Hypertensive Gastropathy Research Articles

The Use of Proton Pump Inhibitors in Patients with Liver Cirrhosis: Real Life Experience.

(1) Background: Proton pump inhibitors (PPIs) are commonly prescribed for gastric disorders. In patients with liver cirrhosis, PPI use is associated with an increased risk of spontaneous bacterial peritonitis and increased mortality rates; therefore, they should be used with caution. This study aims to evaluate the appropriateness of PPI prescriptions in hospitalized cirrhotic patients against current clinical guidelines to identify patterns of misuse and guide better prescribing practices. (2) Methods: A retrospective study was conducted on liver cirrhosis inpatients in an internal medicine department from January 2022 to May 2023. The primary measure was the proportion of PPI prescriptions aligned with clinical guidelines. Medical files were entirely reviewed by researchers to assess the appropriateness of PPI prescriptions using the current guidelines. Outcomes included the identification of common reasons for PPI prescription and the rate of inappropriate PPI use among the study population. (3) Results: The study included 189 cirrhotic patients, with PPIs prescribed to 95 (50.2%) patients during hospitalization and 75 (39.7%) patients at discharge. Among those, 47.4% of the inpatients and 34.7% at discharge had no valid indication for PPI administration. The most common reason for PPI prescription during hospital stays was gastritis, followed by antiplatelet use in high-risk patients, ulcers, and upper gastrointestinal bleeding. The most common inappropriate indication was portal hypertensive gastropathy (PHG), followed by treatment with corticosteroids and anticoagulants alone. We did not find an association between PPI administration during hospital stays and infections. Only in 4% of cases patients should have received PPIs and did not. (4) Conclusions: There is a concerning overprescription of PPIs in cirrhotic patients, often deviating from established guidelines. It subjects patients to unnecessary risks. There is an urgent need for increased awareness and adherence to clinical guidelines regarding PPI prescriptions in cirrhotic patients.

Predictive factors of portal hypertensive enteropathy exacerbations based on long-term outcomes

BackgroundPortal hypertensive enteropathy (PHE) is a small-bowel lesion observed in patients with portal hypertension. The clinical significance of endoscopic findings in PHE remains unclear. We aimed to clarify the clinical significance and predictive factors of capsule endoscopic findings in patients with PHE based on long-term outcomes.MethodsThis retrospective study enrolled 55 patients with PHE (33 males and 22 females; median age, 64 years; range, 23–87) followed for > 3 years using capsule endoscopy (CE) between February 2009 and May 2023. We evaluated the clinical factors affecting PHE exacerbations and the effects of PHE exacerbations on gastrointestinal bleeding by comparing exacerbated and unchanged PHE groups.ResultsOverall, 3 (5%) patients showed improvement, 33 (60%) remained unchanged, and 19 (35%) showed exacerbation on follow-up CE. In the exacerbated group, the rates of worsened fibrosis-4 index, exacerbated esophageal varices, and exacerbated portal hypertensive gastropathy were significantly higher than those in the unchanged group (21%, 32%, and 42% vs. 3%, 6%, and 12%, respectively; P < 0.05), and the rate of splenectomy was significantly lower in the exacerbated group than in the unchanged group (5% vs. 39%, respectively; P < 0.01). In multivariate analysis, exacerbation of esophageal varices and absence of splenectomy were significantly associated with PHE exacerbation. The rate of gastrointestinal bleeding after follow-up CE was significantly high in the exacerbated group (log-rank, P = 0.037).ConclusionsExacerbation of esophageal varices and splenectomy were significantly associated with exacerbation of PHE. Exacerbated PHE requires specific attention to prevent gastrointestinal bleeding.

Upper Gastrointestinal Endoscopic Findings and Their Clinical Correlates in Patients With Liver Cirrhosis in Northern Ghana.

Background and study aim Liver cirrhosis causes portal hypertension that leads to dysfunction of the gastrointestinal tract, which may result in complications including upper gastrointestinal (UGI) bleeding. This study sought to determine the prevalence and the clinical correlates of these UGI abnormalities in patients with liver cirrhosis receiving care at the Komfo Anokye Teaching Hospital in Kumasi, Ghana. Patients and methods One hundred and forty-five participants with liver cirrhosis were consecutively sampled and clinically evaluated for symptoms and signs of liver cirrhosis and then underwent esophagogastroduodenoscopy (EGD). Results The mean age of the respondents was 46.50 ± 12.14 years, with the majority being males (106, 73.10%) and in Child-Pugh class C (111, 76.55%). Fatigue (128, 88.28%) and ascites (127, 87.59%) were the most common symptoms and signs, respectively. Fatigue, itch, and ascites were significantly correlated with the severity of liver cirrhosis, with an adjusted odd ratio (AOR) (confidence interval (CI)) of 3.56 (1.11-11.47), p-value of 0.03, 4.35 (1.34-14.18), p-value of 0.02 and 22.50 (4.88-103.77), p-value < 0.01, respectively. Esophageal varices were the most common UGI endoscopic findings, occurring in 102 (70.34%) patients, and correlated with the severity of liver cirrhosis, AOR (CI) of 5.19 (1.70-15.87), p-value of 0.01. Other common findings included gastritis in 71 (48.97%), portal hypertensive gastropathy in 67 (46.2%), duodenitis in 49 (33.79%), and peptic ulcer in 46 (31.72%). Conclusions Fatigue, ascites, and esophageal varices were the most common symptoms, signs, and EGD findings, respectively. Fatigue, itch, ascites, esophageal varices, duodenitis, and gastric antral vascular ectasia correlate with the severity of liver cirrhosis.

Correlation of Portal Hypertensive Gastropathy with the Size of Esophageal Varices in Patients with Decompensated Chronic Liver Disease:

Objectives: To determine the correlation of portal hypertensive gastropathy with esophageal variceal size. To determine the differences in gender of esophageal varices Study design: A cross-sectional study was done from January 2022- October 2022 on 440 patients reporting to JPMC, Karachi having portal hypertensive gastropathy and were assessed for severity of esophageal varices based on endoscopic findings. Methodology: The new Italian Endoscopic Club criterion was used for portal hypertensive gastropathy (PHG) and the Japanese Research Society for Portal Hypertensive Gastropathy to describe the grading of esophageal varices. Results: Of 440 patients 163 (37%) were female and 277 (63%) were males. The size of esophageal varices correlated with severity and a Spearman p&lt;0.1% was seen which is significant. Male patients showed a significantly higher chance of having larger-sized varices. Conclusions: The size of varices correlates to severe decompensated chronic liver diseases (DCLD). Hence, patients with advanced liver cirrhosis are likely to be at risk of severe upper GI bleeds

Endoscopic band ligation, and Argon plasma coagulation Yields in management of Post-Hepatitis Portal Hypertensive Gastropathy

Endoscopic band ligation, and Argon plasma coagulation Yields in management of Post-Hepatitis Portal Hypertensive Gastropathy

Endoscopic ultrasound‐guided portal pressure gradient identifies patients with previously undiagnosed clinically significant portal hypertension

AbstractAimsPortal hypertension (PH) is a complication of cirrhosis that leads to hepatic decompensation. Assessing the portal pressure gradient (PPG) provides valuable information for disease assessment, staging, and prognosis. In this study, we aimed to report the utilization of endoscopic ultrasound (EUS)‐guided PPG (EUS‐PPG) measurements in a real‐world setting.MethodsThis retrospective analysis included patients at a tertiary care center who underwent EUS‐PPG between February 2021 and May 2022. The most common indication was to establish or exclude the diagnosis of cirrhosis, followed by an assessment of surgical risk in the setting of suspected cirrhosis. Extensive demographic and clinical data were collected, and statistical analysis was performed using the Student's t test.ResultsEighteen patients underwent EUS‐PPG. Technical success was achieved in 17 of the 18 patients. No complications were observed. The mean scores of Child‐Pugh, Model for End‐Stage Liver Disease‐Sodium, and Fibrosis‐4 scores were 5.1 ± 0.5, 9.0 ± 3.0, and 3.7 ± 4.5, respectively. Of the 18 patients, two presented with esophageal varices and six with portal hypertensive gastropathy. The mean PPG was 5.8 ± 4.5 mmHg, and five patients exhibited clinically significant PH (CSPH). Of the 18 patients, 15 underwent concurrent EUS‐liver biopsy, which was 100% successful and provided diagnostic histology for all patients. The PPG data led to changes in the clinical management of 17 patients.ConclusionsEUS‐PPG is safe and technically feasible. The Child‐Pugh score did not correlate well with the presence of CSPH; however, PPG measurements resulted in changes in the management of almost all patients. Larger studies correlating EUS‐PPG with other assessments of liver diseases are required.

Prospective evaluation of patients with non-cirrhotic portal hypertension: A single centre study.

Non-cirrhotic portal hypertension (NCPH) is a spectrum of liver diseases, including porto-sinusoidal vascular disorder, with portal hypertension (PH) in the absence of cirrhosis. The natural history and diagnostic approach to NCPH are not well understood. We aimed to evaluate disease progression and outcomes in NCPH. Patients with or at risk for NCPH were enrolled in a single centre prospective study; two groups were formed based on the presence of specific features of PH, such as varices, collaterals, portal hypertensive gastropathy or portal hypertensive bleeding. All participants underwent a baseline liver biopsy. Liver stiffness measurement (LSM), and imaging were repeated every 6-12 months. Fifteen patients without specific features of PH (Group I), and 35 patients with specific features (Group II) were enrolled. The median follow-up time was 50 months. Group II had higher hepatic venous pressure gradients, non-invasive measures of PH and a lower platelet count (PLT) when compared to Group I. Rates of survival and decompensation were similar in both groups. Patients with PLT ≤100 K/mcL had lower survival compared to those with PLT >100 K/mcL. Patients with LSM ≥10 kPa had lower survival and survival without decompensation when compared to patients with LSM <10 kPa. Patients irrespective of specific features of PH had similar survival or survival without decompensation. Patients without specific features are at risk for disease progression and should be monitored closely. Thrombocytopenia and increased LSM are associated with severe forms of liver disease, which are strongly associated with outcomes.

Management of Thrombocytopenia with Partial Splenic Embolization in Liver Cirrhosis

Thrombocytopenia is a frequent complication in patients with cirrhosis. Thrombocytopenia is generally divided into mild, moderate, and severe thrombocytopenia. Thrombocytopenia in liver cirrhosis not only increases the risk of bleeding during surgery but can also have an impact on patient management, such as liver biopsy, administration of antiviral therapy, and postponement of elective surgery. The pathophysiology of thrombocytopenia in chronic liver disease can be caused by decreased platelet production, sequestration in the spleen, and increased platelet destruction. Partial splenic embolization (PSE) is one option for treating thrombocytopenia in chronic liver disease. PSE is an effective procedure in treating complications associated with hypersplenism and portal hypertension, such as esophageal varices, pancytopenia, portal hypertensive gastropathy and ascites.

Mitochondrial dysfunction induced by HIF-1α under hypoxia contributes to the development of gastric mucosal lesions.

Hypoxia is an important characteristic of gastric mucosal diseases, and hypoxia-inducible factor-1α (HIF-1α) contributes to microenvironment disturbance and metabolic spectrum abnormalities. However, the underlying mechanism of HIF-1α and its association with mitochondrial dysfunction in gastric mucosal lesions under hypoxia have not been fully clarified. To evaluate the effects of hypoxia-induced HIF-1α on the development of gastric mucosal lesions. Portal hypertensive gastropathy (PHG) and gastric cancer (GC) were selected as representative diseases of benign and malignant gastric lesions, respectively. Gastric tissues from patients diagnosed with the above diseases were collected. Portal hypertension (PHT)-induced mouse models in METTL3 mutant or NLRP3-deficient littermates were established, and nude mouse gastric graft tumour models with relevant inhibitors were generated. The mechanisms underlying hypoxic condition, mitochondrial dysfunction and metabolic alterations in gastric mucosal lesions were further analysed. HIF-1α, which can mediate mitochondrial dysfunction via upregulation of METTL3/IGF2BP3-dependent dynamin-related protein 1 (Drp1) N6-methyladenosine modification to increase mitochondrial reactive oxygen species (mtROS) production, was elevated under hypoxic conditions in human and mouse portal hypertensive gastric mucosa and GC tissues. While blocking HIF-1α with PX-478, inhibiting Drp1-dependent mitochondrial fission via mitochondrial division inhibitor 1 (Mdivi-1) treatment or METTL3 mutation alleviated this process. Furthermore, HIF-1α influenced energy metabolism by enhancing glycolysis via lactate dehydrogenase A. In addition, HIF-1α-induced Drp1-dependent mitochondrial fission also enhanced glycolysis. Drp1-dependent mitochondrial fission and enhanced glycolysis were associated with alterations in antioxidant enzyme activity and dysfunction of the mitochondrial electron transport chain, resulting in massive mtROS production, which was needed for activation of NLRP3 inflammasome to aggravate the development of the PHG and GC. Under hypoxic conditions, HIF-1α enhances mitochondrial dysfunction via Drp1-dependent mitochondrial fission and influences the metabolic profile by altering glycolysis to increase mtROS production, which can trigger NLRP3 inflammasome activation and mucosal microenvironment alterations to contribute to the development of benign and malignant gastric mucosal lesions.

Does Portal Hypertension Increase the Risk of Helicobacter pylori Infection and Pre-Malignant Gastric Lesions?

Background and Aims: The presence of portal hypertension in cirrhotic patients is a major prognostic factor associated with the development of severe complications and increased mortality. The gold standard for diagnosing portal hypertension is the hepatic venous pressure gradient. More recently, spleen stiffness has emerged as a new and non-invasive diagnostic tool, and has already been included in the last Baveno VII guidelines. The exact prevalence of Helicobacter pylori infection, pre-malignant lesions and their relation to portal hypertension have never been described. The aim of our study was to evaluate the relationship between the presence of portal hypertension assessed via liver and spleen elastography and Helicobacter pylori infection and pre-malignant gastric lesions. Methods: An observational study was conducted, including consecutive patients admitted from December 2020 to December 2022. All patients underwent upper endoscopy and were also subjected to liver and spleen elastography (using the new probe of 100 Hz) by the same blinded operator in a tertiary center. Results: We included 155 cirrhotic patients, with a mean age of 64.1 years (±8.8), and 81.3% were male. The most common etiology was alcoholic liver disease (72.9%). The median value of liver stiffness measurement was 24.4 kPa [3.1-75.0], and the spleen stiffness measurement was 49.1 kPa [12.8-100.0]. Akin to endoscopic findings, 50.3% presented esophageal varices, 5.2% gastric atrophy, 11.6% gastric metaplasia, and 32.9% portal hypertension gastropathy. Regarding histologic findings, we found that 34.8% presented H. pylori infection, 35.5% gastric atrophy (OLGA 1-58.2%) and 38.7% gastric metaplasia (OLGIM 1-63.3%). Liver stiffness and spleen stiffness measurements were associated with the presence of portal hypertensive gastropathy (p < 0.01), but not with H. pylori infection or pre-malignant gastric lesions. Conclusions: Although present in almost one third of cirrhotic patients, H. pylori infection and pre-malignant gastric lesions are not associated with liver stiffness and spleen stiffness measurements. On the other hand, we found an association between liver stiffness and spleen stiffness measurements and portal hypertensive gastropathy.

A216 MODERATE TO SEVERE ACUTE UPPER GASTROINTESTINAL BLEEDING IN RURAL NORTHERN ONTARIO: AN EPIDEMIOLOGICAL ANALYSIS OF AETIOLOGIES, GEOGRAPHIC LIMITATIONS, AND OUTCOMES

Abstract Background Hospitalizations for upper gastrointestinal bleeds (UGIBs) are resource-demanding as they often require blood transfusion, endoscopy, and intensive care unit admission. Referral centers that provide higher levels of care to remote regions treat illnesses, including UGIB, in much later stages of disease and of higher severity. The Thunder Bay Regional Health Sciences Center (TBRHSC) is a referral center servicing over 250,000 people over a geographically expansive region of Northern Ontario. Despite known barriers to accessing care, little data is currently available to guide our understanding of UGIB aetiologies, severity, and outcomes among patients living remotely in Canada. Aims This retrospective study aimed to evaluate epidemiological data among patients with UGIB at TBRHSC. Methods Of 441 patients with a discharge diagnosis of gastrointestinal hemorrhage from 2016–2022, inclusion criteria were met for 333. Patients under 18 y or with lower GIB were excluded. Patients were classified as regional if their primary address was outside the District of Thunder Bay. Results Patients were highly comorbid (median CCI = 5) and presented with a median (IQR) GBS of 9 (6) and Clinical Rockall Score of 3 (1). Of those who received inpatient endoscopy (n=248), findings included erosive gastritis (21%), gastric ulcer (14%), esophagitis (12%), duodenal ulcer (8%), AVM (7%), and variceal (6%). No definite lesion was observed in 62 patients (22%). The median (IQR) Complete Rockall Score was 4 (2) with major stigmata of recent hemorrhage found in 20%. There was a high prevalence (19%) of cirrhosis, of which 83% had a history of liver decompensation. In 49% of cirrhotic patients, culprit lesions did not include portal hypertensive gastropathy or variceal bleeding. Regional patients accounted for 14% of the population and travelled an average of 424 km to seek care at TBRHSC. Regional patients were younger and required more ICU admissions (p=0.01). ICU admission primarily due to UGIB was 5.4% and all-cause thirty-day mortality was 3.3%. Oral anti-coagulation use prevalence was 43.2% and was associated with a longer length of stay (pampersand:003C0.0001), higher proportion of all-cause 30-day mortality (pampersand:003C0.005). Forty-eight patients did not receive endoscopy due to bleeding stability, palliation, and preference. Conclusions Patients with UGIB at TBRHSC are a highly multimorbid population with a significantly burden of anticoagulant use, cirrhosis, and variceal bleeding. Comparative analysis with metropolitan centers will expand our understanding for providing UGIB care in Northern Ontario. Funding Agencies NOAMA

Gastric antral vascular ectasia, also known as watermelon stomach - diagnosis and treatment

Gastric antral vascular ectasia (GAVE), also referred to as watermelon stomach is a rare disease accounting for about 4% of non-variceal upper gastrointestinal bleeding. It can manifest as occult bleeding requiring transfusion or acute gastrointestinal bleeding. This condition often coexists with liver cirrhosis, autoimmune diseases, heart failure, in patients post-bone marrow transplantation, or kidney failure. It is crucial to differentiate GAVE from portal hypertensive gastropathy (PHG), because despite a similar clinical presentation, the treatment for these conditions is different.&#x0D; Endoscopic diagnosis is necessary and in some cases, it may require further investigation and histopathological examination of the biopsy. Treatment is administered to patients with bleeding symptoms. Currently, the most commonly used treatment method is endoscopic thermal ablation using argon plasma coagulation.&#x0D; The focus of this work is to present essential information regarding the clinical picture, diagnosis and treatment of watermelon stomach.

Mitochondrial Dysfunction by FADDosome Promotes Gastric Mucosal Injury in Portal Hypertensive Gastropathy.

Mucosal epithelial death is an essential pathological characteristic of portal hypertensive gastropathy (PHG). FADDosome can regulate mucosal homeostasis by controlling mitochondrial status and cell death. However, it remains ill-defined whether and how the FADDosome is involved in the epithelial death of PHG. The FADDosome formation, mitochondrial dysfunction, glycolysis process and NLRP3 inflammasome activation in PHG from both human sections and mouse models were investigated. NLRP3 wild-type (NLRP3-WT) and NLRP3 knockout (NLRP3-KO) littermate models, critical element inhibitors and cell experiments were utilized. The mechanism underlying FADDosome-regulated mitochondrial dysfunction and epithelial death in PHG was explored. Here, we found that FADD recruited caspase-8 and receptor-interacting serine/threonine-protein kinase 1 (RIPK1) to form the FADDosome to promote Drp1-dependent mitochondrial fission and dysfunction in PHG. Also, FADDosome modulated NOX2 signaling to strengthen Drp1-dependent mitochondrial fission and alter glycolysis as well as enhance mitochondrial reactive oxygen species (mtROS) production. Moreover, due to the dysfunction of electron transport chain (ETC) and alteration of antioxidant enzymes activity, this altered glycolysis also contributed to mtROS production. Subsequently, the enhanced mtROS production induced NLRP3 inflammasome activation to result in the epithelial pyroptosis and mucosal injury in PHG. Thus, the FADDosome-regulated pathways may provide a potential therapeutic target for PHG.

«Арбузный» желудок — редкая причина хронической железодефицитной анемии

Aim. Demonstration of the rare in general medical practice cause of iron deficiency anemia in a patient with acute and chronic blood loss from vascular ectasias of the gastric mucosa. Key points. Iron deficiency anemia is one of the most common diseases in the world. The most common cause of anemia in gastroenterological practice is chronic or acute blood loss. Gastric antral vascular ectasia, or GAVE syndrome, is the cause of 4% nonvariceal bleeding from the upper gastrointestinal tract. Diagnosis of the disease requires careful endoscopic and histological examination to differentiate GAVE from similar changes (e.g. portal hypertensive gastropathy) and to choose the correct treatment ways. The presented clinical case demonstrates the difficulties of diagnosing the disease in a polymorbid patient, refractory to endoscopic treatments. Conclusion. GAVE syndrome is a rare but clinically significant cause of bleeding from the upper gastrointestinal tract. GAVE syndrome may be asymptomatic or accompanied by a clinical picture of anemia or obvious bleeding. Endoscopic treatment using argon plasma coagulation is considered first-line therapy in patients with GAVE syndrome, but most authors confirm the high rate of recurrence of gastrointestinal bleeding after the procedure. The presented clinical case clearly demonstrates a difficult path to the diagnosis of GAVE syndrome, which was finally verified after 7 years of follow-up of a patient with severe, refractory to the therapy iron deficiency anemia, only when a typical endoscopic picture of vascular ectasias in the antrum of the stomach organized in radial bands — the “watermelon” stomach was formed. At the same time, even the use of modern endoscopic treatment methods was not effective. Keywords: iron deficiency anemia, gastrointestinal bleeding, “watermelon” stomach, GAVE syndrome.

Outcomes of meso-Rex bypass for prehepatic portal hypertension in pediatric patients

Portal hypertension in pediatric patients is often associated with prehepatic portal hypertension (PHPH), frequently linked to thrombosis and cavernomatous degeneration of the portal vein (CDVP). This study evaluates the efficacy of the MesoRexBypass (MRB) in managing PHPH and associated thrombosis. MethodsA retrospective prognostic cohort design was employed to analyze the clinical outcomes of nine pediatric patients who underwent MRB between 2020 and 2022. Clinical and surgical variables were examined, including graft type, surgical time, and complications. Postoperative follow-up confirmed MRB functionality. ResultsThe MRB proved highly successful, with improved clinical parameters observed in all patients. Significant reductions in gastrointestinal bleeding, esophageal varices, and hypertensive gastropathy were observed postoperatively. Thrombocytopenia and liver enzyme levels showed substantial improvement, indicating enhanced liver function and amelioration of hypersplenism. The MRB's adaptability was demonstrated using autologous grafts and various graft sources.One patient experienced shunt thrombosis, another experienced minor gastrointestinal bleeding, and another died. The MRB exhibited a high success rate and few complications. ConclusionThe MRB is an effective and versatile surgical technique for managing PHPH in pediatric patients. This study emphasizes its promising outcomes and suggests its potential for enhancing treatment approaches and quality of life in this patient population. Further research with larger cohorts is needed to strengthen the evidence presented. The MRB holds promise as a valuable addition to the management of PHPH in children. Level of Evidence IV.

Endoscopic Evaluation among Patients Presenting with Upper Gastrointestinal Tract Bleeding

Background: Bleeding from the upper gastrointestinal tract is a critical medical condition that requires prompt diagnosis and management. Endoscopic evaluation plays a pivotal role in identifying the source of bleeding, determining its severity, and guiding appropriate interventions. Objective: The objective of this study was to conduct a comprehensive endoscopic evaluation in patients who have presented with bleeding originating from the upper gastrointestinal tract. Study Design: Descriptive cross-sectional study. Settings: Department of Gastroenterology, Islamic International Medical College, Rawalpindi Pakistan. Duration: Study duration was 7 months from November 2021 to April 2022. Methods: Patients who were 18 years of age or older and presented with active or recent upper gastrointestinal bleeding, regardless of gender, and were scheduled for endoscopic examination, were incorporated into the study. Upper gastrointestinal endoscopies were performed. The procedure was involving the direct visualization of the esophagus, stomach, and duodenum using an endoscope. Any visible lesions or bleeding sources were documented. Data regarding the location and nature of bleeding sources and the endoscopic diagnosis were recorded in a standardized data collection form and analyzed by SPSS version 26. Results: The study included 59 patients with a mean age of 52.27 years. Esophageal endoscopic findings revealed "Grade I to III Esophageal varices (EV) being less common (3.4%, 11.9%, and 13.6% respectively). LAX LEs, esophagitis and Hiatus hernia were observed in 10.2%, 3.4%, and 6.8% of cases. Rarer findings, including Venules, Ecstatic vein, Candidiasis, and various combinations, each accounted for 1.7% of cases. Portal hypertension gastropathy was the most prevalent condition (20.3%), followed by Antral gastritis (45.8%), Erosive gastropathy (10.2%), and other less frequent conditions, such as fundal varices, GOVI varices, diffuse gastritis and Ulcer. Grade II and III EV, and PHTN gastropathy, were significantly more prevalent among males, while Antral gastritis was notably higher among females (p &lt; 0.05). Although the endoscopic findings did not show any statistically significant differences based on gender (p &gt; 0.05). Conclusion: PHTN gastropathy, antral gastritis, grade III EV and erosive gastropathy were the most common conditions among patients with Hematemesis, along with less frequent findings like grade I to III Esophageal varices, Venules, Ecstatic vein, Candidiasis, and combinations of these conditions.

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 &amp;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.

Risk Stratification in Egyptian Patients with Upper Gastro Intestinal Bleeding

Abstract Introduction Acute upper gastrointestinal bleeding is a common and life-threatening condition. It remains a common cause of visits to the emergency department with an estimated incidence of about 100 per 100000 hospitalizations and being associated with significant morbidity, 30 day mortality and health-care costs. Urgent triage in emergency departments and risk stratification can help to identify patients who warrant urgent diagnostic and therapeutic procedures. We aimed to assess the correlation between Glasgow-Blatchford Bleeding Score, the AIMS65 score and Rockall score in sixty Egyptian patients with upper gastrointestinal bleeding, and to evaluate the best scoring system for risk stratification in these patients. Methods This prospective study included 60 Egyptian patients presented to Ain shams university hospital with upper gastrointestinal bleeding. All patients underwent emergency endoscopic evaluation within 12 hours of presentation. Surgical and radiological interventions were considered for patients who failed or were not feasible for endoscopic therapy. Rockall score, Glascow-Blatchford and AIMS65 were calculated for each patient. Results the age of the studied patients ranging between 20 and 81 years old with a mean age of 55.57 ± 13.14, of them 66.7% were males and 33.3% were females. Most of the patients (90%) had co-morbidities in the form of hepato-billiary diseases (70%), HTN (30%), DM (26.7%), cardiac disease (8.3%), and GIT related disorders (6.7%). Portal hypertension gastropathy was the most common finding in UGIT endoscopy (58.3%) followed by esophageal varcies (56.7%), then gastritis (30%), then peptic ulcer (20%) and lastly gastric mass (6.7%). Rockall score had significant association with altered mental status and liver cirrhosis. Rockall score was found to be the most effective predictor for mortality (sensitivity 100%, specificity 67.92% and AUC 91.0%). Conclusion complete Rockall score is the most effective scoring system for prediction of in hospital mortality in patients with upper gastrointestinal bleeding.

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

Diagnostic Approach and Pathophysiological Mechanisms of Anemia in Chronic Liver Disease—An Overview

Hematological abnormalities are frequently linked to chronic liver disease of any etiology. About 75% of patients with advanced chronic liver disease experience anemia. The causes of anemia are complex and multifactorial, particularly in cirrhotic patients. Acute and long-term blood loss from the upper gastrointestinal tract, malnutrition, an enlarged spleen brought on by portal hypertension, hemolysis, and coagulation issues are the main causes of anemia. Alcohol, a common cause of chronic liver disease, determines anemia through direct toxicity on the bone marrow, with the suppression of hematopoiesis, through vitamin B6, B12, and folate deficiency due to low intake and malabsorption. In patients with chronic hepatitis C virus infection, antiviral drugs such as pegylated interferon and ribavirin can also cause significant anemia. The use of interferon has been linked to bone marrow toxicity, and hemolytic anemia brought on by ribavirin is a well-known dose-dependent side effect. Within six months of the infection with hepatitis B, hepatitis C, and Epstein–Barr viruses, aplastic anemia associated with hepatitis is seen. This anemia is characterized by pancytopenia brought on by hypocellular bone marrow. Esophageal varices, portal hypertensive gastropathy, and gastric antral vascular ectasia can all cause acute and chronic blood loss. These conditions can progress to iron deficiency anemia, microcytic anemia, and hypochromic anemia. Another common hematologic abnormality in liver cirrhosis is macrocytosis, with multifactorial causes. Vitamin B12 and folate deficiency are frequent in liver cirrhosis, especially of alcoholic etiology, due to increased intestinal permeability, dysbiosis, and malnutrition. Many chronic liver diseases, like viral and autoimmune hepatitis, have a chronic inflammatory substrate. Proinflammatory cytokines, including tumor necrosis factor and interleukin 1, 6, and 10, are the main factors that diminish iron availability in progenitor erythrocytes and subsequent erythropoiesis, leading to the development of chronic inflammatory, normochromic, normocytic anemia.