Gastric Hyperplastic Polyps after Argon Plasma Coagulation for Gastric Antral Vascular Ectasia in Patients with Liver Cirrhosis: A Case Suggesting the "Gastrin Link Theory".

We herein report a case of gastric hyperplastic polyps after argon plasma coagulation (APC) for gastric antral vascular ectasia (GAVE) in the antrum of a 65-year-old man with liver cirrhosis and hypergastrinemia induced by long-term proton pump inhibitor (PPI) use. Two years after APC therapy, endoscopy demonstrated multiple gastric polyps in the antrum and angle. A gastric polyp biopsy indicated foveolar epithelium hyperplasia, which was diagnosed as gastric hyperplastic polyps. One year after switching to an H2 blocker antagonist, endoscopy revealed that the polyps and GAVE had disappeared, with normal gastrin levels suggesting that PPI-induced hypergastrinemia had caused gastric hyperplastic polyps after APC therapy, and the polyps had disappeared after discontinuing PPIs.

Gastric antral vascular ectasia in systemic sclerosis: Association with anti-RNA polymerase III and negative anti-nuclear antibodies.

OBJECTIVE: Gastric antral vascular ectasia (GAVE) is a vascular manifestation of systemic sclerosis (SSc) that can lead to iron deficiency anemia or acute gastrointestinal (GI) bleeding. We aimed to identify clinical features associated with GAVE. METHODS: We performed a cohort study of SSc patients who were seen at Stanford between 2004 and 2018 and had undergone esophagogastroduodenoscopy (EGD). We compared the clinical features of those with and without GAVE, and multivariable logistic regression was performed to identify clinical correlates with GAVE. RESULTS: A total of 225 patients with SSc who underwent EGD were included in this study and 19 (8.4%) had GAVE. Those with GAVE were more likely to have scleroderma renal crisis (SRC) (21% vs 3%; p < 0.01), positive anti-RNA polymerase III antibody (71% vs 19%; p < 0.01), nucleolar pattern of anti-nuclear antibody (ANA) (33% vs 11%; p=0.04), and negative ANA (<1:80 by immunofluorescence) (33% vs 11%; p=0.02). On multivariate analysis with multiple imputation, anti-RNA polymerase III positivity (OR 4.57; 95% CI (1.57 - 13.23), p < 0.01) and ANA negativity (OR 3.75; 95% CI (1.21 - 11.62), p=0.02) remained significantly associated with GAVE. CONCLUSION: Positive anti-RNA polymerase III antibody and ANA negativity were significantly associated with GAVE. Further studies are necessary to determine whether patients with these autoantibody profiles should undergo screening endoscopies for GAVE.

Gastric Antral Vascular Ectasia Pathogenesis and the Link to the Metabolic Syndrome.

PURPOSE OF REVIEW: Gastric antral vascular ectasia (GAVE) is a well-described source of chronic blood loss. We aim to review the previously hypothesized etiologies of GAVE and focus on recent proposed mechanisms, including metabolic syndrome. We will support these theories with newly discovered clinical associations and possible therapeutic implications. RECENT FINDINGS: Historically, GAVE has been associated with connective tissue disease and liver disease. Based on these associations and its histologic appearance, GAVE has presumed to be caused by mechanical- and hormonally mediated injury. Recent findings have been notable for a clinical association with aspects of the metabolic syndrome. Therefore, the pathogenic etiology may be akin to aspects of the metabolic syndrome via microvascular injury and neoangiogenesis. The potential etiologies of GAVE include hypergastrinemia, mechanical injury, and microvascular injury with neovascular proliferation particularly in the metabolic syndrome. Further research is needed to evaluate these proposed mechanisms and potential targets for treatment.

Orthotopic liver transplantation changes the course of gastric antral vascular ectasia: a case series from a transplant center.

BACKGROUND AND AIM: Gastric antral vascular ectasia (GAVE) is an important cause of upper gastrointestinal bleeding and anemia in patients with cirrhosis. The aim of our study was to evaluate the effect of orthotopic liver transplantation (OLT) on GAVE and associated anemia. PATIENTS AND METHODS: We performed a chart review and identified all cirrhotic patients with GAVE who underwent OLT at the University Of Alabama at Birmingham between 2005 and 2013. Population's demographics, etiology of cirrhosis, comorbidities, presentation and treatment modalities of GAVE, endoscopic and histopathologic reports, hemoglobin values before and after transplant, and immunosuppressive regimens were collected. RESULTS: Twelve patients were identified, mean age 52.4±4.4 years; seven were men (58.3%); 11 (91.7%) were White; and 6 of 12 patients had biopsy-proven GAVE. The most common etiology of cirrhosis in the cohort was chronic hepatitis C and obesity was the most common chronic condition in 50 and 83.3%, respectively. Anemia resolution was observed in 9/12 (75%) patients who underwent OLT with an increase in hemoglobin from 8.1±2.4 (5.7-13.1) before transplant to 12.0±1.4 (10-15) after transplant (P<0.0001). Esophagogastroduodenoscopy after transplant was performed in all 12 (100%) patients. The mean time between transplant and post-OLT esophagogastroduodenoscopy was 13.8±18.28 (2-57) months; complete resolution of GAVE was observed in 10 (83.3%) patients, with resolving GAVE in one (8.3%) patient. CONCLUSION: GAVE is an important cause of anemia and upper gastrointestinal bleeding in patients with liver cirrhosis. Our findings show that liver transplantation can resolve GAVE and related anemia.

Gastric antral vascular ectasia in systemic sclerosis: Where do we stand?

Gastric antral vascular ectasia (GAVE) continues to be a challenge in both diagnosis and treatment. GAVE has a diverse group of associations and presumed causes, including cirrhosis, chronic renal failure and autoimmune connective tissue diseases. However, in most occasions, the management plan of GAVE itself is the same whatever the underlying disease by using Argon plasma coagulation (APC). Herein, we will discuss three cases of systemic sclerosis-associated GAVE presenting with either acute or chronic gastrointestinal bleeding showing variable responses to APC. Anemia and telangiectasia may be the first striking presentation of systemic sclerosis (SSc). Renal artery stenosis, aortic stenosis, widespread cutaneous and mucosal telangiectasia and hypertension seem to be associated with poor prognosis and should prompt rapid intervention and careful follow-up. Moreover, the hunt for molecular underpinnings of the broad array of vascular lesions in SSc has to include von Willebrand factor and endoglin. Eventually, we will review the recent alternatives that can be effective in SSc-GAVE, such as band ligation, hematopoietic stem cells transplantation and immunotherapy.

The Efficacy of Virtual Chromoendoscopy in the Diagnosis of Portal Hypertensive Gastropathy.

BACKGROUND: Diagnosis of portal hypertensive gastropathy (PHG) is based on endoscopic criteria. I-scan technology, a new technique of virtual chromoendoscopy, increases the diagnostic accuracy for lesions in the gastrointestinal tract. AIM: To establish the role of i-scan endoscopy in the diagnosis of PHG. METHOD: In this prospective study, endoscopic examination was conducted first by using white light and after that i-scan 1 and i-scan 2 technology in a group of 50 consecutive cirrhotic patients. The endoscopic diagnostic criteria for PHG followed the Baveno criteria. The interobserver agreement between white light endoscopy and i-scan endoscopy was determined using Cohen's kappa statistics. RESULTS: Forty-five of the 50 patients met the diagnostic criteria for PHG when examined by i-scan endoscopy and 39 patients were diagnosed with PHG by white light endoscopy. The strength of agreement between the two methods for the diagnosis of PHG was moderate (k=0.565; 95%CI 0.271-0.859; p<0.001). I-scan 1 classified the mosaic pattern better than classic endoscopy; i-scan 2 described better the red spots. CONCLUSION: I-scan examination increased the diagnostic sensitivity of PHG. The diagnostic criteria (mosaic pattern and red spots) were easier to observe endoscopically using i-scan than in white light.

Systemic mastocytosis: A rare cause of non-cirrhotic portal hypertension.

Mastocytosis is a clonal neoplastic disorder of the mast cells (MC) that can be limited to the skin (cutaneous mastocytosis) or involve one or more extracutaneous organs (systemic mastocytosis). The clinical manifestations of mastocytosis are heterogeneous ranging from indolent disease with a long-term survival to a highly aggressive neoplasm with survival of about 6 mo. Although liver involvement in aggressive systemic mastocytosis (ASM) is relatively common, the development of portal hypertension with or without cirrhosis is rare. We report a case of ASM without skin involvement in a 72-year-old caucasian male who presented with non-cirrhotic portal hypertension based on clinical, analytical, imagiological and endoscopic findings. Given the hematological picture, the correct diagnosis was established based on ancillary tests for MC using bone marrow aspirates and biopsy. Extensive involvement of the liver and gastrointestinal tract was histologically documented. The disease progressed rapidly and severe pancytopenia and recurrent upper gastrointestinal bleeding became the dominant problem. This case illustrates the challenge in establishing a diagnosis of ASM especially when the clinical picture is atypical and without skin involvement. Gastroenterologists should consider infiltrative disease, particularly systemic mastocytosis, as a differential diagnosis in a clinical case of portal hypertension of unknown etiology.

Gastrointestinal Issues in Liver Disease.

Gastrointestinal (GI) complications of cirrhosis are frequent in patients who require intensive care support and are often the primary indication for intensive care unit (ICU) admission. Perhaps the most worrisome GI complication for the intensivist is variceal hemorrhage. Bleeding from esophageal or gastric varices represents a life-threatening event for cirrhotic patients and provides management challenges for the ICU team. Nonvariceal GI bleeding, impaired GI motility, and malnutrition also provide significant challenges for the intensivist. This article reviews GI issues that present in critically ill cirrhotic patients and their management in the acute setting.

Interpretation of an Extended Autoantibody Profile in a Well-Characterized Australian Systemic Sclerosis (Scleroderma) Cohort Using Principal Components Analysis.

OBJECTIVE: To determine the relationships between systemic sclerosis (SSc)-related autoantibodies, as well as their clinical associations, in a well-characterized Australian patient cohort. METHODS: Serum from 505 Australian SSc patients were analyzed with a commercial line immunoassay (EuroLine; Euroimmun) for autoantibodies to centromere proteins CENP-A and CENP-B, RNA polymerase III (RNAP III; epitopes 11 and 155), the 90-kd nucleolar protein NOR-90, fibrillarin, Th/To, PM/Scl-75, PM/Scl-100, Ku, topoisomerase I (topo I), tripartite motif-containing protein 21/Ro 52, and platelet-derived growth factor receptor. Patient subgroups were identified by hierarchical clustering of the first 2 dimensions of a principal components analysis of quantitative autoantibody scores. Results were compared with detailed clinical data. RESULTS: A total of 449 of the 505 patients were positive for at least 1 autoantibody by immunoblotting. Heatmap visualization of autoantibody scores, along with principal components analysis clustering, demonstrated strong, mutually exclusive relationships between CENP, RNAP III, and topo I. Five patient clusters were identified: CENP, RNAP III strong, RNAP III weak, topo I, and other. Clinical features associated with CENP, RNAP III, and topo I were consistent with previously published reports concerning limited cutaneous and diffuse cutaneous SSc. A novel finding was the statistical separation of RNAP III into 2 clusters. Patients in the RNAP III strong cluster had an increased risk of gastric antral vascular ectasia, but a lower risk of esophageal dysmotility. Patients in the other cluster were more likely to be male and to have a history of smoking and a history of malignancy, but were less likely to have telangiectasia, Raynaud's phenomenon, and joint contractures. CONCLUSION: Five major autoantibody clusters with specific clinical and serologic associations were identified in Australian SSc patients. Subclassification and disease stratification using autoantibodies may have clinical utility, particularly in early disease.

[Gastric vascular lesions in cirrhosis: gastropathy and antral vascular ectasia]. / Lesiones vasculares gástricas en la cirrosis: gastropatía y ectasia vascular antral.

Portal hypertensive gastropathy (GHP) is a complication of portal hypertension usually associated with liver cirrhosis. The pathogenesis is unclear but the presence of portal hypertension is an essential factor for its development. GHP may be asymptomatic or present as gastrointestinal bleeding or iron deficiency anemia. Endoscopic lesions vary from a mosaic pattern to diffuse red spots; the most common location is the fundus. Treatment is indicated when there is acute or chronic bleeding, as secondary prophylaxis. There is insufficient evidence to recommend primary prophylaxis in patients who have never bled. Drugs that decrease portal pressure, such as non-cardioselective beta-blockers, and/or endoscopic ablative treatments, such as argon-beam coagulation, may be used. The role of transarterial intrahepatic portosystemic shunt) or bypass surgery has been insufficiently analyzed. Antral vascular ectasia (EVA) is a rare entity in liver cirrhosis, whose pathophysiology is still unknown. Clinical presentation is similar to that of GHP and endoscopy usually shows red spots in the antrum. Biopsy is often required to differentiate EVA from GHP. There is no effective medical therapy, so endoscopic ablative therapy and, in severe cases, antrectomy are recommended.