. They were clinically assessed and laboratory investigations were done including liver biochemical profile, and viral markers. Severity of liver disease was assessed by Child-Pugh, model for end stage liver disease (MELD) and updated (uMELD) scores. The presence of PHG was diagnosed by esophago-gastroduodenoscopy. Results: Serum VEGF increased in patients with liver cirrhosis compared to healthy control. But there was no significant difference between patients with PHG and patients without PHG as regard to serum VEGF.VEGF expression in the gastric mucosa was highly significant in patients with PHG than patients without PHG and control group. Serum VEGF has no correlation with severity of liver disease or PHG grade. Conclusion: VEGF was highly expressed in gastric mucosa rather than elevation of serum VEGF in patients with PHG.

Lowering hepatic venous pressure agent carvedilol versus variceal banding ligation for clinical outcomes of cirrhotic portal hypertension.

ObjectiveCarvedilol is nonselective beta-blocker with a mild anti-alpha-1-adrenergic effect. Several studies proposed improved hemodynamic effects of carvedilol compared with propanolol. Our study was to perform a systematic review and meta-analysis of randomized control trials comparing carvedilol with variceal banding ligation (VBL).MethodsStudies were searched on online databases MEDLINE, EMBASE(Ovid), the Cochrane Library, Chinese Wanfang Database, and China National Knowledge Infrastructure between January 2000 and May 2018. Incidence of bleeding and mortality were main outcome measures. Subgroup analysis and sensitivity analysis were conducted to ensure the robustness of pooled estimates.ResultsTen randomized control trials including 1,269 cirrhotic patients were chosen. Compared with VBL, carvedilol showed similar preventive efficacy of risk ratios (RRs) in variceal bleeding, and bleeding-related mortality over different follow-up periods from 6 months to 24 months. Also, significant differences between carvedilol and VBL in overall mortality and other causes of mortality were failed to be found. Carvedilol achieved a lower incidence of portal hypertension gastropathy in both 6 months (RR=0.49, 95% CI: 0.38–0.64, P<0.00001) and 12 months (RR=0.35, 95% CI: 0.26–0.47, P<0.00001). Two trials compared combination of carvedilol and VBL with VBL alone; however, the results failed to find an improved preventive efficacy of bleeding (RR=0.71, 95% CI: 0.15–3.30, P=0.67).ConclusionCarvedilol is equivalent to invasive VBL for variceal bleeding prevention. It can be well tolerated and may be of benefit to portal hypertension gastropathy. However, available data during 24 months follow-up did not support a potential advantage of carvedilol for prognosis as a lowering hepatic venous pressure agent.

Utilidad de la histología para el diagnóstico de la gastroenteropatía por hipertensión portal. Concordancia entre la imagen endoscópica y las biopsias gastrointestinales. Papel del marcador CD34

IntroductionUpper gastroscopy in patients with cirrhosis often reveals non-specific lesions, which are usually oriented as portal hypertensive gastropathy (PHG). However, the diagnosis of PHG can be difficult, both from an endoscopic and histological point of view. The study of CD34 expression, which enhances the endothelial cells of the microvasculature, could help the differential diagnosis. The objectives of this study were to evaluate the correlation between endoscopy and histology in the diagnosis of PHG and to assess the utility of CD34 in the diagnosis of PHG. Material and methodsThe results of immunostaining with CD34 gastric fundus biopsies from 100 cirrhotic patients and 20 controls were compared with the endoscopic images. ResultsThe correlation between the histology and the endoscopic diagnosis of PHG was very low (kappa=0.15). In addition, the measurement of the diameter of the gastric vessels enhanced by the use of immunohistochemical staining (CD34) did not show good correlation with the endoscopic diagnosis (p=.26) and did not provide relevant information for the histological diagnosis of PHG either. DiscussionThe correlation between histology and endoscopy is low for the diagnosis of PHG. The use of immunostaining for CD34 does not seem to improve the diagnostic yield of the histological study.

Video Capsule Endoscopy in the Assessment of Portal Hypertensive Enteropathy.

Background The features of the portal hypertension enteropathy (PHE) vary from mild mucosal changes to varices with or without bleeding. The prevalence and the development are not fully understood. Aim Our aim is to examine the prevalence and the different manifestations of PHE using video capsule endoscopy (VCE). Methods It is a single center retrospective study of patients with cirrhosis, who had VCE. Based on the published literature, we divided the PHE lesions into vascular lesions and mucosal lesions. Results Of the 100 patients with cirrhosis that had a VCE study, the mean age was 62.82 years. Male gender was predominant (64%), while Caucasians represented 82% of the cohort. The most common etiology of cirrhosis was chronic alcohol abuse followed by chronic hepatitis C virus and nonalcoholic steatohepatitis. VCE detected small bowel lesions in 71% of the patients while the features of PHE were found in 65% from the total cohort. AVMs and inflammatory changes were the most common findings, followed by bleeding. More than 50% of the lesions were vascular in nature. The risk of finding PHE in decompensated cirrhosis is twice that in compensated cirrhosis. Forty-five patients had negative EGD exam for any active bleeding, esophageal varices, portal hypertensive gastropathy, or gastric varices. Of these, 69% had features of PHE in their VCE. Conclusions VCE detected small bowel lesions in 71% of our cohort. There is a high prevalence of PHE in decompensated cirrhosis. Vascular lesions are the most common finding in the small bowel of this population.