Portal Hypertension and Chronic Kidney Disease Significantly Increase the Risk of Early Unplanned Readmissions in GAVE- Related Admissions.

BACKGROUND AND AIMS: Gastric antral vascular ectasia (GAVE) is an uncommon cause of non-variceal upper gastrointestinal bleeding that is characterized by dilation of blood vessels in the antrum of the stomach. Various co-morbidities are associated with the development of GAVE, but the impact of co-morbidities on unplanned GAVE readmissions is unclear. The aim of this study was to assess the national incidence, 30-day mortality rate, and 30-day readmissions related to GAVE. Secondary outcomes were evaluation of predictors of early readmission, hospital length of stay (LOS) and total hospitalization charges. METHODS: Using the 2016 National Readmission Database, we analyzed discharges for GAVE. ICD-10 CM codes were utilized to identify associated comorbidities and inpatient procedures during the index admission. 30-day readmissions were identified for GAVE. Secondary measures of outcomes including LOS and hospitalization charges were also calculated. Risk factors for early readmission were also evaluated using multivariate analysis to adjust for confounders. RESULTS: A total of 18,375 index admissions for GAVE were identified. 20.49% (n=3,720) of the discharged patients were readmitted within 30 days. 30-day mortality of GAVE-related admissions was 1.82% (n=335). Early readmissions accounted for 20,157 hospital days along with $189 million in hospitalization costs. Multivariate analysis revealed that the presence of portal hypertension (OR 1.63; 95% CI 1.37-1.93; p=0.0001) and chronic kidney disease (CKD) (OR 1.62, 95% CI 1.44-1.82; p<0.0001) significantly increased the odds of early readmission. CONCLUSIONS: Our analysis demonstrates that the overall 30-day mortality rate of GAVE-related admissions is relatively low, but the 30-day readmission rate is significantly high. Patients with comorbid CKD and portal hypertension have a significantly higher risk of readmission. Further studies are required to determine if therapeutic interventions such as argon plasma coagulation or radiofrequency ablation during the index admission may prevent readmissions in these specific subgroups.

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.

Antral mucosal perfusion is not increased in GAVE.

OBJECTIVES: Although a common cause of intestinal blood loss, the pathophysiology of gastric antral vascular ectasia (GAVE) is not well understood. We aimed to evaluate gastric antral and body mucosal flow in GAVE patients compared to a control population using laser Doppler flowmetry. METHODS: 27 patients with GAVE and 11 control patients without GAVE were evaluated using an endoscopic LDF probe. The probe was placed in the gastric antrum and body in order to calculate standardized mucosal flow rates recorded as perfusion units (PU). RESULTS: Despite its hyperemic appearance and propensity to bleed, antral blood flow was not increased in GAVE: 115.5 PU (IQR: [94.4, 135.9 PU]) in GAVE versus 123.7 PU (IQR: [109.7, 186.5 PU]) in controls. There was a significant gradient between the gastric body and antral blood flow in GAVE (p < 0.001) that was not evident in controls. CONCLUSION: These results indicate that antral mucosal blood flow is not increased in GAVE despite its grossly hyperemic appearance. A mild but statistically significant gradient was noted between the gastric antrum and body in patients with GAVE compared to controls. The pathophysiological significance of this finding is uncertain.

[VENOUS ECTASIA OF GASTRIC ANTRUM].

Gastric antral vascular ectasia (GAVE) is an uncommon but often severe cause of upper gastrointestinal bleeding. GAVE may be asymptomatic or accompanied by clinical anemia or overt gastrointestinal bleeding. The diagnosis is mainly based on pathognomonic endoscopic pattern, defined as «watermelon stomach¼, located in antrum. Autoimmune disorders aye co-existing in about 60% of patients with GAVE, chirrosis in about 30%, and cardiac or renal failure in 10%.The "golden standarden" treatment of GAVE is endoscopic argon plasma coagulation (APC). There is poor information about diagnostics and treatment of GAVE in the domestic literature. The analysis of the presented materials shows that correct diagnostics takes much time and the choice of the optimum optimal treatment strategy encounters difficulty. Our experience with diagnostics and therapy of GAVE is based on the treatment of 4 patients. The diagnosis of GAVE was established within the period from 5 months to 1.5 years after onset of the disease. In two cases, GAVE was asymptomatic. Two patients with severe anemia completed endoscopic treatment; in one case, APC was supplemented by laser coagulation and bipolar coagulation. The implementation of laser coagulation caused some technical difficulties. Treatment of both patients was successful. Endoscopy pivotal for diagnosis of GAVE is the main method of its treatment. Due to the large number of diagnostic errors and the importance of correct diagnosis of GAVE, it is necessary to pay attention to this issue in training programs for endoscopists.

[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.

Successful treatment of refractory gastric antral vascular ectasia by distal gastrectomy: a case report.

Gastric antral vascular ectasia (GAVE) is an uncommon and often neglected cause of gastric hemorrhage. The treatments for GAVE include surgery, endoscopy and medical therapies. Here, we report an unusual case of GAVE. A 72-year-old man with a three-month history of recurrent melena was diagnosed with GAVE. Endoscopy revealed the classical "watermelon stomach" appearance of GAVE and complete pyloric involvement. Melena reoccurred three days after argon plasma coagulation treatment, and the level of hemoglobin dropped to 47 g/L. The patient was then successfully treated with distal gastrectomy with Billroth II anastomosis. We propose that surgery should be considered as an effective option for GAVE patients with extensive and severe lesions upon deterioration of general conditions and hemodynamic instability.

Review article: the management of portal hypertensive gastropathy and gastric antral vascular ectasia in cirrhosis.

BACKGROUND: Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are important causes of both acute and chronic gastrointestinal bleeding in patients with cirrhosis. AIM: To review the current management of PHG and GAVE. METHODS: PubMed was searched for English language articles using the key words 'GAVE', 'gastric antral vascular ectasia', 'cirrhosis', 'gastrointestinal bleeding', 'acute', 'chronic', 'portal hypertensive gastropathy', 'watermelon stomach', 'radiofrequency ablation', 'band ligation', 'thermoablation' and 'TIPSS'. RESULTS: GAVE and PHG are both encountered in patients with cirrhosis. They can be seen in asymptomatic patients and in those with either acute or chronic gastrointestinal bleeding. PHG, by definition, requires the presence of portal hypertension, with or without cirrhosis, whereas GAVE requires neither cirrhosis nor portal hypertension. They can often be diagnosed on endoscopic appearance alone, but may require biopsy in certain cases. The treatment of PHG is aimed at reducing hepatic venous pressure gradients, most often by pharmacologic means, but may require shunt procedures in severe cases. Management of GAVE on the other hand is predominantly endoscopic, focusing on various ablative techniques. CONCLUSIONS: Gastric antral vascular ectasia and portal hypertensive gastropathy are distinct entities and are both encountered in cirrhotic patients. Management of portal hypertensive gastropathy is centred on reduction in portal pressures, whereas treatment of gastric antral vascular ectasia is predominantly endoscopic.

Coronary artery calcification score is increased in patients with isolated coronary artery ectasia.

PURPOSE: Coronary artery calcification (CAC) is an indicator of coronary atherosclerosis and is associated with future adverse cardiac events. Isolated coronary artery ectasia (CAE) is defined as localized or diffuse dilation of the coronary arteries without coronary stenosis. The aim of this study was to assess the relationship between CAC and isolated CAE. METHODS: Thirty-four patients with isolated CAE and 50 controls subjects, with normal coronary arteries, were enrolled in the study. Baseline demographic features and atherosclerosis risk factors were similar in both groups. RESULTS: Patients with CAE had higher total CAC than control subjects (84±111 vs. 33.5±103.5; p<0.001). There was also a significant correlation between per-segment CAC and ectatic segment length (r=0.32; p=0.01) but no correlation with diameter (r=0.09; p=0.5). CONCLUSION: Patients with isolated CAE had higher CAC than control subjects, suggesting that atherosclerosis may be involved in the pathogenesis of isolated CAE. Patients with isolated CAE may have increased cardiovascular risk and should receive appropriate risk stratification and relevant medical treatment.

Gastric antral vascular ectasia and its clinical correlates in patients with early diffuse systemic sclerosis in the SCOT trial.

OBJECTIVE: To describe the prevalence and clinical correlates of endoscopic gastric antral vascular ectasia (GAVE; "watermelon stomach") in early diffuse systemic sclerosis (SSc). METHODS: Subjects with early, diffuse SSc and evidence of specific internal organ involvement were considered for the Scleroderma: Cyclophosphamide Or Transplant (SCOT) trial. In the screening procedures, all patients underwent upper gastrointestinal endoscopy. Patients were then categorized into those with or without endoscopic evidence of GAVE. Demographic data, clinical disease characteristics, and autoantibody data were compared using Pearson chi-square or Student t tests. RESULTS: Twenty-three of 103 (22.3%) individuals were found to have GAVE on endoscopy. Although not statistically significant, anti-topoisomerase I (anti-Scl70) was detected less frequently among those with GAVE (18.8% vs 44.7%; p = 0.071). Similarly, anti-RNP antibodies (anti-U1 RNP) showed a trend to a negative association with GAVE (0 vs 18.4%; p = 0.066). There was no association between anti-RNA polymerase III and GAVE. Patients with GAVE had significantly more erythema or vascular ectasias in other parts of the stomach (26.1% vs 5.0%; p = 0.003). CONCLUSION: Endoscopic GAVE was present on screening in almost one-fourth of these highly selected patients with early and severe diffuse SSc. While anti-Scl70 and anti-U1 RNP trended toward a negative association with GAVE, there was no correlation between anti-RNA Pol III and GAVE. Patients with GAVE had a higher frequency of other gastric vascular ectasias outside the antrum, suggesting that GAVE may represent part of the spectrum of the vasculopathy in SSc.

The management of portal hypertensive gastropathy and gastric antral vascular ectasia.

Portal hypertensive gastropathy and gastric antral vascular ectasia are gastric mucosal lesions that can cause chronic gastrointestinal haemorrhage and, consequently, chronic anaemia, in patients with cirrhosis. Although chronic anaemia is the most common clinical manifestation, these entities may also lead to acute gastrointestinal bleeding. Despite similar clinical manifestations, their pathophysiology and management are entirely different. Their diagnosis is endoscopic and although generally each of them has a characteristic endoscopic appearance and distribution, there are cases in which the differential is difficult and must rely on histology. This review focuses on the management of both entities. The mainstay of management of portal hypertensive gastropathy is based on portal-hypotensive pharmacological treatment whilst gastric antral vascular ectasia benefits from endoscopic therapy. More invasive options should be reserved for refractory cases.

Management of gastropathy and gastric vascular ectasia in portal hypertension.

Portal hypertensive gastropathy and gastric antral vascular ectasia may cause gastrointestinal hemorrhage in patients with portal hypertension. Whereas the former presents exclusively in patients with portal hypertension, gastric antral vascular ectasia can also be observed in patients with other conditions. Diagnosis is established with upper gastrointestinal endoscopy, although some cases may require a biopsy to confirm the diagnosis. The most frequent manifestation is ferropenic anemia, which may become transfusion dependent. Treatment in portal hypertensive gastropathy is focused on portal pressure reducing drugs, mainly nonselective beta-blockers, whereas in gastric antral vascular ectasia treatment is based on endoscopic ablation. More invasive options can be used if first-line therapies fail, although these should be evaluated on a case-by-case basis.

Portal hypertensive gastropathy: a review.

Portal hypertensive gastropathy (PHG) occurs as a complication of cirrhotic or non-cirrhotic portal hypertension. Although the pathogenesis of PHG is not completely understood, evidence suggests that the key factor for the development of PHG is portal hypertension. PHG is clinically important because it may cause acute (and even) massive or insidious, blood loss. The diagnosis of PHG is (only) made endoscopically; it is most often characterized by an abnormality of the gastric mucosa described as a mosaic-like pattern resembling 'snake-skin', with or without red spots and the endoscopic pattern is key its diagnosis. Unfortunately, standardization of the endoscopic diagnostic criteria for PHG is poor and consensus is generally lacking, resulting in a wide range of reported prevalence. Pharmacological therapies, presumably reducing portal pressure and gastric blood flow, have been used to treat acute bleeding; propanolol, a non-selective beta-blocker (24-480 mg/day), has been used most frequently. Endoscopic treatment for PHG bleeding plays a small, if any, role in the treatment of PHG. TIPS and shunt surgery have not been extensively analysed as a treatment for acute or chronic PHG bleeding, but they appear to lessen the severity of PHG. Secondary prophylaxis of PHG bleeding with non-selective beta-blockers is recommended. There is not enough evidence to support the use of beta-blockers in primary prophylaxis of PHG bleeding, even in cases of severe PHG (however, non-selective beta-blockers are recommended if varices are present). Further studies are needed to clarify the role of PHG in suspected chronic gastrointestinal bleeding.

Gastric antral vascular ectasia (GAVE) in a non-cirrhotic patients with diabetes: case report and possible pathophysiological mechanism.

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon but well-described cause of recurrent upper gastrointestinal bleeding or iron deficiency anaemia. Atiology is unknown but several associated diseases have been reported like connective tissue or autoimmune disorders or cirrhosis. Cases have been reported in systemic sclerosis, achlorhydia, atrophic gastritis and chronic renal failure. The most common cause is portal hypertension and portal hypertensive gastropathy. This is especially so after eradication of oesophageal varices by sclerotherapy or banding. Diabetic complications are characterised by microvascular diseases especially in the retina, glomerulus and vasa nervorum. It involves apoptosis and remodelling of endothelial cells. Hyperglycaemia is an essential cause of reactive oxygen species (ROS)-mediated oxidative stress in this complication. Angiopathy of gastric mucosa in diabetes mellitus has not been reported so far in the literature. We are presenting an interesting case of diabetes mellitus with gastric vascular ectasia without evidence of any other systemic illness.

Argon photocoagulation in the treatment of gastric antral vascular ectasia and radiation proctitis.

Gastric antral vascular ectasia (GAVE) and radiation proctitis are two vascular disorders of the gastrointestinal tract that typically present with recurrent gastrointestinal bleeding. Although the pathogenesis of either condition is not known, they are unlikely to be similar. GAVE appears to be related to autoimmune disorders or cirrhosis, while radiation proctitis is the result of pelvic irradiation, most commonly used for the treatment of pelvic malignancies. Medical therapies for both conditions are not typically effective, and surgical therapies are usually not required because endoscopic treatment, aimed at coagulation of the underlying vascular lesions, has evolved as the most effective therapy. There is limited evidence in the literature for the use of medical and surgical therapies, with most of the evidence coming from case reports involving small numbers of patients. In the present article, we review the evidence for the use of argon plasma photocoagulation (APC, the most commonly used endoscopic modality) in the treatment of GAVE and radiation proctitis.

Gastric antral vascular ectasia (GAVE): an update on clinical presentation, pathophysiology and treatment.

Gastric antral vascular ectasia (GAVE), though a rare disorder, causes up to 4% of non-variceal upper GI bleeding. This paper gives an overview of studies examining clinical presentation and pathophysiology, and reviews the current evidence for invasive and non-invasive treatments. GAVE is often associated with systemic illnesses, such as cirrhosis of the liver, autoimmune connective tissue disorders, bone marrow transplantation and chronic renal failure. The pathophysiological changes leading to GAVE have not been fully explained and remain controversial. Patient presentation varies from chronic iron-deficiency anaemia to heavy acute gastrointestinal bleeding. It is important to differentiate GAVE from portal hypertensive gastropathy as GAVE does not respond to measures reducing portal pressures. Endoscopic ablation (Nd:YAG-laser or argon plasma coagulation) is the first-line treatment of choice. As evidence for pharmacological therapy with oestrogen (and/or progesterone), tranexamic acid or thalidomide stems from case reports only, these should be used if endoscopic measures have failed to stop chronic blood loss. Surgical antrectomy should be reserved for unresponsive cases as it is associated with a high mortality. Ultimately, treatment of the underlying medical co-morbidities may lead to resolution of GAVE.

Watermelon stomach: pathophysiology, diagnosis, and management.

Watermelon Stomach (WS) has been increasingly recognized as an important cause of occult gastrointestinal blood loss. Clinically, patients develop significant iron deficiency anemia and are frequently transfusion dependent. The histologic hallmark of WS is superficial fibromuscular hyperplasia of gastric antral mucosa with capillary ectasia and microvascular thrombosis in the lamina propria. Endoscopic findings of the longitudinal antral folds containing visible columns of tortuous red ectatic vessels (watermelon stripes) are pathognomonic for WS. Trauma to the mucosal epithelium overlying engorged vessels by gastric acid or intraluminal food results in bleeding. Treatment options for WS include endoscopic, pharmacologic, and surgical approaches. Endoscopic therapy, including contact and non-contact thermal ablations of the angiodysplastic lesions, is the mainstay of conservative therapy. However, many patients fail endoscopic therapy and develop recurrent acute and chronic GI bleeding episodes. Surgical resection may be the only reliable method for achieving a cure and eliminating transfusion dependency. Traditionally, surgery was used only as a last resort after patients failed prolonged medical and/or endoscopic therapy. However, based on the experience garnered from the literature we recommend a more aggressive surgical approach in patients who fail a short trial of endoluminal therapy.

Portal hypertension and portal hypertensive gastropathy in patients with liver cirrhosis: a haemodynamic study.

BACKGROUND/AIM: The relationships between the levels of portal hypertension and the morphologic alterations of gastric mucosa in patients with liver cirrhosis--generally described as portal hypertensive gastropathy--are poorly defined. PATIENTS: In total, 62 patients with cirrhosis of different aetiologies, were examined by endoscopy and measurement of portal hypertension by hepatic venous pressure gradient. RESULTS: Portal hypertensive gastropathy was observed in 49 cases; six patients showed gastric antral vascular ectasia always associated with gastric lesions described as severe portal hypertensive gastropathy with different localizations. Hepatic venous pressure gradient showed severe portal hypertension in 37 cases, and averaged 17.7 +/- 4.3 mmHg. It was much higher in patients with severe lesions (p=0.0004). Hepatic venous pressure gradient in patients with endoscopic signs of isolated antral gastropathy was lower (p=0.04) than in those with isolated lesions in body-fundus. No relationship was found between hepatic function, as assessed by the Child-Pugh score, and portal hypertensive gastropathy. CONCLUSIONS: The present data suggest that the severity of portal hypertensive gastropathy is related to portal hypertension, but portal hypertension is not the sole determinant of the occurrence of endoscopic abnormalities of gastric mucosa. The derangement of liver function does not appear to play any role in the occurrence of portal hypertensive gastropathy.

Cure of gastric antral vascular ectasia by liver transplantation despite persistent portal hypertension: a clue for pathogenesis.

Gastric antral vascular ectasia (GAVE) is a rare cause of chronic bleeding in cirrhotic patients. It has been suggested that these gastric lesions might be related to portal hypertension, hepatic insufficiency, or both parameters. We report two cases of cirrhotic patients in whom GAVE was the source of recurrent bleeding. These patients also had complete portal vein thrombosis. Liver transplantation was performed and an end-to-end cavoportal anastomosis was performed, leaving patients with persistent portal hypertension after surgery. We observed complete disappearance of the antral lesions several weeks after transplantation, which shows that the GAVE is not related to portal hypertension but is rather a direct consequence of liver failure. Possible pathophysiologic mechanisms are discussed.