Severe Portal Hypertensive Gastropathy Research Articles

Association between Blood Ammonia Level and Severity of Portal Hypertensive Gastropathy in Egyptian Patients with Post Hepatitis C Virus Cirrhosis

Abstract Background Cirrhosis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, characterized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. In most persons, approximately 80 to 90 percent of the liver parenchyma must be destroyed before liver failure is manifested clinically. When complications of cirrhosis occur, they typically are related to impaired hepatic function or actual physical disruption and re organization of the liver parenchyma. Aim of the Work The aim of this study is to assess the correlation between blood ammonia level and severity of PHG (to determine if serum ammonia level could be used as a non invasive predictor for severity of PHG). Also, to find out if there is a causal relationship between blood ammonia level and severity of PHG which encourage trials of ammonia-lowering treatments for the management of severe PHG with a tendency to bleed) Patients and Methods This case control study was conducted upon 100 Egyptian cirrhotic patients attending at Ain Shams University Hospital (gastroenterology and hepatology department) and Kafr –El Sheikh liver center after informed written consent. Results There was a significant difference between studied groups regarding ammonia levels, with a significant increase in serum ammonia level in group 1, group 2 and group 3 versus group 4 (Pvalue ˂ 0.001). There was a significant difference between studied groups regarding haemoglobin, Platelet count, serum albumin, INR, serum bilrirubin (P-value 0.006, ˂0.001, ˂0.001, ˂0.001, ˂0.001, ˂0.001 respectively). There was a significant difference between studied groups regarding SLD (P- value ˂0.001). Splenic longitudinal diameter can be used as a good predictor for OVs. There was a significant difference between studied groups regarding PVD, portal vein flow direction and PVV (P-value ˂0.001, ˂0.001,˂0.001 respectively). There was a significant positive correlation between blood ammonia level and Child Pugh score (P 0.004), PVD (P 0.005) and SLD (P˂0.001), but ammonia has a negative correlation with PVV (P ˂0.001). There was a positive correlation between PHG score and serumammonia level (r0.830, P ˂0.001). Conclusion Blood ammonia levels correlate with the presence, severity, and score of portal hypertensive gastropathy in cirrhosis

Serum Kallistatin Level as a Predictor of Esophageal Varices in Patients of Liver Cirrhosis

Abstract Background Esophageal varices are porto-systemic collaterals resulting from portal hypertension, and considered the most lethal complication of liver cirrhosis so early diagnosis of varices can improve prognosis of liver cirrhosis. Kallistatin a tissue kallikrein-binding protein and a serine proteinase inhibitor (serpin) is mainly formed and secreted in liver and its serum level diminished in liver cirrhosis. It has anti-angiogenic, anti-oxidant, anti-inflammatory and anti-tumor effects. Kallistatin level is believed by many literature to be related to the severity of liver disease. Aim of the Work The aim of this study was to assess the relation between serum kallistatin level and presence of OVs. This study also aimed to evaluate serum kallistatin level as a non-invasive predictor of OVs. Patients and Methods This study was conducted in the Gastro-enterology unit, Internal medicine department, Ain Shams University hospitals &Theodor Bilharz Institute. This is a case control study including 60 cirrhotic patients and 20 healthy. Results There was no significant differences between the studied groups regarding demographic data. There was no significant differences between the studied groups as regards Hb, WBCs, ALT, AST, creatinine and, urea but there was highly significant differences between cirrhotic groups and healthy group in the means of platelet count, serum albumin, serum sodium, total and direct bilirubin but no significant difference between groups I and II. Regarding to prothrombin time, there was highly significant differences between the 3 groups as it was higher in group I more than II more than III. There was also no significant difference between the cirrhotic groups regarding to Child Pugh score, MELD score and portal hypertensive gastropathy (PHG). There were significant differences between the 3 studied groups regarding to the means of splenic diameter and portal vein diameter. Kallistatin level showed significant decrease in both patients with OVs and patients without OVs vs. healthy individuals and there was highly significant difference between patients with OVs and patients without OVs. The level of Kallistatin concentration is not correlated with size of varices or risky signs suggesting that Kallistatin level can predict presence of O.V but it can’t reflect the size and severity of varices. There was no significant correlation between serum level of Kallistatin and age, gender and smoking. There was positive correlation to hemoglobin, platelet count, albumin level and negative correlation with PT, INR and urea. There was positive correlation to portal hypertensive gastropathy (PHG) and negative correlation with MELD score and portal vein diameter. Conclusion Serum level of Kallistatin level may express the degree of liver dysfunction. It is correlated with presence of O.V but not correlate to size or risky signs of OVs suggesting that Kallistatin level can’t reflect the presence of O.V. It can predict the presence of severe PHG.

A133 PORTAL VENOUS STENTING FOR THE TREATMENT OF NON-CIRRHOTIC PORTAL HYPERTENSION-RELATED GASTRIC ANTRAL VASCULAR ECTASIA: A CASE REPORT

Abstract Background Pancreatic and hepatobiliary cancers account for 15-24% of extrahepatic portal hypertension. Treating portal hypertensive bleeding associated with these tumors has been challenging with the delayed effect of chemoradiation and patients with active bleeding being unfit for such therapies. Portal vein stenting has been described in the literature for the treatment of variceal bleeding in such patients. We present the first report of its use for the successful treatment of refractory gastric vascular ectasia (GAVE)-related bleeding. Purpose To review portal vein stenting as a treatment for non-cirrhotic portal hypertension-related GAVE bleeding. Method Chart review was performed with the patient's informed consent. Result(s) A 53-year-old female patient with locally invasive pancreatic cancer presented with one week of melena and presyncope. She had a history of gastroesophageal reflux disease. Her tumor encased the celiac trunk, hepatic and splenic arteries, and abutted the superior mesenteric artery. She had been treated with chemotherapy and radiation. On examination, she was afebrile, blood pressure was 132/87, pulse 110 beats/min, and oxygen saturation 99% on room air. Her abdomen was soft and non-tender. Her hemoglobin was 63 g/L, which represented a 64-point drop over 4 months, leukocytes 4.5 x109/L, platelets 238 x109/L, INR 1.1 and normal electrolytes and creatitine. Alkaline phosphatase was 399 U/L, aminotransferases normal, albumin 38 g/L and total bilirubin 6 umol/L. She was started on pantoprazole and octreotide. On admission, gastroscopy revealed copious blood in the stomach with no clear source despite gastric lavage; hemospray was applied. Given persistent bleeding, repeat gastroscopy the following day revealed 4 columns of Baveno grade III esophageal varices with no high-risk stigmata, as well as severe portal hypertensive gastropathy and GAVE. Argon plasma coagulation and esophageal banding were performed. Over the next month, she continued to have maroon-colored stools. CT angiogram revealed portal vein occlusion and contrast extravasation within the gastric lumen, in keeping with her known gastric antral bleed, with no evidence of lower gastrointestinal bleeding. She had 5 further gastroscopies where APC and GAVE banding were performed. Despite that, she developed hematemesis. Interventional radiology was consulted and performed transhepatic portal venous recanalization, angioplasty and stenting using a 10mm x 60mm self expandable nitinol stent from the superior mesenteric vein to the main portal vein. After stenting, previously seen collateral veins and cavernous transformation were significantly reduced on angiography. She was started on clopidogrel to maintain stent patency. Two days following stent insertion, she stopped clinically bleeding and her hemoglobin stabilized. She was discharged home one month later. Conclusion(s) In patients with GAVE-related bleeding refractory to standard therapeutics, portal venous stenting is possibly an effective treatment modality. Please acknowledge all funding agencies by checking the applicable boxes below None Disclosure of Interest None Declared

Spray coagulation as an alternative to argon plasma coagulation for bleeding portal hypertensive gastropathy

Spray coagulation as an alternative to argon plasma coagulation for bleeding portal hypertensive gastropathy

The Spectrum of Oesophagal Varices, Portal Hypertensive Gastropathy and Child Pugh’s Class in Cirrhotic Patients at Tertiary CareHospital

Objective: To find the association of Child-Pugh’s Class with oesophagal varices and portal hypertensive gastropathy in cirrhotic patients at CMH Lahore.
 Study Design: Cross sectional study
 Place and Duration of Study: Department of Gastroenterology and Department of Pathology, Combined Military Hospital Lahore Pakistan, from Feb to May 2021.
 Methodology: All patients with cirrhosis of the liver, irrespective of aetiology, who underwent upper gastrointestinal endoscopy, were included in the study. Lab data was retrieved from the Pathology Department to calculate Child Pugh’s score. Endoscopic findings of oesophagal varices and portal gastropathy were recorded and their correlation/association with Child-Pugh’s Class was calculated separately by using Pearson’s coefficient.
 Results: A total of 148 patients were included in the study. Male patients were 90(60.8%) and female were 58(39.2%). The age range was 27-85 years, with the mean of patients being 55.93±13.19 years. Association of Child Pugh’s Class with oesophagal varices and portal hypertensive gastropathy revealed that higher grades of oesophagal varices (Grade-lll) and severe portal hypertensive gastropathy were found in Child Pugh’s Class-B (13.51%, 14.18%) and C (15.54%, 16.2%) as compared to Class- A (4.72 %, 1.35%). Child-Pugh’s Class positively correlates with both oesophagal varices and portal hypertensive gastropathy by Pearson’s coefficient r=0.594 and 0.035, respectively; both have significant p values (p <0.05).
 Conclusion: Child-Pugh’s Class has a positive correlation with both oesophagal varices and portal hypertensive gastropathy in patients with cirrhosis

Narrow band endoscopic diagnosis of portal hypertensive gastropathy in cirrhotic patients

ABSTRACT Background Portal hypertensive gastropathy (PHG) is an overlooked complication of liver cirrhosis, as it is a source of acute upper gastrointestinal bleeding and cause of chronic blood loss. Objective To assess the role of narrow band endoscopy in the diagnosis of PHG in cirrhotic patients. Methods Fifty patients with liver cirrhosis were examined by both conventional White Light Endoscopy (WLE) and Narrow Band Technology Variable Intelligent Staining Technology (VIST) using Sonoscape endoscope HD500. Biopsies were taken from the body of gastric mucosa during endoscopy. Results The prevalence of PHG among patients with liver cirrhosis is around 94% by WLE, 92% by VIST, and 55.3% by pathology. There is no statistical significance between VIST and WLE in case of PHG p = 0,750. The risk of developing oesophageal varices grade 3 in severe PHG is higher than in no or mild PHG (OR = 6.8571, 95% CI 1.6270 to 28.9001, p = 0.0087). Conclusion VIST is comparable and complementary to WLE in diagnosis of PHG. There is poor correlation between pathology and WLE in diagnosis of PHG.

The Association of Helicobacter pylori With Portal Hypertensive Gastropathy in Patients With and Without Cirrhosis.

Cirrhosis and its associated complication of portal hypertensive gastropathy (PHG), amongothers, remaina significant cause of deathin resource-poor countries with limited capacity for liver transplantation.This research aimed to assess the association of Helicobacter pylori (H. pylori) with portal hypertensive gastropathy and its severity in patients with and without cirrhosis. The study was conducted at a tertiary care hospital in Pakistan from April 2021 to May 2022. Liver cirrhosis was diagnosed by clinical manifestations, ultrasonography, and laboratory investigations. The severity of liver cirrhosis was assessed using the Child-Pugh scoring system. The association of H. pylori with portal hypertensive gastropathy in patients with and without cirrhosis was assessed using the chi-square test. A total of 120 patients participated in the study, of which 40 were without liver cirrhosis, while 80 were with cirrhosis. Amongpatients with cirrhosis, 24 were in Child-Pugh class A, 26 in class B, and 30 in class C. Of patients with liver cirrhosis who were H. pylori-negative, 37.5% (15/40) had portal hypertensive gastropathy. Of these, 12.5% (5/40) had severe PHG, while 25% (10/40) had mild PHG. Of patients with liver cirrhosis who were H. pylori-positive, 62.5% (25/40) had PHG. Of these, 2.5% (1/40) had severe PHG, while 60% (24/40) had mild PHG.Helicobacter pylori contributed nonsignificantly (p=0.080), showing no association with portal hypertensive gastropathy. Helicobacter pylori does not appear to have any significant association to cause or worsen portal hypertensive gastropathy in patients with liver cirrhosis.

P1020: SCREENING FOR PORTAL HYPERTENSION IN PATIENTS WITH PHILADELPHIA NEGATIVE MYELOPROLIFERATIVE NEOPLASMS

Background: Portal hypertension (PH) is a well-recognized complication of BCR-ABL negative myeloproliferative neoplasms (MPNs) and is associated with significant morbidity and mortality. However, the prevalence of PH and its associated risk factors have not been studied systematically in this patient population. Screening by esophagogastroduodenoscopy (EGD) can facilitate early diagnosis of PH and opportunity for intervention to prevent complications. Aims: To investigate the prevalence of PH and its patient and disease-related risk factors. Methods: From May 2013 to March 2019, MPN patients ≥ 18 years old with spleen >5 cm below the costal margin in myelofibrosis (MF) or any size in Polycythemia Vera (PV) or Essential Thrombocythemia (ET) were enrolled prospectively (NCT01816256). Patients with a known history of portal or hepatic vein thrombosis, liver cirrhosis, and esophageal varices were excluded. Screening for PH was done by EGD to evaluate for esophageal varices (EV) or gastric varices (GV), and portal hypertensive gastropathy (PHG). Abdominal Doppler ultrasonography (USG) was performed to evaluate for portal vein thrombosis and spleen size. PH severity was based on the size of varices or severity of PHG. For sample-size calculation, a precision approach was used, considering scenarios where PH prevalence ranged from 5 to 10% and an upper limit for sample size of 100. At a prevalence estimate of 8%, the 90% confidence interval (CI) was 4-14%, with an acceptable lower limit for moving forward with a screening program. Prevalence of PH was calculated as a proportion and CI are exact using Clopper-Pearson method. Results: Among 102 enrolled patients, EGD and USG were completed in 85 and 84, respectively. Primary and Post-PV/ET MF comprised the majority of the study population (93% [79/85]). Evidence of PH was found in 32 patients (38%, [90% CI 29-47]) of whom 12 (14% [90% CI 9-22]) had moderate to severe PH. EV, GV, and PHG were found in 81% (26/32), 13% (4/32), and 31% (10/32) of patients, respectively. The prevalence of PH among MF and PV/ET patients was 35% (28/79) and 67% (4/6), respectively. In MF patients, PH was moderate-to-severe in 13% (90% CI 8-20). No cases of portal vein thrombosis were identified on USG. Apart from a palpable liver observed more frequently in non-PH patients, there were no other significant differences in baseline characteristics among patients with and without PH. The frequency of JAK2, MPL and CALR mutations among PH patients was 78% (25/32),13% (4/32), and 6% (2/32). There was a trend towards more JAK2 mutations in PH patients (78% [25/32] vs 64% [34/53], p=0.23), but no difference in DIPSS risk or frequency of high molecular-risk mutations. Overall survival was similar in both groups. PH-directed interventions were initiated in 59% (19/32); 28% (9/32) were started on beta blocker (BB) prophylaxis, 16% (5/32) were treated with BB and variceal banding, and 16% (5/32) continued on surveillance EGDs alone. Three patients with moderate PH at baseline developed variceal bleeding (2) and ascites (1). All 3 patients were on BB prophylaxis, and 1 had prior prophylactic banding. There were no adverse events related to study procedures EGD or USG. Image:Summary/Conclusion: Given the study population, our results are generalizable to MF patients. Our study shows that clinically significant PH is common in MF patients, and led to additional clinical interventions in significant number of patients. These data support the inclusion of asymptomatic PH screening in the work up of MF patients.

Helicobacter pylori Infection in Cirrhotic Patients With Portal Hypertensive Gastropathy: A New Enigma?

The relationship between Helicobacter pylori (H. pylori) infection and Portal hypertensive gastropathy (PHG) is still a debatable matter. The aim of this study is to find out how common H. pylori infection is in cirrhotic patients with PHG and to see if there’s a link between H. pylori infection and PHG severity. Out of 340 cirrhotic patients who had upper Gastrointestinal Tract (GIT) endoscopy for early varices screening, 160 cirrhotic patients were selected and divided into 2 groups; 80 cirrhotic patients with PHG (cases) and 80 cirrhotic patients without PHG (controls). Gastric biopsies were taken from all enrolled patients for histological evaluation for the presence or absence of H. pylori infection. H. pylori was found in 44 cirrhotic patients (55%) who had PHG (cases), compared to 22 cirrhotic patients (27.5%) who did not have PHG (controls). The prevalence of H. pylori infection was significantly higher in patients with PHG (p < 0.001). The severity of PHG was associated with H. pylori infection (p < 0.001). The response to eradication therapy of H. pylori infection was must better in patients without PHG (p = 0.045). By multi-variant analysis, H. pylori infection, splenic diameter, and portal vein diameter were independent predictors for PHG presence. After treating H. pylori infection in patients who tested positive for H. pylori, there was a significant reduction in PHG severity (p < 0.001). Patients with PHG have a greater prevalence of H. pylori infection. PHG is more severe in patients infected with H. pylori. To improve PHG severity, cirrhotic patients must have their H. pylori infection eradicated.

Serum serotonin as a non-invasive marker of portal hypertensive gastropathy in Egyptian patients with HCV-related liver cirrhosis.

Portal hypertensive gastropathy (PHG) is an important complication of portal hypertension (PHT) in cirrhotic patients. We aimed in the current study to investigate the validity of serum serotonin as a probable non-invasive marker for PHG in cirrhotic patients with PHT. We conducted this study on 100 HCV-related cirrhotic patients divided into three groups according to their endoscopic findings; group I: patients with no endoscopic signs of PHG; group II: patients with mild PHG; and group III: patients with severe PHG. All subjects had routine laboratory investigations, serum serotonin level using ELISA kits, calculation of Child's score, abdominal ultrasound, and upper GIT endoscopy. Serum serotonin was significantly higher in those with PHG than those without (t= 5.128, p <0.001). Moreover, it was significantly higher in patients with severe degree of PHG than those with mild PHG (t=7.357, p<0.001). Furthermore, a significant positive correlation was observed between serum serotonin and Child Pugh score (t=7.357, p<0.001). Roc curve analysis revealed that serum serotonin at a level ? 26.5 ng/ml had a 78.82% sensitivity, 73.33% specificity, and accuracy of 78% to discriminate between those with signs of PHG and those without. Serum serotonin is a valuable non-invasive marker of PHG in HCV-cirrhotic patients. Furthermore, its serial measurements could be used to monitor disease progression.

Portal Hypertensive Gastropathy in Liver Cirrhosis: Prevalence, Natural History, and Risk Factors.

Objective Portal hypertensive gastropathy (PHG) is a common finding in patients with liver cirrhosis (LC) and may cause both acute and chronic bleeding. A number of risk factors for PHG have been identified. The present study explored the characteristics of Japanese patients with LC who develop PHG.MethodsClinical findings (age, sex, etiology, the presence of esophageal varices, splenomegaly and severity of LC), laboratory data, and whether or not atrophic gastritis was found on endoscopy were retrospectively reviewed in patients with LC who had undergone esophagogastroduodenoscopy. PHG was endoscopically graded as absent, mild, or severe.ResultsOf 262 patients with LC (mean age, 69 years old; 145 men), 158 had no PHG, 41 had mild PHG, and 63 had severe PHG. In a univariate analysis, a younger age, male sex, non-viral etiology, absence of atrophic gastritis, presence of esophageal varices, splenomegaly, severe LC, low platelet count, and low hemoglobin concentration were associated with PHG. A multivariate analysis showed a significant association of PHG with the absence of atrophic gastritis (p<0.048), presence of esophageal varices (p<0.001), non-viral etiology (p<0.033), splenomegaly (p<0.048), and severe LC (p<0.005). There were no cases of massive bleeding from PHG during follow-up.ConclusionEsophageal varices, splenomegaly, severe liver cirrhosis, the absence of atrophic gastritis, and etiology were found to be risk factors for PHG in Japanese patients.

AUTO IMMUNE HEPATITIS AS A LIVER MANIFESTATION OF COMMON VARIABLE IMMUNODEFICIENCY: A CASE REPORT

Common variable immunodeficiency (CVID) is a primary immunodeficiency disorder characterized by impaired differentiation of B cells with defective immunoglobulin production and paradoxically the development of autoimmune disorders. It is estimated that the prevalence of the liver disease is less than 10%. The most reported is focal nodular hyperplasia and, to a lesser extent, primary biliary cholangitis, primary sclerosing cholangitis and autoimmune hepatitis (AIH). present the case of a 22-year-old male who was admitted for hematemesis. He was diagnosed with immune thrombocytopenia 12 years ago without treatment and common variable immunodeficiency six years ago, currently three years without treatment. No family history of autoimmune or liver diseases. After extraction of the 4th molars, he presented swelling, redness, heat in the left submandibular region, unquantified fever, for which he received antibiotic treatment and non-steroidal anti-inflammatory drugs; 12 hours before admission, he began with hematemesis and hematochezia with data of hemodynamic instability, for which crystalloids are administered, the physical examination presents scleras with jaundice, an edematous, erythematous area with local heat in the left submandibular region, flat, symmetrical abdomen, absence of collateral circulation, Non-painful hepatomegaly, without shifting dullness. Laboratory admission with anemia, thrombocytopenia, cholestatic pattern in liver biochemistry tests, chronic viral infectious processes are ruled out and antibodies are made for autoimmune diseases, ANA 1:1200 is documented, other antibodies negative. Esophagogastroduodenoscopy where large esophageal varices of Baveno and severe portal hypertensive gastropathy (image 1 panel A). Doppler ultrasound reports diffuse liver disease, 14mm portal vein, with the presence of free fluid perihepatic and perisplenic, without biliary obstruction data (image 1 panel B). Percutaneous liver biopsy: fibrosis F2-3 on the scale of Metavir, interface hepatitis, associated with infiltrate lymphoplasmacytic integrating diagnosis of AIH (image 1 panel C). The prevalence of this condition is estimated at 1 in every 50,000 people worldwide. Up to 25% of patients with CVID will have an association with autoimmune diseases, representing the heterogeneous nature of the disease. The presentation of liver disease commonly reported in case series is anicteric cholestasis, and biopsies show evidence of non-cirrhotic portal hypertension. However, the association of CVID and AIH is rare; its diagnosis requires biopsies due to the lack of expression of antibodies in most cases. In CVID patients with altered liver function tests, the association with autoimmune liver diseases should be ruled out to initiate timely treatment and avoid late complications. The authors declare that there is no conflict of interest.

Case report on Horseshoe kidney with hypothyroidism with cryptogenic cirrhosis of the liver with portal hypertension

Horseshoe kidney is rare non-fatal congenital abnormality of renal development. This conditions usually asymptomatic and in various cases it discovered incidentally. The incidence of horseshoe kidney is approximately 1 in 500 in the average population and this anamoly is found in men than in female. Horseshoe kidney means two kidneys joined together and form the U shape like a horseshoe. It is also known as Renal Fusion. The most problem of horseshoe kidneys is nephrolithiasis. There is no cure for horseshoe kidneys, but supportive treatments can treat symptoms. Patient medical history : The Patient has come with the chief complaints of breathing difficulty, swelling, facial puffiness for 15 days, abdominal distension, repeated episode of vomiting blood (hematemesis), and melena. The Patient had a history of hypothyroidism for two years and cryptogenic cirrhosis of the liver with portal hypertension for one year. Diagnostic evaluation : Endoscopy procedure done to screen esophageal varices, there are large esophageal varices and severe portal hypertensive gastropathy USG: cirrhosis of liver, mild splenomegaly. Echo: Severe portal hypertension, mild Tricuspid Regurgitation with Right Ventricular Systolic Pressure, Mildly dilated Right Atrium and Right Ventricle. Therapeutic intervention : Provide beta-blockers, antibiotics, antiemetics, vitamin supplements, biliary agents, and antidiuretic used to treat the client, but the Patient’s overall health was deteriorating. Conclusion : Treatment and care for horseshoe kidney disease on time will help to prevent further life-threatening consequences.

Accuracy of virtual chromoendoscopy in differentiating gastric antral vascular ectasia from portal hypertensive gastropathy: A proof of concept study

BACKGROUNDAccurate detection of gastric antral vascular ectasia (GAVE) is critical for proper management of cirrhosis-related gastrointestinal bleeding. However, endoscopic diagnosis of GAVE can be challenging when GAVE overlaps with severe portal hypertensive gastropathy (PHG).AIMTo determine the added diagnostic value of virtual chromoendoscopy to high definition white light for real-time endoscopic diagnosis of GAVE and PHG.METHODSWe developed an I-scan virtual chromoendoscopy criteria for diagnosis of GAVE and PHG. We tested our criteria in a cross-sectional cohort of cirrhotic adults with GAVE and PHG when high-definition white light endoscopy (HDWLE) diagnosis was in doubt. We then compared the accuracy of I-scan vs HDWLE alone to histology.RESULTSTwenty-three patients were included in this study (65.2% Caucasians and 60.9% males). Chronic hepatitis C was the predominant cause of cirrhosis (43.5%) and seven adults (30.4%) had confirmed GAVE on histology. I-scan had higher sensitivity (100% vs 85.7%) and specificity (75% vs 62.5%) in diagnosing GAVE compared to HDWLE. This translates into a higher, albeit not statistically significant, accuracy of I-scan in detecting GAVE compared to HDWLE alone (82% vs 70%). I-scan was less likely to lead to an accurate diagnosis of GAVE in patients on dialysis (P < 0.05) and in patients with elevated creatinine (P < 0.05). I-scan had similar accuracy to HDWLE in detecting PHG.CONCLUSIONThis pilot work supports that virtual chromoendoscopy may obviate the need for biopsies when the presence of GAVE is in doubt. Larger studies are needed to assess the impact of virtual chromoendoscopy on success of endoscopic therapy for GAVE.

The relationship between portal hypertension and portal hypertensive gastropathy

Background and aim Portal hypertensive gastropathy (PHG) most commonly occurs in the setting of increased portal pressure in patients with cirrhosis. Here, we aimed to understand the correlation between hepatic venous pressure gradient (HVPG) and the presence and severity of PHG in patients with cirrhosis. Methods We examined patients with cirrhosis who underwent HVPG measurement at the Medical University of South Carolina between 2014 and 2020. Extensive demographic, clinical, laboratory, procedural (including precise grading of PHG severity using standard definitions), and outcome data were abstracted at the time of HVPG measurement. Results Three hundred and ten patients with HVPG measurements and cirrhosis were identified. Seventy-three patients having endoscopy within 6 months of HVPG measurement were included (mean age 54 ± 11, 44% female). The most common causes of cirrhosis were alcohol (41%) and non-alcoholic steatohepatitis (32%). The average HVPG was 15 mmHg (±6) and 62 patients had clinically significant portal hypertension (CSPH) (HVPG ≥ 10 mmHg). Of the 73 patients with HVPG measured, 45 (62%) had PHG, including 40 (89%) of whom had CSPH. Out of the 45 patients with PHG, 41 and four had mild or severe PHG, respectively. MELD scores were similar in patients with and without PHG [15 ± 9 (SD) and 17 ± 9, respectively; p = .37]. HVPG was higher in patients with PHG (17 ± 7 mmHg) than those without PHG (13 ± 4 mmHg) (p = .01) but did not differ between mild and severe PHG. Conclusion A weak correlation exists between HVPG level and the presence of PHG.

Relation between Helicobacter pylori infection and severity of portal hypertensive gastropathy in cirrhotic patients

ABSTRACT Background: Cirrhosis is a great health problem worldwide and is associated with many complications. Portal hypertensive gastropathy (PHG) is one of its most common complications and in some patients may lead to gastrointestinal bleeding. The relationship between Helicobacter pylori (H. pylori) infection and PHG is not clearly identified. Objective: This work aimed to study a possible association between H. pylori infection and PHG and to correlate the severity of PHG with H. pylori infection in cirrhotic patients. Methodology:A cross sectional comparative study included 90 cirrhotic patients, who were classified into 3 groups. G1: included 30 age and sex-matched cirrhotic patients with no PHG. G2: included 30 age and sex-matched cirrhotic patients with mild PHG. G3: included 30 age and sex-matched cirrhotic patients with severe PHG. Endoscopic examination was done to evaluate the presence and severity of portal hypertensive gastropathy and for diagnosis of H. pylori infection. Results: H. pylori infection by histopathology was detected in 61 studied patients (67.8%). H. pylori infection was more prevalent among cirrhotic patients with PHG (78.3%) than patients without PHG (46.7%) (P=0.0029). H. pylori infection was detected in 26(86.7%), 21(70.0%), 14(46.7%) in patients with severe, mild and no PHG respectively. H. pylori infection was more prevalent in patients with severe PHG relative to patients with no PHG (p-value = 0.001). Conclusion: The current study showed a significant relation between H. pylori infection and PHG in cirrhotic patients and it might have a role in the pathogenesis of severe PHG.

Endoscopic profile of acute upper gastrointestinal bleed in adults: A tertiary care center-based study in South India

Background: Acute upper gastrointestinal bleeding (UGIB) is one of the most common causes of medical emergencies and associated with high morbidity and mortality in adults. Although there is decline in peptic ulcer bleed as an etiology of acute UGI bleed due to discovery of proton pump inhibitors, the Emergency Room (ER) visits for UGI bleed are increasing due to other etiologies including variceal bleed and drug-induced gastrointestinal (GI) bleed. This study was designed with the aim to assess the endoscopic profile of UGIB presenting to our tertiary care center in south India. Materials and Methods: This was a prospective analytical study. It was done over a period of 6 months from January 2020 to June 2020. All adult patients presenting with acute hematemesis and/or melena were included in the study. All included patients underwent detailed history, clinical examination, blood tests, and upper GI endoscopy. Results: One hundred and eighty-two patients were included in the study. Out of 182 patients, 76% were males. The most common age group was 51–60 years contributing to 34%. The commonest presentation was hematemesis than that of melena. Out of all patients, 69% of patients were hemodynamically stable and 31% patients were unstable at the time of admission. The causes of bleed included esophageal varices, gastric varix, peptic ulcer, portal hypertensive gastropathy (PHG), Mallory-Weiss tear, gastric cancer, drug-induced gastritis, and esophageal tear. Variceal bleed was the most common cause of UGI bleed comprising 34.16% of cases. Conclusions: From our study, we conclude that the most common cause of upper GI bleed in our part of India is portal hypertension related bleeding which included esophageal varices, gastric varices, and severe PHG. This was in contrary to most of the studies from other part of the country as peptic ulcer is far more common than variceal bleed in other studies.

Helicobacter Pylori Infection is Associated with Portal ‎Hypertensive Gastropathy in Patients with Liver Cirrhosis ‎

Background and study aims‎: Portal hypertensive gastropathy (PHG) is a complication of portal hypertension in patients with liver cirrhosis, and it is considered one of the causes of upper gastrointestinal bleeding. Helicobacter pylori (H. Pylori) is one of the most common pathogenic organism worldwide because it infects 50% of the population all over the world. The role of H. Pylori infection in the development of PHG and its severity is controversial. The aim of this study is to determine the frequency of H. pylori infection in cirrhotic patients with PHG, and to find out the possible association of H.pylori infection with PHG severity. Method: This study was carried out on 90 patient with cirrhotic liver. Patients were divided into two groups according to the presence or absence of PHG diagnosed by upper endoscopy. Child's Pugh score, MELD, uMELD and detection of H.Pylori by histopathological examination were done for all patients. Results: The studied patients 47 were males and 43 were females their mean age was 51.96 ± 7.02 years (ranging between 38-66 years). H.Pylori infection was significantly more frequent in patients with PHG than patients without PHG (P= 0.001). H.Pylori infection was significantly more frequent in patients with severe PHG than those with mild PHG (P=0.012). By multi-variant analysis, splenomegaly, presence of esophageal varices, gastric varices and H. Pylori infection were independent predictors for PHG presence. Conclusion: H. Pylori infection could be an independent predictor for PHG development and ‎associated with its severity.

Endoscopic Eradication of Esophageal Varices Transiently Affects the Development and Severity of Portal Hypertensive Gastropathy

Endoscopic Eradication of Esophageal Varices Transiently Affects the Development and Severity of Portal Hypertensive Gastropathy

Correlation of endoscopic findings with Doppler ultrasound in portal hypertension in children.

Aim of the studyTo determine the correlation of the endoscopic findings with portal Doppler and ultrasound (USG) in children with suspected portal hypertension (PHT).Material and methodsEighty children with extrahepatic portal vein obstruction (EHPVO) and chronic liver disease (CLD) were included in this retrospective study conducted over a period of 1 year. All patients underwent upper gastrointestinal (GI) endoscopy and Doppler.ResultsThe etiology was EHPVO in 30 (37.5%) patients, biliary atresia in 12 (15%), Budd-Chiari syndrome in 11 (13.7%), Wilson’s disease in 10 (12.5%), idiopathic CLD in 8 (10%), autoimmune hepatitis in 4 (5%), glycogen storage disease (GSD) in 3 (3.8%), non-alcoholic liver disease (NAFLD) in 1 (1.3%) and systemic lupus erythematosus (SLE) in 1 (1.3%) patient. Fifty-three (66.25%) patients had esophageal varices on endoscopy, of whom 3 (3.8%) had associated gastric varices. Portal hypertensive gastropathy (PHG) was present in 30 (37.5%) patients, of whom 10 (12.5%) had severe PHG. Forty-one (51.3%) patients had PHT on Doppler (κ correlation 0.43). Kappa correlation was 0.43 in patients with biliary atresia, 0.31 in Budd-Chiari syndrome, 0.23 in idiopathic CLD, 0.21 in CLD, and 0.05 in Wilson’s disease. All (100%) EHPVO patients and 39 (78%) CLD patients had PHT on USG. Endoscopic findings of PHT were seen in 24 (80%) EHPVO patients and 29 (58%) CLD patients. All patients with EHPVO had cavernous transformation of the portal vein on Doppler. For patients with CLD, the common Doppler findings were collaterals seen in 35 patients and reversal of flow in 12 patients.ConclusionsDoppler ultrasound followed by endoscopy should be used to diagnose PHT in children. In children with biliary atresia, Doppler ultrasound may miss changes of PHT.